Immunologist and Infectious Diseases Research Scientist by day, ultra runner and mountain adventurer in my spare time. Blogging about whatever comes up in life.
Seven years
ago a crazy idea was hatched out of an online discussion on 14ers.com, how many
14,000ft peaks was it possible to climb in 24hours, and what would be the
optimal linkup? I love 14ers, and I love logistical challenges, so I set out
working some variations and timing, scouted a few lines and put some wheels in
motion. I made my first go at the linkup in July 2013 as a training run leading
up to UTMB, ultimately bowing out after tagging Sherman in 18h37min, for a
total of 9 summits. At the time it was a good first effort, but I felt that I
had a left a lot more potential out there and that 12 was feasible on a good
day. Since 2013 several others have improved upon my original 9 summits,
pushing the number to 11 summits in 22h, though still no one had crossed the 12
peak threshold.
Smokey views from the Mt Evans Rd, 9/18/20.
After a summer of running around the mountains, I was searching for a little inspiration, something to cap the summer and add a little extra motivation to the weird race-less Covid year it’s been. The opportunity presented itself, so I worked the schedules, lined up a driver and was set to go. Friday morning at 430a my friend Misti picked me up and we headed out for the Mt Evans Rd, the starting point for the journey. At 6:11am on 9/18/20 I clicked the watch and started jogging up the Rd to Mt Evans. It was cool and breezy, smoke hanging in the air from all the wildfires, but on I ran. I hit summit lake at 1:10 and busted up the NE slope to the summit (1:43). For some reason I thought I was behind schedule so I cranked my way across the Sawtooth, gasping as I scampered around the snow on Bierstadt, hitting the summit in 2:38. Even though it was a Friday it was a bit of a cluster, so I wasted no time and hammered down the trail, passing dozens upon dozens of onlookers, not even registering their comments or questions, reaching the Guanella Pass Rd, and eventually 11000ft at 3:25 (10min ahead of schedule).
Headed across the Sawtooth to Mt Bierstadt.
Finally a bit of downhill after dodging the crowds atop Mt Bierstadt.
I jumped in the car, and Misti promptly took off for Stevens Gulch as I packed my water, food and gear for the next leg of the journey. The word of the day was ‘efficient’. We pulled up to the Stevens Gulch TH, I jumped out, poles in hand and headed straight onto the trail for Torreys Peak. I dug into the trail, and found a steady rhythm up and over Torreys (5:31) and over to Grays (5:55). Thankfully the trail wasn’t too busy and CFI has done some great work, allowing me to cruise at a quick pace back down to the car where Misti had a cup o’noodle waiting and off we bounced down the Stevens Gulch Rd, next stop Quandary!
Headed up Torreys and Grays Peak.
We had a good rhythm going, I’d stuff my pack with food, water and gear, eat something solid and do some recovery work on my legs while we drove. After a short nap we navigated our way onto the Blue Lakes Rd on the South side of Quandary Peak, where I again hopped out of the car at 11200ft, intent on making quick work out of the dirt road section. I soon crested the dam at Blue Lake, and struck off on the climbers trail headed for Cristo Couloir. My semi-secret shortcut and little known fact that it’s only 2mi from 11200ft to the summit of Quandary via Cristo (1mi gaining 2300ft!). I’ve always been good at digging my poles in and just grinding out slow vert, so that’s what I did. Reaching the summit of Quandary Peak at 9:06 (1:24 from the car) to cloudy cool skies with only one other person in site. I made quick work of the steep loose descent, getting back to the car in 37min (9:43)! Then began the frantic recovery and repacking effort before we hit the Kite Lake Rd, this would be the shortest turn around, and with a long loop of the DeCaLiBron to come.
Looking down Cristo Couloir on my way up Quandary.
Misti dropped me at 11100ft on the Kite Lake Rd at 10:07 (4:45pm) and I began the long slog up to Kite Lake and Mt Democrat. After 10hours I wasn’t feeling as spry but I just kept grinding away, for the first time starting to struggle a bit on the uphills, reaching the summit of Mt Democrat at 11:52 (1:45 from the car), slower than I’d hoped for, but still on pace overall. I made decent time over to Mt Lincoln (12:48), spurred on by a bitter cold wind that froze my fingertips. Soon after I crested Mt Bross as the evening light faded into blackness, I paused long enough to take in the fact that I’d had the entire DeCaLiBron to myself, a rare occurrence. The darkness made the rocky descent far tougher than I’d expected, and I rolled back to the car at 14:13. For the first time all day I was a bit beat up, and was looking forward to the long drive over to Missouri Gulch, a chance to rest and recharge before the long night ahead. I refueled and napped as Misti drove, and before I knew it we were bumping down the Winfield Rd, screeching to a halt because we’d flow right by the trailhead!
Cold and windy sunset run up Mt Lincoln, all by my lonesome.
After a quick double check of my gear and food stores I bid Misti farewell and set off into the darkness. I put on some music and just focused on strong and solid movement upwards. I was hitting my splits as I neared treeline, but I could feel the strain in my breathing. As I began to climb the endless switchbacks to Mt Belford I knew I was in for a challenging night. My lungs felt congested and I couldn’t seem to get a full breath, forcing me to take breaks far more often that I wanted just to catch my breath. The switchbacks seemed to drag on forever, made worse by the lingering snow and ice that further slowed progress. At this point I was feeling very demoralized, moving as fast as I could muster, reaching the summit of Belford in 2:31 from the trailhead (18:16). It was dark, cold and I was struggling mentally to stay motivated.
Final bit of light fading away on the Rocky Mountains.
I pushed on
to Oxford, once again forced to dodge a bunch of awkward snow and ice blocking
the trail, reaching Oxford in 0:47 (19:03), far slower than what I know I’m
capable of. On the summit of Oxford I did some fuzzy math, realizing that at my
current pace it was gonna be tough to break the current FKT of 11 summits in
22h. When I’d started up from the trailhead 11 summits seemed almost a
certainty and 12 seemed very reasonable, but now I was struggling to fathom
climbing 11 in the allotted time. As I descended back to Elkhead Pass I was
able to talk myself out of the funk….you know these routes, there’s still time
on the clock, so keep pushing forward until you run out of time, nothing is
certain.
The grind
up Missouri felt like death, but I pushed on as hard as I could. 13000ft…..13200ft….13500ft…..
dodging a few more snow patches, and not happy to see that my scree shortcuts
down the SW face of Missouri was blocked by drifted snow from the prior week’s
storm, so I’d have to go around the long way. At last I crested the summit of
Missouri Mt, summit #11 at 21:00, giving me an hour to traverse the ridge and drop
3000ft to Clohesy Lake, a task that felt nearly impossible at the moment, but
still off I went.
The glory of sleep deprivation and the excitement of endurance events…nap time.
I pushed across Missouri’s NW ridge as fast as I could move in the dark, the whole things is a blur in my memory. I finally turned West and began to drop, astonished to find that the popularity of Nolans had hacked a real trail into the ridge (when I began scouting 13 years ago, no trail existed). This gave me a fighting chance, because descending 2800ft on a steep rough trail in 40min was definitely within the realm of possibility! I charged downhill as fast as my legs and lungs would allow, sliding out now and again, but losing elevation in a hurry. At last I dropped out of the upper basin and began descending to Clohesy Lake. The final mile of trail seemed to take forever, but as I neared 11200ft I turned my path straight down the tundra to the lake, collapsing on the edge of Clohesy Lake at 10991ft at 4:01am on 9/19/20, 21hours and 50min after starting my journey on the Mt Evans Rd the previous day. There had been so much doubt and uncertainty the previous 4hours that I’d actually make it to this point that I was relieved, excited, exhausted and beat to shit. The only thing left to do was trudge my way out of the mountains and back down to the Winfield Rd.
Since I don’t own a jeep this meant walking/yogging a slow 3mi back down the jeep road in the coldest part of the night. After wading through the river (twice) I walked up to Lana (my Rav4) and woke Misti to give her the good news… I’d done it, though barely. I’d set out the ultimate goal to climb 12 14ers in 24hours, and while I’d fallen short of that goal, I’d still managed to climb 11 summits and just squeeze in under the previous FKT by 10min, covering 22,300ft of gain and 48.7mi. It may not have been a perfect day; with all the physical struggles and the additional challenges added by the smoke and snow, but it had been one hell of a journey through the mountains. I’d over come the persevered despite the mental struggles and uncertainty, trusting in the process rather than giving in to the doubts. Though that 12th summit still lingers….Mt Huron, I’m coming for you.
Hello my name is Eric Lee and I’m an Asian American (technically multi-racial). Recent event have really pushed to the forefront of thought my personal relationship with racial bias, racism and the systemic social issues that plague our country. As an Asian American I’ve been exposed to my share of negative racial commentary throughout life; comments about eyes, color, language, driving ability, eating habits, how we name our children, penis size (yes I’m being serious), disparaging looks and on and on. Though at the same time I must also admit the privilege I’ve had growing up in a middle class community. Most of these taunts and racial slurs have come from stupid and non-physically threatening sources. Meaning, I never had to fear for my life or feared someone was going to do me physical harm as part of this. Having grown up in an immediate community where violence was not the norm, where law enforcement was not prone to profile individual POC, I was privileged that the abuse was only verbal and emotional, not physical. This may not sound like much of a privilege, but I think we are all realizing (because of recent and ongoing events), that this simple factor IS a privilege.
Which brings me to the much messier question, how have I been a part of them problem for all these years. While Asian Americans have by no means had an easy history in the US, we’ve greatly benefited from the civil rights movements while not being as visible on the front lines. Also, because of the backing of strong Asian economies many have been fortunate to position themselves in more affluent settings. While this doesn’t change the profiling or underlying racial issues, it does ease the reactions/interactions that we’ve endured. I will never know what it’s like to be an African American living in a lower socioeconomic neighborhood, who fears being arrested/beaten or worse every time they leave their home to go to the store, work or school. I will never truly know the frustration of fighting for equal rights for decades, to seemingly make little headway. One of my first exposures to the unrest associated with racial injustice was watching Los Angeles burn in 1992 during the Rodney King riots (and hearing the rise of gangsta rap). As a 10yo I didn’t fully grasp the situation, but the image is still deeply imprinted in my mind. Do I like that these protests have turned violent (whether it’s the protesters or other agitators not related, remains to be seen)? No, but it doesn’t surprise me one bit. If I’d been trying to calmly, logically and peacefully protest and make my voice heard only to be brushed aside time and again, I too would have little faith in a system that keeps promising things will change but never delivering that change. Whether you like it or not, you can’t help notice what’s going on, and the protesters and voices screaming for change have your attention. I know they’ve got mine, and while I consider myself an educated and empathetic human, they’ve got me reconsidering my place in perpetuating the racial inequality that continues to persist. We can all be better, we can all do better, and we must.
By now some
of you know that this past weekend I took a very short trip back to see family
in California, traveling by plane both directions. I know many people are itching
to hop back on a plane, travel and to get away from it all. So to help everyone
make a more informed choice I’ll lay out what I did to mitigate much of the
risk of flying and how my experience went navigating all the public spaces that
come with traveling to a different state. If you want to ask (or scold if you
must) me about my personal reasons for doing this you are more than welcome to
send me a DM or email and I’ll respond individually with that information, but
its personal and thus not suited for a public forum and not the point of this
writeup.
Every departing flight from Denver between 6p-11p on a Friday afternoon….. wow!
My Mitigation Plan For me this whole process was a test of my ability to creation infectious disease mitigation plans, a skill I learned and honed working in tuberculosis and HIV labs for many years. So I did not simply hop on a plane and wait to see what happened, I had a whole step by step plan of all the risks involved with travel, how I would protect myself and how I would act in certain situations. Below is my initial plan that I laid out BEFORE traveling, and it is VERY conservative.
