(Editors’ note: This essay will be appearing in Uncanny Magazine Issue 34, but we felt it necessary to release it immediately. Author Kelly Lagor will be periodically updating the article as more is known. Updated 3/31/20)
The world is a different place today than it was a month ago, as more and more countries adopt increasingly stringent lockdown policies in an attempt to get ahead of the growing coronavirus epidemic. We have entered a state of collective limbo, watching the number of diagnosed cases worldwide climb towards one million, as dramas surrounding access to testing, and availability of personal protective equipment and necessary medical equipment evolve. It’s hard to not feel anxious and wonder when life will ever feel normal again. It’s hard not to worry about what the world will look like on the other side of this, making it easy to feel helpless and alone.
With calls for social isolation and distancing to help reduce rates of transmission, “flatten the curve,” and relieve the serious burden on our medical institutions, these feelings of helplessness are compounded. After all, our communities are where friendships and partnerships are made and sustained. Our communities inspire us, define us, give us drive and a sense of purpose. This is true of any of our communities—from professional to academic to artistic, local to regional to global. Isolated from that sense of purpose and identity, we need to remember we are doing this not only to protect ourselves, but those larger communities, and through them, our collective futures.
It is no surprise that the worldwide lockdown was preceded by the canceling of large meetings of people. Conferences and conventions are notorious spreaders of disease. In fact, the rash of post-con illness is such a common phenomenon there is a special name for it—con crud. Con crud can be anything from the common cold, to norovirus, to an outbreak of H1N1 Swine Flu at the 2009 Penny Arcade Expo in Seattle. The stress, lack of sleep, poor diet, increased inebriant consumption, disruption of exercise routines, and impaired ability to regularly wash your hands all conspire to weaken the immune systems of even the healthiest attendees, all while surrounded by large numbers of people who have traveled from all over the world to hang out together in a confined space.
With the COVID-19 situation evolving daily, it’s understandable to feel apprehensive about leaving your home or interacting with others. The situation isn’t being helped by inconsistent messaging coming from politicians, public health agencies, social media posts, forum comments, and talking heads. And with journalists and medical professionals under high pressure as they scramble to feed a public anxious for updates, misinformation has at times been given a stamp of authenticity on its way into the 24-hour news cycle. So amid a barrage of anxiety and misinformation, how can you best weather this storm? Go about your life thinking it’s a bunch of overblown nonsense, or build yourself a fort of toilet paper and face masks?
As an immunocompromised, asthmatic biologist, and a speculative fiction writer who relies on my communities for my inspiration and sense of purpose, I have been following the continuous flow of coronavirus updates out of a sense of both professional curiosity and personal vigilance. We need to remember we’re all in this together. As a member of a vulnerable population in a state where I have been mandated to stay indoors and practice social distancing, it’s hard to sit by, helpless, watching my retirement funds evaporate and try not to think about the end of the world. While these kinds of situations often bring out the good in many, it brings out the worst in others, and there are already examples of stigmatization of Asians and Asian-run businesses in response to COVID-19 news. Novel diseases have always sparked particularly visceral public reactions—see the AIDS epidemic of the 90s, for one. So whenever I find myself dealing with such an emotionally fraught topic, I try to arm myself with the best information I can, which for many can be challenging when a lot of the useful information about a disease outbreak comes from an evolving understanding of the biology of that disease. Therefore, to help better understand why such a big deal is being made about COVID-19, I’d like to start with a brief lesson in virus biology.
Viruses are considered the minimum form of life on our planet. They’re made up of a handful of genes that sit on a relatively short string of DNA or RNA (which can be single- or double-stranded), wrapped in a coat of proteins that both protect its fragile genetic material, and help that genetic material enter an intended host cell to replicate and thus complete the virus’ life cycle. As long as there has been life on earth, there have been viruses to infect it, and as life evolved in complexity, viruses have evolved right alongside it into an array of species as diverse as there are hosts on our planet.