Now on to the reality of the situation and what I observed and found. I’ll lump both my flights together as a way to give the sum of a couple different experiences for each step listed above.
The whole journey for me started in Boulder boarding the RTD AB bus which heads to the airport. Under normal circumstances these buses are packed and can be standing room only, but right now RTD is limiting the number of passengers on each bus to <20, has suspended fare collections and is requiring all drivers/passengers to wear face coverings. When I got on it was apparent it was going to be a quiet trip, just myself and one other person headed to the airport!
On my way to the airport on RTD, the bus is empty except for one other person and the driver.
The
Airport
Needless to say the ride went smoothly, but I still kept my mask on the whole time. Arriving at the airport I unloaded my own bag and headed up the escalators to security. I was astonished to find 1 person (TOTAL) in line in front of me. I walked up to TSA precheck, handed the security office my ID, she didn’t even request I remove my mask (though they did in Oakland), then I passed on through. In Oakland they didn’t even have a precheck lane running, instead they specially escorted me through normal security (shoes on, liquids in the bag). After security I sanitized my hands and ID and headed to the gate. I only passed by a few people, almost all of whom were wearing masks of some variety (they are mandatory in the airport). As I approached the gate I was astonished to see the bar at Timberline Steaks (Denver) was open and seating patrons at the bar/restaurant? I filled my water bottle, washed my hands and headed over to the gate. At the gate there were only about 20 people heading to Oakland, and 30 people on the return flight, for planes that have a capacity for 140 people. I found a spot at the gate spread out between others, which was easy, and sat down to eat my snacks and grab some water before the flight. This was the first time I removed my mask and it was only for a few minutes in a safely spaced out area. While waiting for my first flight an SWA worker came and sat right behind me, no attempts to space out, and while waiting for my second flight a woman came and stood right in front of me to await boarding. In both instances there was plenty of space to maintain at least 6ft of distancing, but neither person was aware enough to realize the situation.
TSA Checkpoint in Oakland, not a single passenger to be seen. TSA precheck was even closed in Oakland, though it was open (with 1 person) in Denver.
Waiting for the airport train at Denver International, people nicely spaced out, wearing masks.
Walking through Terminal C at Denver International, barely anybody around at 6pm on a Friday evening.
Southwest Airlines boarding process in Oakland, a mad rush to the podium as always (only 10 at a time), not much organization to the boarding process.
The
Flight
Now on to the fun chaos of boarding. Southwest is famous for their open seat policy, normally boarding in groups of 30 at a time, all crammed together in small lines. Now they are calling up 10 numbers at a time to allow people to spread out. The problem is, when they call those 10 numbers it’s a free for all, no organization, so of course everyone immediately rushes to the counter and stands right next to each other trying to be the first on. I simply stood back, let them crowd ahead and walked on once my group had thinned out. Boarding the plane you have to walk by/near people, there’s just no fix for this situation (wearing my N95 still). I chose a window seat about halfway through the plane, spread out from other passengers, right now there is plenty of space on many flights. But, of course, on my first flight someone came and sat right in front of me (there was no need), so I moved over two seats to the aisle. As planes begin to fill up more and more the actual seating part is going to become impossible to not have several people within a 6ft radius of you, so that’s a part of travel risk one will just have to accept as being unavoidable. On the plane almost everyone was wearing masks, including the crew. But not long after take off many people removed their masks for most of the flight (about ½ on my first plane, and 10-20% on my second). I even witnessed one woman call the flight attendant over to ask a question, then promptly pull down her mask to speak directly with her (really???). On the flight I spent most of my time working and reading as I watched the scenery go by. I did sanitize my hands and remove my mask for a brief few seconds to grab a drink of water, but that was the only time in the 2.5h flight my N95 came off. Overall a pretty uneventful flight once we were in the air, no food and beverage service, a few trash collection passes by the friendly flight attendants, but that was it. Both flights landed early so we had to wait a few extra minutes for our gates. Even though very few flights are running (<30-40/day outbound at DIA and Oakland it looked like) each airport is only operating a fraction of it’s gates. When we finally got to the gate and the captain turned off the seat belt sign, the mad rush to the aisles to be the first off was on. Social distancing be damned, everyone did their normal thing and crammed into the aisle way right next to each other. So I simply stayed in my seat at the window, let most of the people deplaned, then grabbed my bag and headed out. I cleaned off my hands, took off my outer jacket and headed to the curb side. Again both airports were fairly empty for now, and getting through was a breeze.
On board headed to Oakland, most people spread out. After all, there’s only 20 of us. Masks still on.
Headed back to Denver, a few more people, but still everyone has their own row and plenty of space. Imagine this plane 2/3 full, with only middle seats empty. People in front and behind you, people across the aisle from you, etc.
People can’t help their natural tendencies. As soon as we land, it’s a rush to the aisle, everyone lines up nice and close to each other to rush off the plane.
Final
Thoughts
Right now the overall take home from my experience is that airports are fairly empty and the airlines are still trying to figure out how to manage travel during the Covid-19 pandemic (which will continue on for many more months ahead). While I was able to protect myself fairly well throughout the entire travel process, it was evident to me that one can not rely on the airline’s good intentions or the unaware strangers around you to protect you. And while right now it’s easy to find some space, once passengers start returning to air travel (and they will) you will be forced into closer quarters/contact with people no matter how hard you try to avoid it. Lines for buses, security, trains, escalators, seating areas at gates and on planes will all become busier to the point where you’ll have to be within 6ft of people, some will wear masks, some won’t (unless it becomes a Nationally enforceable law, unlikely). So if you choose to travel by plane in the next few months be prepared to accept the risk you are taking and knowing that you will be exposing yourself to people outside your realm of control and to people who might not all be acting very conservatively (or even think the virus is real). Hopefully during this lull in travel the airports and airlines can better test and implement their policies (I’ve written to Southwest), but that remains to be seen. And for those wondering, I’m now on a 14 day quaratine/watch for any symptoms (5/21, Day 3, ending 6/1).
This past weekend much of the State of Colorado moved from “Stay-at-Home” to “Safer-at-Home” restrictions. This is the first step to us opening up more businesses and moving slowly back towards a state of ‘new’ normal. As part of this a lot of people across the country are preparing to go back to work (or into an office/store) in some capacity in the coming weeks. Some people think this is all BS and a hoax, you can stop reading now, for those who are worried or uncertain exactly what this return to a ‘normal workplace’ might look like, I’ll try to outline a few best practices that my work has been using and also highlight what the State of Colorado has outlined for businesses that are reopening.
Governor Polis’s outlines what Safer-at-Home means for Colorado. Note that individual Counties may enact additional legislation beyond these basic measures. Here in Boulder County masks are required in public settings where you can not maintain 6ft of separation.
To start with for those that don’t know my background, I work in a vaccine and drug development laboratory. So my workplace will definitely look different than many of yours, but there are still many applicable practices that we’ve implemented that all types of work environments can utilize. Much of my experience in mitigating infectious hazards comes from years of working in Biosafety Level 3 facilities (with airborne, highly infectious, incurable pathogens). The stringent types of biosafety measures we implement in the lab aren’t applicable to daily life, except if you’re working in a healthcare setting in close contact with highly infectious patients (ping me separately if this is of interest to you). I’ll divide the topics up into three categories; general work place practices that should be implemented at the management level, engineering controls (equipment) and lastly how many of the common workplace practices can and should change to help you protect yourself during this uncertain time.
General
Workplace Policy
While some people can work remotely from home (best practice), many of us require specialized equipment/facilities, customer interactions or other tools that are simply not available at home. If your work place is welcoming employees back into the office/store, the State of Colorado has set out several guidelines for how work place policy should be setup to protect the employees. First, spread out the hours people work; work from home, work shifts, segregate tasks people are working on to different areas, etc. Second, the employer should be providing ample cleaning supplies, hand sanitizer and soap. In our office we also have an employee tasked with daily cleaning of the common areas and commonly touched surfaces (door knobs, time clock, fridge, conference table, etc). In addition to this I clean my personal desk each morning, it only takes a few minutes, but alleviates any concern about contamination of my immediate workspace. Third, the wearing of masks should be made mandatory for all employees (and customers) when you’re interacting with anybody else (even in passing or in the bathrooms) or moving around the office. The reason this needs to be made a company wide policy is, otherwise it’s too easy for a portion of the population to not adhere, making the effectiveness of cloth/surgical masks far less on a company wide scale, everybody needs to protect everybody else. Additionally, signage reminding everybody about the policies on staying home if you’re sick, hand washing, cleaning of common areas and wearing of masks are helpful. Many of these measures are requirements of the State of Colorado for reopening a business, check with your individual state about their requirements.
Mandatory cleaning supplies near our front entry. All offices should have these available for employee use.
Masks, gloves and all the protective equipment. Despite what Trump recommends, injecting bleach and UV irradiating yourself are not a good idea. But these are good tools for cleaning equipment and surfaces (just not your body).
Engineering
Controls
Engineering controls is a term used for physical barriers or equipment that is used to reduce the hazards of a workplace. In regards to COVID-19 in the workplace it’s referring to barriers and office setup that can help reduce interactions with coworkers and thus reduce the risk of someone getting sick. One method of limiting the workplace risk is to spread out employees desks/work spaces. Providing all employees with at least 6ft of space as to reduce the likelihood of infectious transmission. Another way is to setup barriers between employees desks/work spaces. This can be done by putting up plexiglass walls (or other materials) to block the direct line of transmission from one person to the next. So the open workspace system that so many tech companies love, is probably going to need to go away for the immediate future. Cubicles (or closed offices) actually provide a fairly safe way for each employee to have their own protected space, where infection risk is low, and you don’t have to wear a mask all the time. Work with your employer to establish these ‘safe zones’, because not only will it reduce the transmission risk, but it makes the employee far less anxious because they have their own personal space (at least in our office it works that way). For those of you working retail, store fronts or other customer based jobs, many of these rules won’t directly apply. My recommendation would be to establish a safe zone for yourself (back room, office, car, outside). Take breaks to get out of the mask for a few minutes (pretend like you’re a smoker) or just to step into the back room/warehouse for a few minutes to relax and breath. Plan and prepare for the long haul.
The dreaded cube farm, a great way for every employee to have their own protected safe space and to minimize COVID-19 transmission risk.
Common
Workplace Practices
While the previous two sections mostly addressed changes that can/should be broadly implemented in the workplace, this section is going to address how the actions of individuals/groups should change. I have a feeling for many people this is going to be the hardest section to incorporate into our daily lives, but these changes are equally as important as those above. The first one is simply an extension of the general social distancing policy that pervades our lives, but applied to the workplace. No group lunches, standing around the coffee/espresso machine, office parties, etc (yes, sad face, I know). It doesn’t mean you can’t chat with coworkers or socialize, but it does mean it has to be done at a safe distance apart and while wearing your masks. If/when you need to use common office equipment (printers, coffee makers, fridge, cash register, etc) either make sure the equipment is well cleaned off or sanitizer/wash your hands afterwards as a precaution. This mitigation measure may be slightly less important for some workplaces, and more important for others (depending on how many people you’re sharing space with). On the far end of the spectrum are people whose jobs require direct contact with others (massage therapist, physical therapist, hair stylist, acupuncturist). For these professions it’s even more important to sanitize all surfaces after each client, wear masks (tough for hair salons), make sure both client and provider clean their hands before interacting, and of course pre-screen your clients to make sure they are not sick or symptomatic.
The last one
is probably fairly obvious for many people, but meetings are going to look quite
a bit different (if they happen at all). The easiest way to mitigate the risk
is to do virtual meetings (Zoom, Skype, Teams, etc) whenever possible. Of
course sometimes it’s much faster and more efficient to meet in person, which can
definitely be done very safely. The smaller the better to start with, but as meetings
grow, ensure there is at least one seat between everybody in the room, and
everybody continues to wear their masks when in the same room.
Workplace meetings in the COVID-19 era. Join virtually, space out, masks for all those who attend in person.
Final
Thoughts
My office/lab implemented most of these procedures the first week of Colorado’s Stay at Home order and shutdown. We have our own cubicles/workspaces that are our own private areas when we’re not working in the common lab spaces. We wear gloves (because it’s a lab) and masks whenever working in close proximity to others, common surfaces are regularly cleaned, our employees with COVID-19 risk factors spend much of their time working from home, or working off shifts, our meetings are done half virtual half in person (with masks). Using all these measures we’ve had no issues with viral transmission and also minimal issues slowing down our workflow. If you or your employer are hesitant to implement many of these actions, just look at the extreme cases of the meat packing plants all over the country. They stayed open but didn’t implement any infection risk mitigation (employees working in close quarters), and ended up suffering large outbreaks forcing their businesses to shutdown. So it’s really in everybody’s best interest to protect themselves and those around them, to stay healthy and keep the business running without the major setbacks that an outbreak would cause.
While company wide policy is up to the employer, you are your own strongest advocate. So it’s important to assess your work place (and how it operates) and how best to mitigate risks. If an employer isn’t providing you at least the minimum levels of protection outlined above, then speak with your local public health department, as they will come in and further assess what more can and should be done. Going back to work in and of itself isn’t a problem, it’s doing so in a responsible and controlled manner that allows your workplace to implement and test out these new policies. For all businesses there will be a trial period of adjustment to the new way of functioning, just be flexible and understand most of these changes really don’t dramatically affect our lives (and definitely don’t impinge our our civil liberties), we’re all going to get through this.
Sorry for
the delay, but this one has taken a lot of time and thought to put together
(and reading some 80 odd Covid research papers). My goal in this edition of
Covid Science Theater 2020 is to talk about what happens when the virus enters
our body, infects our cells and subsequently leads to either mild disease or
more severe infections. It’s going to be a fairly dense article, but I’ll do my
best to keep the science and terminology to something generally understandable and
hopefully educational.
For those who don’t want to delve too much into the specifics of all the virology, immunology and pathology I’ll provide a short 1 paragraph set of clifs notes here. The virus most commonly enters the host through mucus membranes (eyes, nose, mouth) and infects vascular endothelial cells and cells of the lungs, kidneys, GI tract and begins to replicate. The body initially responds to the virus through a host of Innate Immune mechanisms; these generic counter measures are deployed against all invading pathogens as a first line defense and are not specific to the invading pathogen. Unfortunately, these initial immune responses aren’t always adequate to contain the virus (the virus sometimes evades destruction, other times the virus just overpowers the immune response) so our body deploys a second type of response known as the Adaptive Immune response. In this phase, T-cells and B-cells are primed to respond to the specific infectious agent (here, SARS-CoV-2). Often this two-pronged approach works to contain the infection, eliminate the virus and build up lasting memory to subsequent infections. Unfortunately in some people the virus spreads too rapidly and the immune response doesn’t respond appropriately, leading to destruction of their organs (notably the lungs) and potentially death. Sometimes this more severe outcome is caused by the virus itself, but more often it seems to be caused by an overzealous immune system trying to play catch-up. So there’s the quick and dirty; in the following paragraphs I’ll go into more detail about Viral Entry/Binding/Replication, Early Cellular Responses, Clinical Symptoms, Adaptive Immune Response and What Happens and Why the Immune System Sometimes Fails.
The information in the following paragraphs comes from a combination of basic immunology principles (Kuby Immunology textbook), observations and early research released about Covid-19 and conclusions drawn from earlier studies of SARS-CoV-1 (a virus that is very similar to the current SARS-CoV-2, but with some caveats of course). As Covid-19 is still a new disease, we are constantly learning new things about the virus, infection cycle and pathology, so while what I outline here is based on a lot of research, there are definitely aspects of this virus that we don’t fully understand, and need further investigation.
Graphic of the structure of a SARS virus, the S, M and E proteins are the most important in regards to host recognition, Li et al 2020.
Viral Entry and Replication
Coronaviruses get their name from the hallmark shape, a circular capsid (or shell) that is spiked with proteins on the outside and sheltering the virus genetic sequence on the inside. The Spike (S), Membrane (M) and Envelope (E) proteins make up the majority of the viruses outer shell, while the Nucleocapsid (N) protein found inside the virus assists in viral replication. This small assortment of proteins, plus a few others, make up the bulk of the very simple viral structure (Weiss 2005, Li 2020). The novel coronavirus 2019 (COVID-19) shares a lot of homology or similarity with the original SARS virus that was discovered in 2002, genetically 80% similar, while being 76-95% similar for the major proteins listed above (Xu 2020). This allows researchers to draw a lot of conclusions from previous research on SARS-CoV-1, though we must be careful when doing so, as there are some known (and unknown) differences between the two viruses. The infection cycle starts with the virus gaining entry to the host, usually through mucus membranes of the eyes, nose and mouth. Once inside the virus often begins it’s infectious cycle by infecting vascular endothelial cells that line vessels throughout the body. While different viruses have different mechanisms by which they enter host cells, SARS-CoV-2 binds to the ACE2 receptor using its spike protein (same as SARS-CoV-1), allowing it to enter the host cell (Jia 2005, Walls 2020). Like most viruses, SARS-CoV-2 then goes through a multi-stage process by which it hijacks some of machinery inside our own cells to in order to replicate, escape and subsequently infect more cells in a continual cycle (Frieman 2008).
Overview of the SARS viral life cycle inside the host, Frieman et al 2008.
Early Cellular
Response
Thankfully our body has a whole host of immune mechanisms it utilizes to deal with infectious agents of all types. Almost as soon as an invading pathogen has infected our cells the immune system starts going to work. The Innate Immune response is our constantly active sentinel, whose cells are constantly circulating all over our body just looking for foreign invaders to attack and kill. These innate cells use Pathogen Associated Molecular Patterns (PAMPs), or markers of foreign invaders, as the initial signals something is wrong and that it’s time to go to work (Li 2020). Some cells go to work directly attacking the virus and infected cells in an attempt to destroy the virus, others release signaling molecules known as cytokines and chemokines that recruit other cells to help in the fight (Frieman 2008), and some cells just go ahead and sacrifice themselves in an effort to prevent the virus from hijacking them, a process known as apoptosis (Lim 2016).
Symptoms:
What and How They Manifest
While this system works well for many invading pathogens (why we are not sick all the time), allowing our body to control the infection, many viruses (and bacteria) have evolved mechanisms by which to evade, subvert and co-opt the immune response to their advantage. For SARS-CoV-2 it seems to be able to prevent the host immune system from activating one of it’s key anti-viral signaling pathways, the Type 1 Interferon pathway (Lim 2016, Li 2020, Frieman 2008). While it is not known exactly how the virus subverts this system a few hypotheses involve the Nucleocapsid protein (Lim 2016), other non-structural proteins (Lim 2016), and some of the SARS enzymes (Chen 2014). So by reducing the host immune response the virus is able to more effectively replicate and spread, leading to a more systemic infection. This is when we start to experience more of the hallmark symptoms of the infection; fever, sore throat, coughing, fatigue, pulmonary inflammation leading to shortness of breath and possible pneumonia and lymphopenia (a decrease in lymphocytes, more on that later) (Huang 2020, Zhu 2020). Most of these symptoms are a physical outcome of the body’s ongoing fight with the virus, trying to delicately balance destroying the invader, while preserving the host organs and system. The fever is the immune system’s attempt to raise the core temperature enough to burn out the infection. The sore throat/cough is an outcome of our immune system attacking infected cells of the airways and trying to expel the invader (mmm mucus), same for the pulmonary issues (initially, more on this later too). While many of these symptoms may be scary and uncomfortable they are often a normal part of our body’s healing process when dealing with a foreign invader. So under normal circumstances, it’s best to rest and let your body do it’s thing, unfortunately this doesn’t always go as planned, as we’ll find out in the following sections….
Adaptive
Immune Response; Stage 2
In the previous two sections you’ve seen how our well intentioned Innate Immune system can sometimes fail leading to illness, thankfully the body has a backup, the Adaptive Immune response. This secondary wave of the immune response goes into action very soon after the initial infection (several hours to few days, infection dependent) and is mostly comprised of two cell types; T-cells and B-cells. When the levels of virus in the body start to rise, several of the innate immune cells can act as activators of the adaptive immune response, taking pieces of the virus to specialized activation centers know as lymphoid organs. These centers of immune activation are spread all over our body and are the primary site of pathogen specific antigen (virus pieces) presentation. The antigen presenting cells (Dendritic cells are most prominent) present the virus to the T-cells and B-cells as if locks in a door, allowing the T-cells and B-cells to go to work making specific keys (receptors and antibodies) that can attack and destroy the pathogen in a very focused manner. The outer proteins that make up the viral capid (proteins S, M, E) tend to be the most effective as this is what is visible to our body when intact virion are released (Liu 2017). So the body makes a whole army of these specific cells that traffic to the sites of infection; T-cells directly attack the virus and infected cells, while B-cells make antibodies that bind to parts of the virus, preventing them from entering new cells and marking them for destruction (Liu 2017).
These two arms of the Adaptive Immune response are also what comprise our immunological memory. Virus specific T-cells and antibody producing B-cells remain dormant in specialized lymphoid organs (sometimes they also remain in circulation), just waiting for the virus to turn up a second time. This time since they are already primed and ready to go, memory T-cells and B-cells start attacking the virus almost immediately, usually preventing the virus from spreading and preventing us from getting sick. Studies of SARS-CoV-1 have found both memory T-cells and memory B-cells (producing neutralizing antibodies) that are capable of rapidly responding to viral reinfection (Li 2020, Liu 2017, Channappanavar 2014). In human patients who recovered from SARS-CoV-1 infection anti-SARS antibodies and memory T-cells were found in most patients up to 24 months after infection (Liu 2006, Ka fai 2008, Liu 2017). While antibody responses did decline over time in SARS-CoV-1 patients (many undetectable at 6 years), memory T-cell responses were conserved for up to 11 years after infection (Tang 2011, Ng 2016, Liu 2017). Similar high quality neutralizing antibodies have been found in COVID-19 patients, but since the disease is so new the longevity of memory responses to this new virus aren’t exactly known. Encouragingly, since SARS-CoV-2 is so similar to the original SARS virus, and lab testing has even shown that their be might cross-reactive protection between the two diseases (Walls 2020), there is much hope that the long lasting memory responses seen for SARS-CoV-1 would also apply to those who have recovered from COVID-19. All of this evidence, both old and new, does inspire a lot of hope that a functional vaccine would both be likely and very effective in providing some duration of immunity from COVID-19, but how long remains to be seen.
Graphical overview of the many cells and pathways involved in the host immune response to SARS. It’s a complex set of feedback loops and interactions with a lot of variables. Li et al 2020.
When the
Immune System Fails, Severe Disease
The reason COVID-19 is such a scary disease, isn’t because our immune system has no problem fighting it off, but because in some percentage of the cases (uncertain, but estimates are as high as 10-20%) patients need to be hospitalized due to severe complications. If our immune system is so complex and so strong, why do patients with COVID-19 get so sick that they need hospital care? It comes down to numerous very subtle things this virus does that are different than coronaviruses that cause the common cold. One is the effect SARS-CoV-2 has on Type 1 Interferons mentioned earlier, reducing the body’s initial response to infection. Another early symptom seen in many severe cases is lymphopenia, or a loss of lymphocytes (notably T-cells) early on in disease (Huang 2020, Schmidt 2005, Weiss 2005). While the exact cause of this loss of T-cells is not known, it is hypothesized that the viral proteins may lead directly to T-cell death as a mechanism of immune evasion (Lim 2016, Li 2020). These mechanisms of avoiding immune detection along with the efficiency of viral replication can lead to an out of control infection very quickly.