What determines a virus’ infectious properties are the specific proteins it wraps itself in, which are encoded by their genetic material. The role of some of those coat proteins is to recognize and attach to different structures on the surface of potential host cells. Most viruses, once attached, use other specialized coat proteins to penetrate the cell to allow it to slip inside. Protected inside the host cell, the genetic material can shed its coat, then use the host cell’s DNA or RNA synthesis machinery to make copies of its genetic material. There are a few different hypotheses about where viruses came from—from genetic elements that gained the ability to move between cells, to being the remnants of cellular organisms, to thinking viruses predated or coevolved alongside their hosts—but they are still made of the same stuff that all life is made from, and therefore can use the normal replicative machinery of any cell on earth to translate its genetic material into the coat proteins it needs to wrap its new copies in. These new viroids will then escape, usually by bursting and killing the host cell to start the process over again. There are viruses that have different lives than this one, but for many viral infections, this is their cycle.
All organisms have evolved an equally diverse array of defense mechanisms to protect themselves from being completely wiped out by such a relentless, mindless biological simplicity. In humans, viral immunity is handled by our two-tiered immune system. The first is our evolutionarily older, innate immune system. This is the “nuke it from orbit” system that is designed to keep new viral infections from getting out of hand. Infected cells 1) release specialized proteins that tell neighboring cells to be on their guard and 2) take little bits of an invading virus to display on its surface to flag down a type of killer white blood cell to destroy the cell before the virus gains a foothold. But this system is often imperfect, and some viruses have evolved ways of ducking it. The second line of defense is our newer, adaptive immune system, in which a different subset of white blood cells randomly makes antibody proteins until one such cell makes an antibody that recognizes the invading pathogen. Those lucky cells proliferate, using those antibodies to bind up free virus to be later mopped up, preventing further infection. This system operates on a bit of a lag from the innate system, but once the infection is dealt with, a subset of these cells sticks around in perpetuity in case that particular pathogen returns. This system is the intended target of vaccinations—to generate those memory cells without having to have the disease first, so that if you are infected, your immune system can mop it up without you ever noticing.
The danger of viral infections is therefore twofold. First, in a normal, healthy person, if you’re infected with a virus like we described above that you’ve never encountered before, your innate immune system will, along with the virus, cause the death of infected cells. In the case of something like the common cold, your sinuses bear the brunt of the onslaught until your secondary immune system makes the antibodies that help clear things up in 7-10 days. But in the case of more virulent viruses you get more severe infections, such as in influenza, which leads immune cells to release factors which stimulate your hypothalamus to increase your body temperature, which may help to interfere with further viral replication but is what causes a fever and its associated muscle aches and chills. But still, if your immune system is healthy, your body will make antibodies to eventually mop up the infection. Or if you got your flu shot and caught one of the strains the vaccine was raised against, you’ll likely not even notice. Better yet, you get your flu shot every year and you’ve got a whole host of memory cells patrolling for all kinds of flu viruses all year, every year, for years.
But if you’re immunocompromised, things become much more dire. Your innate or adaptive responses to an infection may be impaired, which may cause more cells to become infected than normally would—spreading from the nose to the throat to the lungs, and there to the kidneys or elsewhere. This can cause increased inflammation and cell death, which can lead to pneumonia, where the accumulation of fluids from the inflammatory response accumulates in the lungs, impairing oxygen transfer, leading to hypoxia, organ damage, and even death. There are also lots of different ways to be immunocompromised. You might take immunosuppressants for an autoimmune disease to keep your immune cells from attacking the cells of your own body, or to protect a transplanted organ from being rejected. You could be older and your immune system just doesn’t work as well anymore. Maybe you have reduced white blood cell counts due to a genetic disease, or from AIDS, or from chemotherapy, or because you lost your spleen in an accident. Or maybe you have an underlying condition that may complicate an infection, such as asthma, diabetes, or malnutrition. Often, these are invisible illnesses, and you may not be aware of the number of vulnerable people around you on a given day.
Now let’s talk about COVID-19. COVID-19 is the disease caused by the SARS-CoV-2 virus, which is a member of the coronavirus family of viruses. Coronaviruses are single-stranded RNA viruses that cause diseases in mammals and birds. RNA viruses mutate more rapidly than DNA viruses do, which means coronaviruses can more easily acquire the kinds of mutations in the genes that encode their coat proteins, which makes their shapes slightly different and might let them go from just recognizing their animal host cells to being able to recognize human cells they might encounter, say by being inhaled, or when we touch a contaminated surface, then touching one of the mucous membranes on our face. Coronaviruses cause diseases in humans that range in severity from a few strains that cause the common cold, to the SARS-CoV virus, which killed 11% of the over 8,000 people it infected in a 2002 outbreak originating in China, to the MERS-CoV virus, which has killed over 34.4% of the small number of diagnosed cases (n=2,494) in the Middle East since 2012.