But in the end, it’s only partially about the virus, and largely about an overexuberate immune response. In an attempt to catch-up to the wide-spread infection the immune response goes into overdrive, ramping up a lot of the inflammatory cells and signaling molecules that tell the body to attack the infection (Li 2020). This response does in fact kill the infected cells, but it also destroys lung tissue (primary target), vascular tissue, liver tissue and other infected tissues (Tian 2020, Schmidt 2005). This is often when the more obvious signs of pneumonia set in; the lungs fill with fluid, the efficiency of aveoli decreases (oxygen absorption) and breathing becomes very labored and difficult. This is the tricky thing about COVID-19, making our immune response more efficient would help prevent early infection, but later on would lead to increased tissue damage. But if we reduce the immune function of the body to prevent self-inflicted tissue destruction, we run the risk of allowing the virus to run rampant throughout our body. COVID-19 is a tricky disease to treat for these reasons, and because the disease severity has a wide range of outcomes for different people. In some, infection is very mild and asymptomatic, in others, their entire body shuts down as the virus (and immune system) destroys the host from the inside. The reason many comorbidities are important as risk factors for severe disease is that most of them either affect the immune system or lung function. Obesity, diabetes, auto-immune diseases all alter the immune system’s ability to function, making it harder to fight off the virus. COPD and asthma (though less prominent then thought) make the host pulmonary system more sensitive to damage caused by the virus and immune system.
But not all hope is lost! Because of the large body of evidence suggesting that SARS viruses create robust lasting immunity, this means a vaccine might be very effective at protecting most of the population. Also, now that there are many patients who have recovered from COVID-19, tests are underway to examine if using their plasma (containing antibodies) can help patients who are suffering from more severe cases of the disease (works for other viruses like Ebola). We also have several promising anti-viral agents that are already in clinical trials being tested against COVID-19, with hopes that one or more of them will help improve patient outcomes and be ready for use later this year. Unfortunately all of this does take time, meaning we won’t have a cure next month, but by slowing the spread of the virus, not only do we allow hospitals to manage the patient load, but we allow all the scientist out there to catch-up and produce much needed data, therapies and vaccines.
Thanks for reading. If you see any mistakes please bring them to my attention and I will correct them ASAP. If you have additional questions or want to discuss the immune response in more detail (this is a very high level overview) I’d be happy to do so via text or email. Stay safe and stay healthy.
Literature Citations: Chan et al, Serological Responses in Patients with Severe Acute Respiratory Syndrome Coronavirus Infection and Cross Reactivity with Human Coronaviruses 229E, OC43, NL63. Nov 2005, Clinical and Diagnostic Laboratory Immunology. Channappanavar et al, T cell-mediated immune response to respiratory coronaviruses. May 2014, Immunology Res. Chen et al, SARS coronavirus papain-like protease inhibits the type 1 interferon signalling pathway through interaction with the STING-TRAF-3 TBK1 complex. Jan 2014, Protein Cell. Frieman et al, SARS Coronavirus and innate immunity. 2008, Virus Research. Huang et al, Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Jan 2020, Lancet. Jia et al, ACE2 Receptor Expression and Severe Acute Respiratory Syndrome Coronavirus Infection Depend on Different Human Airway Epithelia. Dec 2005, Journal of Virology. Ka-fai Li et al. T cell responses to Whole SARS Coronavirus in Humans. Oct 2008, Journal Immunology. Li et al. Coronavirus infections and immune responses. Jan 2020, Journal of Medical Virology. Lim et al. Human Coronaviruses: A Review of Virus-Host Interactions. 2016, Diseases. Lu et al. Immune responses against severe acute respiratory syndrome coronavirus induced by virus-like particles in mice. June 2007, Immunology. Ng et al, Memory T cell responses targeting the SARS Coronavirus persist up to 11 years post-infection. March 2016, Vaccine. Schmidt et al. Coronaviruses with a special emphasis on First Insights Concerning SARS. 2005, Birkhauser Advances in Infectious Diseases. Tang et al, Lack of Peripheral Memory B cell responses in Recovered Patients with Severe Acute Respiratory Syndrome: A Six-year Follow-up Study. May 2011, Journal of Immunology. Tian et al, Pulmonary Pathology of Early-Phase 2019 Novel Coronavirus (COVID-19) Pneumonia in Two Patients with Lung Cancer. Feb 2020, Journal of Thoracic Oncology. Walls et al, Structure, Function and Antigenicity of SARS-CoV-2 Spike Glycoprotein. Apr 2020, Cell. Weiss et al, Coronavirus Pathogensis and the Emerging Pathogen Severe Acute Respiratory Syndrome Coronavirus. Dec 2005, Microbiology and Molecular Biology Reviews. Xu et al, Systematic Comparison of Two Animal-to-Human Transmitted Human Coronaviruses: SARS-CoV-2 and SARS-CoV. Feb 2020, Viruses. Zhou et al, Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study. March 2020, Lancet.
There’s
been a lot of debate and misinformation floating around about the use of masks
for the general public as a measure to prevent the spread of infectious
diseases, specifically Covid-19 in the United States. Do they help, do they
not? Is an N95 really better than a surgical mask, is this better than a cloth
mask? How and when should they be used? On 4/3/20 the CDC in the United States finally
came out with a blanket recommendation that ALL citizens of the United States
wear some sort of face covering whenever in public. This was a dramatic change
of direction from the previous recommendation that masks were completely unnecessary,
except for front line hospital workers and for the infected. In this rendition
of Eric’s Science Corner I’ll do my best to present some of the data and
studies that have looked at the questions above, in an attempt to clarify the
misunderstandings and the mixed messages. The topics I’ll try and cover are;
what are the different types of masks and what are they designed to do? How useful
are the different types of masks for the general public? And finally, a few
best practices on how to wear and use a mask or face covering. Rule #1, just
ignore anything Donald Trump says, now on with the info.
Defining
Mask Types
To start
there are three main categories of face masks that I’ll be discussing; fitted
N95 respirators, professional grade surgical masks and cloth masks (variety of
materials). There are numerous sub-categories for each and also other types of
protective face wear I won’t discuss because they aren’t really relevant to the
general population, only to those in the hospitals and those of us who work in
laboratories. The first type is the fitted N95 respirator, these are face
fitted respirator masks that have been certified to filter out approximately
95% of aerosols and particulate matter (when worn properly). You breath through
either a small filtration unit in the front of the mask or directly through the
filtering material of the mask, NOT around the sides (as it should be sealed).
The professional grade surgical masks that many of us have seen in the
hospitals are loose fitting non-sealed masks that are designed to block the
wearer from inhaling large droplets/splashes and to block their respiratory emissions
(protecting others around them). They are not designed to prevent the wearer
from inhaling aerosolized particles as they are not sealed around the edges
(cdc.gov, crosstex.com). The final group are the cloth masks which can be made
from various materials. Their main purpose is to allow more comfortable
widespread facial covering for the general public; to reduce the inhalation of larger
droplets and to reduce one’s own exhalation and aerosol creation. These types
of masks are not specifically certified in any way, though I will discuss the research
that has been done looking at filtration, efficacy and utility of the different
materials.
On the left is a standard N95 Respirator mask, on the right is a surgical mask.
So now on
to how well do these different types filter out microparticles, specifically in
regards to viral transmission (because that’s what’s on everyone’s mind). Numerous
studies that compare N95s and surgical masks and how they prevent infection in
hospital settings have shown both to be similarly effective when dealing with droplet
based respiratory viruses like influenza (Randanovich 2016, Smith 2016). Laboratory
testing of these two types of masks does confirm that the smaller the particle
size, the better an N95 performs compared to a surgical mask (van der Sande
2008, Shakya 2016), thus they are more effective for those dealing with high
level risk of aerosolized viral exposure. These two types of masks are
certified, so it’s no surprise they perform fairly well, but what about the
cloth and homemade masks? The first thing to consider is the type and thickness
of material being use for the mask. Things that allow easy breathing or light
to penetrate aren’t going to filter the air as efficiently, but if it’s too thick
that you can’t breathe through it then it becomes extremely hot, uncomfortable
and unwearable (and you breath around the sides, rather than through the
material). One study comparing the filtration efficiency (of masks in a lab test,
not on a person) of different materials found that items such as tea towels and
cotton mixed fabrics did the best job of filtering particulate matter (up to 70%
mean filtration) out of the air, while silk, scarves (like buffs), pillow cases
and normal cotton T-shirts did not perform as well (45-60% mean filtration efficiency),
with surgical masks being their standard (90-96% mean filtration) (Davies 2013). When commercially available cloth
masks were compared to surgical masks on humans (again in a lab) filtration
efficiency was more variable; with cloth filtering out 30-50% of microparticles
while surgical masks filtering out 60-90% of microparticles and N95s
consistently filtering out 80-95% (Shakya 2016). The efficiency of filtration
directly correlated to the size of the particle, with cloth masks performing
the poorest on particles small than 1µm in size. So that’s a little background
about how the masks are INTENDED to be used and how they function in a
laboratory, how about in real life?
Use in
the General Public
By now you’ve
probably heard many times that the public should not hoard or use N95s because
we need them for our frontline workers (very true) and they don’t work for the
public (partially true). The first piece is that because of the size of this
pandemic we don’t have sufficient supplies of N95s for highly trained hospital workers
who are coming into direct contact with the virus on a daily basis, thus need
this heightened level of protection, first (and most important) reason not to
stock up or hoard them. The second is that for an N95 to be at it’s most useful
and functional you have to have it fit tested, you need to be trained in proper
techniques to don/doff a mask and you have to actually use it correctly (you
can’t be taking it off to talk, to eat, to drink, basically you can’t break the
seal unless in a clean contained environment). They are also designed to be
disposable, meaning you can’t wash them, though sadly our healthcare workers
are being forced into extreme measures to try and sterilize/reuse them for lack
of options. For the general public a surgical mask would be a descent option
because they are designed to reduce droplet transmissions and to block one’s exhalations
(protecting those around you), but sadly our hospitals are also short on these
too, so for now they need to be saved for the frontline works (and patients) where
they’ll do the most good. Also remember that both of these are designed to be
disposable, so can’t be washed and aren’t designed to be reused for weeks on
end (like the public would need).
So this brings
us to cloth masks and their use in the general public. Mistakenly the US government
(CDC) originally came out saying that cloth masks don’t work and that they aren’t
necessary. By now most people have realized this isn’t exactly true, because
why else would they change their minds and recommend people wear them? Yes,
cloth masks are NOT designed to stop all tiny viral particles (and aerosols)
from passing through, and yes they are not highly efficacious, but that doesn’t
mean they don’t help. While a cloth mask won’t fully stop one from inhaling aerosols
and microparticles, they do filter out some of the smaller aerosols (30nm-1µm)
but more importantly block larger droplet transmission both inward and outward
(Davies 2013, Shakya 2016). So while they do filter some of the air you’re
inhaling, the major benefit of a mask is to protect those around you by minimizing
the amount of aerosols you create. This is especially true with the knowledge
that those infected with COVID-19 can be asymptomatic but still capable of
spreading the infection. For masks to be most beneficial we all should wear
them in any public setting where we’ll be interacting with others (even if we’re
socially distancing).
Best
Practices for Masks
Now on to a few personal suggestions for best practices when using a face mask. Note that much of this stems from my own personal training having worked in Biosafety Level 3 laboratories (blood and aerosol transmitted infectious diseases) and in hospitals, but some additional guidance can be found on the CDC website (CDC.gov). First off, once you’ve made/acquired your mask, put it on at home and work on the fit, comfort, breathability. A mask that doesn’t stay on or that you can’t semi-comfortably wear (to the point you’ll touch it a lot or take it off) isn’t very useful. Look to make sure it fully covers your nose and mouth, has a pretty good fit around the bridge of your nose and the sides, and that it won’t slip down when you turn/move your head.
Once you’ve
established it works, wear it around for 20-30min inside your house to get used
to the idea of breathing through a mask. It’s probably going to be a bit awkward
at first, as for most people they’ve never had to do it before. This exercise
will make it easier to wear in public without thinking about it too much. Now
on to that more critical step, wearing it out. The main times the mask should
be worn is whenever you’re going into a public area where you might have close contact
with others. If you’re just sitting in your car and driving around, no need to
wear a mask, but if you go to the grocery store, pharmacy, liquor store, gas
station, work, or even walk around your neighborhood it’s best to wear the mask
to protect those around you, even if you don’t think you’re sick.
To put on the mask, do so BEFORE entering that public space, meaning your home entry if you’re walking around the neighborhood or inside your car before you walk into a shop. Then clean your hands off so that you are less likely to contaminate other surfaces (hand sanitizer or washing). When you’re wearing you mask you SHOULD NOT be taking it off or moving it off your nose/mouth until you’re back in your non-public safe area. Wearing it half the time, pulling it down half the time, taking a break to eat or drink in public negates some of the benefits and protection and also adds to the chance that anything you pickup on your hands will be transferred to your face. When you’ve exited the public space, wash/clean your hands then grab the strings/band of the mask and remove it (do not grab the front of the mask itself). If you have a washable reusable mask proceed to wash it with soap and water. Disposable masks are supposed to be discarded into the trash (hence why not ideal for daily use in public). While your mask is your barrier of protection, remember it’s not foolproof, and is merely a way to further reduce your risk of becoming infected and infecting others. IT DOES NOT change the fact we should be social distancing and providing each other space or that we should be staying at/near home and avoiding any unnecessary travel/errands. Wearing a mask is just another tool in our arsenal to help slow the spread of the virus and reduce transmission rates.
One last note about gloves. Wearing gloves for most people in a public setting is useless (yes I said useless). Gloves are a very effective piece of PPE for trained healthcare and lab workers, but in our daily lives most people treat gloves just like their normal hands. They touch common surfaces, pick up food items, open doors, text on their cell phone, touch their mask, etc. All of these practices together make the use of gloves just as bad as dirty naked hands. You’re better off just considering your hands as dirty whenever you’re in public and not touching any of your personal belongings (including that cell phone) until you’ve cleaned them. If you have to touch your phone or food items while in public, there are many ways to also clean these surfaces as well. Don’t waste gloves and don’t touch your face.
Citations Balazy et al. Do N95s respirators provide 95% protection level against airborne viruses, and how adequate are surgical masks. American Journal of Infectious Control, 2006. cdc.gov/hai/pdfs/ppe/ppeslides6-29-04.pdf . CDC Guidelines for Selection of PPE in Healthcare. cdc.gov/niosh/npptl/pdfs/UnderstandDifferenceInfographic-508.pdf . Understanding the Differences, Surgical Masks, N95 Repsirators. crosstex.com/sites/default/files/public/educational-resources/products-literature/guide20to20face20mask20selection20and20use20-202017.pdf . Guide to Face Mask Selection. Davies et al. Testing the Efficacy of Homemade Masks: Would They Protect in an Influenza Pandemic. Disaster Medicine and Public Health Awareness, 2013. osha.gov/Publications/osha3079.pdf . OSHA Respiratory Protection Guidelines. Randanonvich et al. N95 Respirators vs Surgical Masks for Preventing Influenza amount Healthcare Personnel. JAMA, 2019. Sande et al. Professional and Home-Made Face Masks Reduce Exposure to Respiratory Infections among the General Population. PLOS One, 2008. Shakya et al. Evaluating the Efficacy of Facemasks in Reducing Particulate Matter Exposure. Journal of Exposure Science and Environmental Epidemiology, 2016. Smith et al. Effectiveness of N95 Respirators vs Surgical Masks in protecting healthcare workers from acute respiratory infection: a systematic review and meta analysis. CMAJ, 2016.
It’s been a week since my first Covid-19 blog on 3/18/20, and I will have to admit how amazed I am at the feedback and attention it got. A LOT has happened since that day, and not all of it has not been so positive. Here in Colorado Governor Jared Polis officially announced today (3/25/20) that ALL residents of Colorado are under a ‘Stay at Home’ order. Meaning we’re supposed to stay in our place of residence with the exception of essential trips (medical, food, work for us exempt jobs) and exercise, all the while maintaining social distancing from anyone not in our immediate household (which is just me and my cat). For many of us this isn’t too much of a change, but for those who didn’t think this was serious it’s probably a bit of a rude awakening. Since my post LAST WEEK (now 3/26/20) the number of worldwide confirmed cases has more than doubled to 530,000 (from 219,243), the number of deaths has increased to over 24,000 (from 8,968) and on 3/26/20 the United States confirmed over 17,000 NEW cases, making us the country with the most confirmed cases in the world (go us?) (worldometers.com, washingtonpost.com).
I’m hoping by now that most people realize how serious this is, and that there is definite need to slow the spread; both to allow our medical care teams to keep up and to allow scientist to keep working (please no arguments on the political actions or economic impact, yes it’s going to be bad). My goal in this blog write up is to outline the things that help us bring this pandemic to an end (or at least slow it down). I’ll be focusing on the status of testing in the US (what those tests are), the current drug pipeline and what is being tested, the process and timeline for a vaccine and whether there’s anything to the claim of seasonality with the infection. So here we go, Round 2, diving back into the Science!
Testing
So in my last post I wrote about how much of a mess the Covid-19 testing and surveillance were in the United States, well sadly that has not improved a whole lot. While we’ve definitely tested a lot more people, I’ve been hearing from providers and hospitals all over the country that they’re only testing people who are in high risk populations or have advanced/severe cases of disease. Very recently a rash of new tests have become available to providers and hospitals, meaning the surveillance is starting to grow and hopefully this will continue. There is definitely hope as we are soon to have two different types of tests available, the PCR based tests that we’re currently using for diagnosing active disease and an Antibody based test.
The PCR based test is the one I spoke about previously where labs are able to look for pieces of the viral genome in human samples (usually a nasopharyngeal swab). This test can be quite sensitive and is used to identify infected patients even during the early stage of disease. Though, being such a sensitive test it is more prone to errors and false positives (though they are still very well validated), hence why the original CDC test failed. The other issue right now is that because there’s not a lot of top down coordination in the United States we have dozens of different labs who have created PCR based tests that are being used in different parts of the country. Here are a few of the companies/hospitals who have created PCR based tests; ThermoFisher, Roche, Cepheid, Mayo Clinic, Stanford University, University of Pittsburgh, Atrium Health and the list goes on and on. The CDC even setup a website to allow researchers to develop their own tests and to provide some general guidelines. While on the surface this seems smart, it also means we don’t have any national coordination in our Covid-19 testing on the ground.
The second type of test that is just now being release is a test to look for IgM and IgG antibodies in the blood of patients. You might remember in the previous post where I talked about us building immunity to the virus? Well, antibodies are one of the hallmarks of immunity, and we can test for them, even after we’re no longer infected. A simple prick of the finger (a little blood) on a indicator strip and we have a positive or negative for SARS-CoV-2 antibodies in minutes rather than hours or days, think of it like a pregnancy test for Coronavirus (United Biomedical, Aytu Bioscience). The problem with these tests is that SARS antibodies may not be detectable until 7-14 days after onset of symptoms (Chan et al 2005), so there’s a good chance they won’t identify people who are in the early stages of disease. They WILL help us dramatically as we attend to understand the true prevalence of the disease and how many people are now immune. Once a person is immune and recovered you’re very unlikely to pickup or spread the disease.
Drugs and Clinical Trials
Much to the chagrin of many of us in the biomedical research sciences and healthcare, Donald Trump touted hydroxychloronquine as a ‘game changer’….wow wow, let’s pump the breaks for a second, back it up, and talk about the process by which drugs are created, rigorously tested and finally produced for mass distribution (if they even make it there). The first step is identifying potential drugs and targets then testing them in a laboratory to see if they actually work like you hoped and they’re not excessively toxic. This usually involves some mix of cell culture and animals models. If a candidate is lucky enough to make it through the lab testing phase (known as pre-clinical trials, only 1 in 1000 do) then the company can apply to the FDA to move it’s drug on to a multi-stage Clinical trial in human subjects. Phase I of the clinical trials process involves taking healthy individuals and dosing them with the new drug (usually starting low and escalating). They have to look for safety, effects on the body, toxicity, side effects, maximum tolerate dose, tissue distribution, half-life and on and on. IF the drug makes it through this initial phase then it’s on to Phase II where the drug is tested in a medium size group of diseased individuals (in this case Covid-19 positive). All of this under careful supervision of doctors who are specially trained to assess dosing and efficacy. If the drug proves efficacious in this Phase II study it will move on to a larger Phase III randomized double blind study where the drug being tested is compared to a placebo control (sugar pill) to ensure that it’s really the drug having an effect. These large studies can include 1000s of people and take many years depending on the nature of the disease being tested. Finally, once a drug survives Phase III; proving safe, efficacious and with the dosing amount and regimen worked out, the company can file for approval from the FDA (1 in 5000 make it this far)(medicine.net). This whole process can take up to 12 years for chronic diseases, but of course right now things are moving much more rapidly, and a lot of the regulations and paperwork are being modified to speed up the process.
So what about all the drugs that are being tested against Covid-19 right now? There are several drugs that were identified as being potential therapeutics, and thankfully they had already passed Pre-clinical testing and Phase I trials, so this dramatically expedites the process of testing. The most promising seem to be Remdesivir (from Gilead), Favipiravir (anti-viral), and the previously mentioned hydroxychloroquine (cdc.gov, Dong et al, Wang et al). Even though all of these drugs have successfully completed varying levels of clinical trials, using them against a new disease requires a new round of efficacy, dosing and safety testing. Patients with different diseases respond to drugs differently, dosing needs to be adjusted for the new disease and of course the drug needs to be thoroughly tested to ensure that the differences seen in early studies weren’t simply because of patient selection, population bias or other factors that were not controlled for with the small sample set. In short, all these drugs, while promising, are many months away from being approved for safe use in a wide array of Covid-19 patients, if they get there at all. See the comment below from my college friend Aileen, who’s a pharmacist in the San Francisco Bay Area in response to the small test of hydroxychloroquine in patients in France (Gautret et al)….
More PSA from a pharmacist….to detail out certain claims Hydroxychloroquine used in this case is in particular HIGH DOSE (usual dose of the drug is 200-400mg daily, in this case…600mg daily and we only use that dose in Q Fever patients). When the hydroxychloroquine in high dose and azithromycin are taken together, there are risks for GI side effects…and most importantly…POTENTIAL ARRHYTHMIA. First azithromycin is a known QT prolonging agent…but also…hydroxychloroquine can either cause direct mycocardial toxicity or exacerbate underlying mycocardial dysfunction. This is a RISK that must be weighed by physicians and healthcare professionals vs. the unproven benefits. Is there promise? potentially….but we NEED MORE EVIDENCE TO EVALUATE SAFETY AND EFFICACY. Please…do not demand for it….leave it to healthcare professionals to make that decision and do our jobs….
The next question is in regards to a vaccine against Covid-19. Unfortunately, the process I outlines above for drugs, also applies to vaccines, but we’re starting from ground zero. Prior to this pandemic there were no coronavirus vaccines available (though plenty of background research), so companies have gone into serious overdrive trying to develop something, and amazingly in just two months Moderna, in collaboration with the NIH, took the first vaccine candidate to Phase I clinical trials this month (March 2020) (nih.gov). A process that usually takes 6-12 months took them 2, let that sink in for a moment. And they’re not the only company working hard on creating a vaccine, as there are numerous others with vaccine designs being tested in Pre-Clinical trials as we speak. But, this bring us back to question of time. Before a vaccine can be deployed to the general public it has many hurdles to pass, and only if it successfully passes those hurdles can it be mass produced and distributed. So, as Dr Fauci has explained many times, we’re looking at best case 12-18months for a vaccine. Guess we’re going to have to hang tight and weather this storm for a bit longer.
Seasonality
Most people have probably heard the claim at one point or another that this thing (Covid-19) is like the flu and it’ll go away when the weather warms up. Even our President claimed “…you know, a lot of people think that (the virus) goes away in April with the heat — as the heat comes in. Typically, that will go away in April.” Is there any logic or scientific evidence to support this claim? The short answer is, no, but it’s definitely more complicated than that.
The idea of seasonality was brought up because the influenza virus does see a very seasonal pattern of spread and retraction. During the cooler winter months in the Northern Hemisphere we see a dramatic rise in influenza infection rates, then a drop as the weather warms in April, as Trump suggested. There are many reasons for this; reduced contact time between people (stuck inside, schools) as weather improves, improvements in immune responses due to people being outside more and increases in Vitamin D, potential increase in duration of infection during winter months, and decreased survival of some pathogens in warmer environments (Fisman et al). While we do have the first three things going for us as they are environmental changes that aren’t pathogen specific, what about the survival time of different viruses? It’s been well documented that influenza viruses survive and transmit best at lower environmental temperatures in the range of 5C and 20C. Though starting at 20C, depending on humidity, influenza virus transmission becomes much more variable, and at 30C a dramatic decrease is seen in viral transmission (Lowen et al). Unfortunately, coronaviruses don’t seem to have the same susceptibility profile. Testing on the original SARS-CoV-1 virus showed that it was fairly stable at environmental temperatures as high as 33C (91F), and only when temperature was increase to 38C (100F) did the virus infectivity begin to dramatically drop (Chan et al 2010). SARS-CoV-2, the causative agent of Covid-19 seems to be more temperature resistant than the influenza viruses that we commonly associate with having seasonal cycles. So with the virus currently spreading in the Southern Hemisphere and in several warm weather countries we shouldn’t expect too much help with the virus from Mother Nature’s change of seasons.
But not all hope is lost! I’ve heard recently that the extreme measures taken by many states have allowed the hospitals in the US a little breathing room. Even if this is short lived it means that staff and supplies can be replenished and that buys more time for widespread testing to come on line. Countries like Germany and South Korea are good case studies for how excellent testing and surveillance can lead to minimizing the number of fatalities (testing large percentages of their populations, and doing so quickly). Even though cases and number of deaths are still increasing, we’re slowly catching up on testing, and keeping our death rate low, but the fact that we have 2,122 serious or critical Covid-19 cases is still a little scary. For now, we’re all going to have to sacrifice a bit, be more compassionate to our fellow humans and just realize that we’re living through unprecedented times, that we will get through, though it’s going to take some time. If you’re interested in reading about some potential scenarios on how the pandemic plays out in the next 3-12months this article from the Atlantic outlines them pretty well in my opinion.
Citations aytubio.com/covid-19/ cdc.gov/coronavirus/2019-ncov/hcp/therapeutic-options.html Chan et al. The Effects of Temperature and Relative Humidity on the Viability of the SARS Coronavirus. Advances in Virology, 2011. Chan et al. Serological response in patients with Severe Acute Respiratory Syndrome Coronavirus infection and Cross-Reactivity with Human Coronavirus 229E, OC43, and NL63. Clinical and Diagnostic Laboratory Immunology, 2005. Dong et al. Discovering Drugs to treat Coronavirus disease 2019 (Covid-19). Drug Discoveries and Therapeutics, 2020. Fisman et al. Seasonality of Viral Infections: mechanisms and unknown. European Society of Clinical Microbiology and Infectious Diseases, 2012. Gautret et al. Hydroxychloroquine and azithromycin as a treatment for Covid-19: results of an open-label non-randomized clinical trial. Journal of Antimicrobial Agents, 2020. Lowen et al. Roles of Humidity and Temperature in Shaping Influenza Seasonality. Journal of Virology, 2014. nih.gov/news-events/news-releases/nih-clinical-trial-investigational-vaccine-covid-19-begins unitedbiomedical.com/COVID-19/ Vincent et al. Chloroquine is a potent inhibitor of SARS coronavirus infection and spread. Virology Journal, 2005. Wang et al. Remdesivir and chloroquine effectively inhibit the recently emerged novel coronavirus (2019-nCov) in vitro. Cell Research, 2020. washingtonpost.com/world/2020/03/24/coronavirus-latest-news/ worldometers.info/coronavirus/
Society is in some state of chaos at the moment, and there’s so much misinformation and misunderstanding floating around. So in this blog I’m hoping to provide some of the scientific knowledge based on the research and observations. First, here are my credentials; Masters of Science in Immunology and Infectious Diseases, I’ve spent 14 years in the laboratory doing research (HIV, Tuberculosis, West Nile, Autoimmune diseases, cancer) and worked in a BSL3 laboratory. So with that out of the way, I’m going to try and stay away from giving too many opinions, talking about the politics or debating the models because there’s just too much speculation there. So if you’re interested just in the scientific research about the virus, the immune system and the current case study numbers hang on, this is going to be a long one (all references cited will be at the end).
Background
In early December 2019 a cluster of pneumonia cases appeared in Wuhan, China with clinical characteristics similar to SARS-CoV-1. Of the initial patients studied the mortality rate was extremely high (10-15%, now estimated closer to 2-3.5%), which gave rise to great concern that this virus would be a serious health issue. Sampling from the initial patients and sequencing identified the causative agent as a novel (new) coronavirus that was originally named 2019-nCoV (Huang C et al). Subsequent sequencing and analysis of the virus from those original cases showed that the founding virus has similar characteristics to coronaviruses found in bats, but is also related to those found in pangolins. There are currently two sub-strains of the virus circulating in the population; S-type and L-type. The S-type is thought to be the founding strain, while the L-type is a slightly altered variant that is now the predominant virus circulating in the population (70% of cases), though the consensus sequence for both strains only differ by a few base pairs (Tang et al). As of now (3/18/20) there is no evidence that SARS-CoV-2 can sustain infection and spread through any other animals other than humans. As of 3/18/20 China has experienced 80,894 confirmed cases on COVID-19 (disease caused by the virus SARS-CoV-2 formerly 2019-nCoV) and 3,237 deaths from the virus (worldometers.info). While daily number of new cases in China has significantly waned in recent weeks, it has spread to the rest of the world and is currently spreading rapidly throughout Europe, the Middle East and the United States.
How the Virus Spreads
Viruses can spread by either direct (touching, kissing, sex) and indirect (coughing, sneezing, aerosols) methods. Early on during the epidemic of SARS-CoV-2 it was realized that the virus was capable of spreading by indirect contact and possibly survived in aerosols. Though the primary route of transmission is still thought to be direct or close contact with an infected individual. Studies showed that aerosolized liquids containing SARS-CoV-2 could survive on surfaces (specifically plastic and steel) as long as 72 hours in a controlled laboratory setting (Doremalen et al). Though the half-life of the virus on all surfaces was 16 hours or less. Meaning that while the virus can be detected up to 3 days after deposition most of it dies much earlier, though we don’t know exactly what the survival time in a natural environment is. The main take home from this should be, the virus can be transferred from one host to another fairly easily and surface contamination can be an issue if an infected person sneezes/coughs, so cover your mouth and clean common areas! One thing that has made the virus especially difficult to track and control is the presence of what are known as asymptomatic carriers. These are individuals who become infected with the SARS-CoV-2 virus and are contagious without showing any symptoms (Bai et al). Thus, while they appear fully healthy, they are in fact vectors for the disease without even knowing it. Additionally there can be long incubation times between becoming infected and showing symptoms, thus allowing people to spread the viruses unknowingly.
Standard hygiene rules apply for SARS-CoV-19; Wash your hands frequently. Clean common surfaces in shared areas. Cover coughs and sneezes with an elbow or arm. Do not touch your nose, eyes and mouth (this is how the virus gains access to the body). Social distancing (the practice of staying 2m away from potential contacts). Stay home if you’re sick and self-quarantine. This one is very important and something Americans do not do well.
The question of using masks and gloves has come up numerous times, so I’m going to try and dispel some of the rumors and misinformation. These items are known as PPE (Personal Protective Equipment) to those in healthcare and the medical sciences. They are used to protect one’s self from infectious and hazardous materials when used properly. Both N95 masks (fitted and tested, designed to filter out 95% of microparticles) and surgical masks (loose fitting masks that cover your mouth, no seal) are designed to create a barrier between the user and the surrounding environment. N95 masks when worn properly will filter out most particulate and infectious matter, protecting the wearer, when USED PROPERLY. Proper use does not include wearing it around your chin, pulling it off your nose to breath or touching the mask with unwashed hands, in short most of the public is not trained well enough to properly use these and thus negates a lot of the benefits they can provide. Surgical masks on the other hand are designed to protect those surrounding the user by blocking some of the aerosolization of material, they ARE NOT designed to protect the user from inhaling microparticles (same goes for cloth masks) (Balazy et al). The reason the government does not want the public using and hoarding these disposable masks is that there is a HUGE shortage for our healthcare workers, the people who have to take care of the sick and injured on a daily basis (which may be you). They come into contact with the infectious and at risk at levels exponentially higher than the average person and if they don’t have these protective equipment then it’s almost a certainty they’ll get infected, and then either be forced to take time off (leaving our hospitals understaffed) or infect those around them such as patients who are at risk. If you’ve been hoarding masks or bought a bunch think of donating them to your nearby hospital, every nurse or doctor I’ve spoken with says they are rationing and running very low on these supplies. If you need to wear a mask buy a cloth reusable mask (and wash it regularly) in order to protect those around you from anything you might be carrying. As with the N95s above, disposable latex and nitrile gloves are not very practical or helpful for most people. Every time you touch your body, your cell phone, your hair, your mask on your face, you contaminate the gloves and spread that contamination around. Save yourself the waste and trouble and just regularly wash your hands.
Symptoms and Testing
The main symptoms as outlined by the Center for Disease Control (CDC) are; fever, cough and shortness of breath along with a host of other minor symptoms (CDC.gov). What sets SARS-CoV-2 apart from influenza or the common cold is the lower respiratory involvement. Symptoms usually appear in 2-7days, but there have been cases where symptoms are very delayed (beyond a week). The state of Colorado recommends that if you have these symptoms or are concerned due to exposure to a positive case to call your primary care doctor first, do not go to an ER unless it’s an Emergency.
Once the virus enters the body it binds to ACE2 (Angiotensin-Converting Enzyme 2) receptors on vascular endothelial cells and uses these cells as a host to replicate. ACE2 receptors are also found in the lungs, kidney and GI tract, all locations known to harbor coronaviruses (Jia et al). In addition to the more general symptoms, in moderate to severe cases pulmonary inflammation and damage are seen and these are considered the more critical issues when looking at long term prognosis. CT scans of the lungs were found helpful in diagnosing patients with more advanced disease (Zhu et al). Patients over the age of 65 and those having a host of other chronic disorders (hypertension, diabetes, auto-immune diseases, immunocompromised) are more likely to progress to severe COVID-19 disease than those without (Zhou et al). Though recently it has been seen that even younger patients can have lasting pulmonary damage beyond disease resolution.
Which brings us to the next issue, testing…oh testing….. When the epidemic first began in China researchers isolated and sequenced the viral genome (this is an RNA virus). Allowing them to identify unique sequences in the virus that they could use as a genetic finger print. In January of 2020 a group at the Charité University Hospital in Berlin released information on an assay that would guide the creation of the first large scale PCR testing to be adopted by the WHO (Corman et al). Since then several other countries have released different versions of the test. Since January over 1million tests have been run around the world, with China (320,000), South Korea (286,000) and Italy (148,000) leading the way (ourworldindata.org). Sadly the estimates in the United States are that only 41,000 people have been tested. I say ‘estimates’ because right now we have no National testing strategy or centralized facility monitoring our testing. Tests are being run by government labs, hospitals, private diagnostic labs and even some private biotech companies have created their own tests, but the short of it is there’s no central coordinated effort as of 3/18/20. If you’re interested in reading more about what went wrong with our testing, check this article from the New Yorker.
Which brings us to how can you get tested? Well, the short
answer is most people can’t. Because of testing shortages the guidelines on who
can get tested vary wildly from state to state and county to county. The standard
criteria in Colorado as of 3/18/20 is that you must have an order from your
healthcare provider, stating known contact with another infected patient and/or
presenting with symptoms. Even if you do meet that criteria there’s no guarantee
you can or will get tested right now, I personally know several people who fit
the criteria but have been turned away to self-quarantine and monitor. So how
do you know if you are infected with the virus? Well, in the United States right
now you really don’t, and in lieu of broader testing to identify the spread of
the virus social distancing and limitations on group gatherings (including concerts,
bars, restaurants) have been put in place.
Treatment Options
Right now there’s no fully validated and approved treatments
for COVID-19 (SARS-CoV-2). For those with more mild forms of the disease the
CDC recommends; quarantine, rest, monitor your symptoms and continue with the
preventative measures listed above. For those with more severe symptoms go to
the hospital for care.
As of 3/18/20 there are numerous companies in the early stage of testing vaccines against COVID-19, one has even begun Phase I human trials, which simply looks at whether or not the vaccine is safe in humans, it’s a long way from mass production though. There are also several approved medications that are being tested in Phase II and III clinical trials in patients suffering from COVID-19; Remdesivir, Chloroquine and Favipiravir appear to be the most promising. All three were originally developed for other diseases (Ebola, malaria, influenza) but are being repurposed to fight COVID-19 and have shown promise in early patient testing. It’s quite common for drugs to be tested and used for numerous different indications, because this expedites testing as the safety has already been proven in previous studies. EDIT: Because Trump and the FDA made specific announcements about Hydroxychloroquine today (3/19/20) I’ll add an extra note here. Hydroxychloroquine has been been used as an anti-malarial (parasite) for almost 70 years, and is also used to treat Lupus and rheumatoid arthritis, so you might ask, how does this drug help us fight a virus??? The drug alters the pH inside special compartments inside our cells (for the scientist; lysosomes, endosomes and the Golgi) having an affect on several pathways. One such pathway is the process of breaking down antigens and presenting them to immune cells (Fox et al). For autoimmune diseases this means the drug helps slow the immune response to your own body, but this is counter productive to fighting a virus that we want to kill, so what gives? Ah, but there’s an alternate pathway that the drug affects, modification of proteins in the Golgi. These modifications are essential for viruses to replicate and produce more functional virion! So the drug does function to slow down some parts of the immune system (not all) BUT it also serves to reduce viral replication (in experiments with HIV showed modest reduction, SARS-CoV-2 specifically has not been tested yet) (Romanelli et al).
Immunity?
With most infections, your body has two stages of response. First is the non-specific innate immune response where our body recognizes that there’s a foreign invader (bacteria, virus, parasite, etc) and attempts to kill it. Sometimes the number of the microbe is too great and they infect and spread in the body causing disease. All infectious organisms have a minimum infectious dose that’s required to get a person sick, though this exact amount varies from person to person, for route of entry and is different for each microbe. Once the initial non-specific response fails our body goes into overdrive to try and kill off the rapidly replicating organism. This includes running a fever to burn the pathogen out and creating a pathogen specific memory response via T-cells and B-cells selection. These specific memory responses are the backbone of what is known as pathogen specific immunity, or our ability to fight off a disease. As of now (3/18/20) it appears as though people who survive and recover from COVID-19 are immune to the virus. Recently there have been news articles about how several recovered COVID-19 patients have retested positive for the virus, these cases most likely fall into one of two categories; first that the patients were released prematurely from the hospital and thus still had low levels of virus remaining in their system, second the recovered patient came into contact with another infectious patient who transferred the virus to them allowing them to retest positive. Being immune does not mean that another person who is infected can not transfer the virus to us, it simply means our body is able to destroy the invading pathogen before it causes disease, this is how a vaccine works. Note that in both cases the affected individuals did not get sick a second time (as far as we know) and for those who become immune it is not believed they can further spread the virus once fully recovered.
Current Statistics (3/18/20)
As of 10pm on 3/18/20 there have been 219,243 people who have tested positive for COVID-19, 124,530 cases are still active (6,814 are in serious/critical condition), 85,745 have recovered (mostly in China) and 8,968 have died (worldometers.info). The current world wide mortality rate stands at 4.09% but as many have and will point out that is a flawed number because of the lack of testing and the lack of understanding what the actual case load is. COVID-19 is different than other viral infections we have because it does seem to be killing patients at a higher rate than other viruses currently in circulation. On Wednesday March 18th alone 976 people worldwide died from COVID-19, that’s a pretty astounding number, especially considering the pandemic is still spreading in many countries. In the United States we had 2,848 NEW cases on March 18th, and that’s with our testing infrastructure greatly lagging and many people not being tested. What makes the potential for this virus so scary is that it has a disproportionately negative effect on those who are elderly, immunocompromised and those who have a number of specific risk factors that depress the body’s normal immune responses. The pandemic is far from over and while none of us know exactly what will happen, it’s not looking good in the short term.
Cited Literature and Sources Bai et al, Presumed Asymptomatic Carrier Transmission of COVID-19. JAMA Network, Feb 2020. Balazy et al, Do N95 respirators provide 95% protection level against airborne viruses, and how adequate are surgical masks? American Journal of Infectious Control, March 2006. cdc.gov/coronavirus/2019-nCoV/index.html Chiang et al. Inhibition of HIV-1 replication by hydroxychloroquine: mechanism of action and comparison with zidovudine. Clinical Therapeutics, November 1996. Corman et al, Detection of 2019 novel coronavirus (2019-nCoV) by real-time RT-PCR. Eurosurveillance, Jan 2020. Doremalen et al, Aerosol and surface stability of HCoV-19 (SARS-CoV-2) compared to SARS-CoV-1. New England Journal of Medicine, March 2020. Fox et al, Mechanism of action of hydroxychloroquine as an antirheumatic drug. Seminars in Arthritis and Rheumatism, Oct 1993. Huang et al, Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Lancet, Jan 2020. Jia et al, ACE2 Receptor expression and severe acute respiratory syndrome coronavirus infection depends on differentiation of human airway epithelia. Journal of Virology, Dec 2005. Newyorker.com/news/news-desk/what-went-wrong-with-coronavirus-testing-in-the-us Ourworldindata.org/covid-testing Romanelli et al. Chloroquine and Hydroxychloroquine as Inhibitors of Human Immunodeficiency Virus (HIV-1) Activity. Clinical Pharmaceutical Design, 2004. Smith et al, Effectiveness of N95 respirators versus surgical masks in protecting healthcare workers from acute respiratory infection: a systematic review and meta-analysis. Canadian Medical Association Journal, Dec 2015. Tang et al, On the origin and continuing evolution of SARS-CoV-2. National Science Review, March 2020. Wang et al, Establishment of a reference sequences of SARS-CoV-2 and variation analysis. Journal of Medical Virology, March 2020. Who.int/emergencies/diseases/novel-coronavirus-2019 Worldometers.info/coronavirus/ Zhou et al, A pneumonia outbreak associated with a new coronavirus of probable bat origin. Nature, Feb 2020. Zhou et al. Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study. Lancet, March 2020. Zhu et al, Initial clinical features of a suspected Coronavirus disease 2019 in two emergency departments outside Hubei, China. Journal of Medical Virology, March 2020.
We threw up our hoods, put our heads down and leaned into
the wind as we left the Alpine Visitor Center. The wind ripped across the
Continental Divide and we ran, partly to make good time, partly to stay warm.
An already challenging route promised to be extra challenging on this day.
11hours in and I’d made it to the Narrows on Longs Peak!
Twelve years after running my first National Park ultramarathon in the Grand Canyon I still hadn’t completed my Rocky Mountain National Park (RMNP) ultra, despite it being my home park. I’d spent a lot of time debating the best route, settling on a ridge traverse through the park’s interior. The difficulty of the route was that almost the entire route was above treeline, holding snow late into the summer and being exposed to thunderstorms for most of the summer. My friend Ben and I picked a nice clear crisp September day (9/22/19), the one factor we didn’t count on was the wind. As we traversed the Ute trail along the Continental Divide a bone chilling wind howled from the NW.
Sunrise from the Alpine Visitor Center with the Continental Divide stretched out in front of us.
Following a section of the Ute trail early in the run. Most of the ridgeline was trailless.
We soon bailed off the trail and onto the ridge proper, where we’d stay for most of the day. As we made our way to Mt Ida, the first summit of the day, we had to duck onto the East side of the ridge to warm our hands and put on all our layers. The wind chill was brutal, and we could barely feel our hands and face. We trudged our way up and over Mt Ida to Chief Cheley (2:11, 7.3mi). Lake Azura and Highest lake were still crusted in ice and the views of the park were phenomenal. This section of the park is one of the most remote and seldom visited, miles from any trailhead and the nearest trail. We put our heads down and continued our trudge into the wind.
Proper Rocky Mountain ridge running near Mt Ida.
Highest Lake near the base of Chief Cheley, with Forest Canyon far below.
Tundra running near Sprague Mountain. Longs Peak still looks really far away (square top)
I tagged Sprague Mountain, Gabletop and Knobtop before finally reconnecting with the Flattop mountain trail (5:35, 15.6mi). Ben opted to bail off Flattop back to the car, as the wind was getting worse and there was uncertainty whether the route would go under the conditions. Solo, I crawled my way up Hallett and Otis, barely able to stand without being blown over. As I huddled in the wind block atop Otis peak, I debated my options….. Push on to the technical part of the route (the Class 5 McHenrys Notch), bail down the long East ridge of Otis Peak or return back the way I’d come to the Flattop mountain trail. Being over halfway across the traverse I opted to push on and try my luck.
Flattop Mountain with Hallet and Oatis in the background.
View from Taylor Peak towards Powell with Longs looming behind.
On the long slog up Taylor Peak (the first 13er of the day) my legs were starting to feel heavy, but the wind was actually lessening. From atop Taylor Peak (7:21, 19.1mi) I peered down on Skypond far below, and for the first time all day it looked as though the traverse would actually go! The traverse over to Powell Peak went slowly, but soon I found myself on the summit staring down the SE couloir, ready for the fun to begin. I descended a little over 200ft and located the grassy ledge system to skier’s left that would allow easy passage to McHenrys Notch. From McHenrys Notch the route is obvious, but far from easy. Directly across the Notch are two vertical Class 5 gulleys that lead to the NW ridge of McHenrys Peak.
Looking into McHenry’s Notch. The two gulleys in the middle are your class 5 options to reach the ridgeline above.
I scrambled my way up the lefthand ledge system to the broad ledge on the South side of the peak, and finished the easy traverse over to the summit of McHenrys Peak (8:39, 21.3mi). It felt great to have surmounted the crux, until I looked across Glacier Gorge at Longs Peak, oy vey, I still had a long way to go. I picked my way down through the talus field to Stoneman Pass (not the low point, but the first notch) and descended into Glacier Gorge. This would be the only time I descended into the valley. Glacier Gorge (especially the upper section) is an absolutely magical gem and one of the most iconic hiking destinations in all of Rocky Mountain National Park. Sheer granite faces surround one on all sides, Arrowhead and Spearhead jut abruptly out of the middle of the valley and numerous alpine lakes have carved out depressions amongst the barren white landscape.
Looking across Glacier Gorge from Stoneman Pass. The Trough is the obvious gulley that ascends just right of the Longs Peak summit block.
Frozen Lake tucked in the shadows of Chief’s Head Peak.
I refilled my water in one of the side streams, crossed over the head of Frozen Lake and made my way to the base of the Trough, a 2500ft gulley that swoops its way from Glacier Gorge up to the West face of Longs Peak. I felt like death as I crawled my way up through the talus and slabs just climbers right of the gulley. Time seemed to be passing in slow motion, 100 vertical feet at a time. At last I pulled myself through the windy notch at the top of the Trough and out onto the Narrows. For as many times as I’ve climbed Longs (30?), this was the first time I’d been on the Keyhole route in non-winter conditions alone. I pulled myself up the Homestretch and onto the summit block (11:16, 24.4mi), collapsing with exhaustion, but also with a smile on my face. It was 6:15pm, I was the only person on the summit, the wind had stopped, and long shadows draped themselves across the park.
Feeling like death as I slog my way up the Trough towards Longs.
The shadows of Longs Peak stretching East into the foothills.
After taking a few long breaths in, I knew I had to get moving, sunset was only an hour away, and I wanted to be below the Loft before it got dark, so back down I went, dropping down Keplinger’s couloir, ascending up past Clark’s Arrow and into the Loft between Longs Peak and Mt Meeker. I summitted Mt Meeker just as the final rays of warm sunlight disappeared over the shoulder of Pagoda Peak (12:04, 25.6mi), bathing the talus in a soft orange glow. I took off at a fairly rapid pace down through the talus, in search of the climbers ledge that would lead below the cliffs. As the light began to fade, I started to panic a little bit as I hadn’t reached the climbers trail yet, but luckily, as the last bit of daylight turned to darkness I spotted the trail just below me. Once on the ledge I knew I would be able to navigate myself back down to trail, and in the end the Longs Peak Trailhead.
The Pallisades guarding easy entry to the Loft, down and around I go.
Sun flare over the shoulder of Pagoda Peak with the Longs Peak summit block on the right. What a day.
Progress was slow as I picked my way down the Class 3 slabs and into the talus below. Once I reached the trail in Chasm meadow I was finally able to jog again….it had been over 13miles since I’d last been on trail, so being able to slowly jog felt wonderful. Tired, beat down and totally satisfied I took my time jogging down the Longs Peak trail back to the trailhead. At 8:45pm, 13:46 after leaving the Alpine Visitor center early that morning I stumbled my way onto the pavement, sat on the bench and hung my head in exhaustion. I had only covered 30.6mi and 12000ft of vertical gain, but it had taken 13h46min and I was worked.
At first glance Rocky Mountain National Park may look just
like the rest of the Colorado Rockies, but for those with the time and energy
to delve a little deeper into it’s depths, the rewards are some of the most stunning
scenery anywhere. From the 2000ft high Diamond of Longs Peak to the glacial
carved valleys of Glacier Gorge, Sky Pond and Dream Lake to the deep forests
teaming with wildlife of the North Boundary; RMNP has it all. I chose my route
because it showcased some of the most remote sections of the park, the high
alpine terrain, the crystal blue lakes, the glacial carved valleys and of course
Longs Peak in all her majesty. There are countless number of adventures within
the park, but for me this route offered a taste of all the best. For those looking
for something less committing I highly recommend the hike to Glacier Gorge and
Mills Lake, Dream Lake and Emerald Lake and for those with summit fever and some
scrambling skills Longs Peak.
This route, being a point to point was not possible without the help of a couple of good friends. So a special thanks to Michael Hodges from McGregor Mtn Lodge for helping with the car shuttle and to my friend Ben for the company on the first half of the loop and for waiting patiently at the end for me to slog my way home. And as always a special thanks to Vfuel for keeping me trudging along through such crazy adventures. My RMNP traverse was National Park Ultra #20, and I completed #21 only 3 weeks later in the Great Smokey Mountains. Even after all the time, suffering and misery I can say I’m super excited to see where this project continues to take me.
Well here goes nothing…. At 5am I set off into the darkness, slowly climbing my way up from Davenport Gap into the silence of the hardwood forest. It was Oct 14th, just over a month after my disappointing race at Ultra Trail Monte Rosa, a very unfulfilling would be end to a big year of training, so I immediately went searching for the next big challenge. Naturally my National Parks project came to the forefront, and at the very top of that list was the “Smokies Challenge Adventure Run” (SCAR). If you’re not from the East Coast I totally get your confusion at the name of the route, I was equally surprised when I first came across it in blogs in early 2019.
Pre-scouting Davenport Gap the day before the big dance. Oh boy, oh boy!
In short, the SCAR is a 72mile traverse of Great Smokies National Park from Davenport Gap to Fontana Dam (or the other way) along the Appalachian Trail, it was a logical, aesthetic and seriously challenging line (72mi, approx. 18000ft, current FKT 14h28min). My goal was to simply survive it, experience it, and take a lot of photos (it would be my first time in the Smokies). So as I power hiked and jogged up the hill from Davenport Gap, my head was swirling with doubts… was I trained enough, did I pack enough food/supplies, would the natural springs be flowing, would the weather hold? The only thing I was certain of was that I was in for one hell of an adventure.
First light hitting hitting the Appalachian Mountains in Great Smoky National Park.
A little splash of fall colors along the AT.
The initial climb went by fairly quickly, and as I crested
the ridgeline near Mt Cammerer the first glow of sunrise was showing in the
East (5.2mm, 2:45). Now atop the ridgeline I settled into my goal pace for the
day, hike up each knob/peak, then jog the descents and flats. The trail was a
mix of deep hardwood forest with fleeting views from the various lookouts and
knobs along the trail. Finally, I crested Mt Guyot and jogged my way down to
the Tricorner Knob shelter (15.7mm, 4:10), my first reliable water source. 2019
was a dry year in the Smokies, as such many of the springs had dried up, and
even the ever reliable Tricorner Knob was reduced to a piped trickle, though
just enough to treat a bottle before moving on.
Early morning light filtering through the deep forest.
Tricorner Knob shelter, the trickle of water is on the right.
The route stuck pretty close to the ridge for the next
section, with several beautiful narrow sections of ridgeline where one could
look down both the North and South sides of the ridge. Over Mt Sequoyah, Eagle
Rock, Laurel Top, Porter’s Gap and The Sawteeth. The foliage was several weeks
behind, but the hillsides were dotted with yellows, oranges and reds, just
enough to break up the endless sea of green. As I passed Charlie’s Bunion I
began to encounter a steady stream of hikers. By the time I reached Ice Water
Spring and Mt Kephart there was an almost endless line of hikers strung out
along the trail. Thankfully most people were aware enough to allow me to cruise
on by, and I soon popped out of the woods into the madness that was Newfound
Gap (30.3mm, 7:15).
Splashes of yellow adorn the Great Smoky Mountains.
A little fun rocky single track along the AT.
I knew Great Smoky NP was the most visited National Park in
the US, but I was definitely not ready for crowds. Cars were backed up for a
mile on either side of the pass as many more endlessly circled the parking lot.
By a stroke of luck I was actually able to find my mom, who had offered to meet
me at the trailhead for a food and water resupply. I reloaded my S-lab 12 and
jogged out of the parking lot, quickly leaving the masses behind. I hike/jogged
along the rolling forested AT up towards Clingmans Dome, the high point of Tennessee
and the day. As I neared Clingmans Dome I had my first low point of the day, I
bonked hard, slowly slogging my way up the Clingman Dome fire tower (39.6mm, 10:05).
Selfie atop the lookout at Clingmans Dome, back from the dead….for now.
View from Clingmans Dome into Tennessee.
The soft afternoon light makes the forest glow.
The views were 360 degree panoramic and the air was
unusually clear, allowing one to see a long way into both Tennessee and North
Carolina. After taking in the views I again disappeared back into the dense
hardwood forest, losing all the crowds instantly. It was all downhill from
here, literally and figuratively. The trail slowly became rockier, and my legs
were definitely not getting any spunkier. Down, then up, then down again, then
up…. I didn’t seem to be losing any elevation, even though I’d passed the high
point? I finally reached the Derrick Knob shelter (49.3mm, 12:45) for a water
resupply, the pipe was again trickling, just enough.
Derrick Knob shelter, water refill station and new friends.
A little solo silent single track running soothes the soul.
I paused for a moment to chat with the group staying at
Derrick Knob, and the inevitable question came up…”So where are you coming
from”….”Davenport”….”How many days did it take you”……”I started this
morning”……”WHAT?!?!?”. I don’t know why I bother trying to explain, but they
were nice enough to point me in the right direction, so off I went. The light
was slowly fading away, and the end didn’t seem to be getting any closer. The
short steep climbs up Thunder Mountain and Mt Squires were soul crushing, the
last just as the sunset faded away in the West, it was going to be a long dark
road (54.4mm, 15:15).
Sunset from Mt Squire on a long day, with many miles to go.
The miles seemed to drag on, over Mollies Ridge and down to Ekaneetlee Pass. I had been dreading the climb to Doe Knob, though knew it was my last significant uphill before what I hoped would be a cruiser downhill to the Fontana Dam. The power in my legs had disappeared on Thunder Mountain and it took all my concentration just to stay upright and on my feet. The dense forest seemed to wrap the darkness tight around me, and it felt as though there was nothing but me and the trail. Finally, I reached the turn where the AT leaves the ridgeline of the Great Smoky Mts and heads due South (64mm, 17:18). I started to jog down the overgrown track, only to find my legs were jello, and I was struggling to not stumble off the trail with every single step. I finally gave up and settled into a soul crushing 16min/mile stumble down the trail, frustrated I couldn’t run, usually my strength.
Just after midnight at the Fontana Dam, happy to be done, and completely worked.
Spending the day after the SCAR quietly recovering along one of the many gentle rivers in Great Smoky National Park.
The miles seemed to pass be excruciatingly slow in the darkness, but at last I popped out of the dense woods at the trailhead, only 0.5mi of road left to the dam! Now back on smooth ground I was able to slow jog down to Fontana Dam and the sign marking the boundary of Great Smoky Mts National Park. 72miles (+/-), 18000ft (+/-) and 19h and 25min after leaving Davenport Gap I’d completed the SCAR. I had received a thorough ass whooping on some beautiful but challenging East Coast trail and my first introduction to the Great Smoky Mts had been one hell of a ride. I definitely underestimated the run, but was grateful to have had the opportunity to experience such a classic AT route. Special thanks to my Mom for helping me out with logistics and making the run possible, and to Vfuel for keeping my energy up throughout most of the run. 21 National Park ultramarathons down….only 35 more to go!