If the 2002 outbreak of SARS sounds like a familiar story, that’s because it is. The first case was reported in November 2002, and the virus, thought to have arisen originally in bats, was propagating in animals like wild civets, which were caught and sold in a meat market in Guangdong Province. The Chinese government drew intense international criticism after failing to inform the World Health Organization (WHO) for two months, and not disseminating information about the disease to healthcare providers, which impaired early efforts to control the epidemic before it spread to dozens of other countries prior to its containment in July 2003. China subsequently banned the kind of markets where animals like the infected civets were sold. The initial hypothesis that the origin of the SARS-CoV-2 virus, which was first identified in December 2019, came from pangolins at a meat market in Wuhan may not be accurate, but the genetic sequence similarity of the virus may again point to an origin in bats before it jumped to humans at a seafood market in Wuhan. What’s different this time is that China reacted quickly and publicly, going from the first case reported to identification and determining the genetic sequence one month later.
There are two important differences between the 2002 SARS-CoV and the SARS-CoV-2 viruses. The first is, unfortunately, how quickly and widely it has spread, with over 200,000 confirmed cases (and counting) in countries all over the world. The reason for this is twofold. 1) Our immune systems haven’t encountered the SARS-CoV-2 virus before, so we are more at risk for developing symptoms and being contagious if we catch it, as we don’t have memory cells in place from previous infections or a vaccine to help quash it quickly, and 2) this means we are more likely to be able to pass it on to those around us once we become contagious. There appears to be a lag time of—on average—five days between catching SARS-CoV-2 and developing symptoms (as determined by a study of 181 case files). Public health agencies initially reported that infected individuals were most contagious after they became symptomatic as the virus spreads through droplets expelled when coughing or sneezing, but a recent paper released by the journal Science indicates the the reason for the rapid spread of the disease is likely due to asymptomatic transmission. This is why such an abundance of caution is being taken—five days is a long time to walk around unaware that you are spreading disease. As such, the quarantine the world is implementing may help slow its spread by keeping those who are infected but asymptomatic away from others.
The second important difference is that the mortality rate of those diagnosed cases is lower than for SARS-CoV, hovering at about 3%. Let me put that into perspective. One of the bigger annual threats to the immunocompromised and those with complicating conditions is the seasonal flu, which has a mortality rate this 2019-2020 season of 0.06%. By contrast, COVID-19 so far has a higher mortality rate than the 1918 H1N1 Spanish Flu (Spanish Flu – 2.5% vs. 4.8% with COVID-19 as of March 30th, 2020). While Spanish Flu disproportionately killed young, otherwise healthy adults (due to how the virus strongly activated the innate immune system, triggering what’s known as a cytokine storm, which caused rapid onset respiratory failure), COVID-19 disproportionately kills a similar demographic to the seasonal flu—the immunocompromised and those with complicating conditions. Furthermore, young and healthy individuals should not assume they are immune to COVID-19 complications—hospitalization and fatality rates are much higher for any population than for the seasonal flu. Because it is spreading so easily and puts at-risk populations at an even greater risk that there is such an abundance of caution being taken worldwide. The goal of these measures is to “flatten the curve”—i.e. to slow the spread of the disease to prevent already overtaxed healthcare systems from potentially becoming overwhelmed, which could lead to further loss of life.
In this time of increasing social isolation and anxiety, we can’t forget that we are all part of a global community that has to look out for each other. While the decision ultimately will lie with you if you decide to flout the advice of your local governments and public health agencies, it is important to be mindful of the unique risks your actions will be having on your larger communities, be it if you’re a member of a vulnerable population, or if you have regular contact with members of that population. Everywhere in the world is now at high risk for COVID-19 transmission, and our ability to test for the virus continues to be hampered by the lack of availability of tests. During this critical time, it is essential we all adhere to the advice of our public health agencies, remember that our decisions may have wider, unintended consequences, while trying not to give too much weight to emotionally charged, secondhand information.
- Wash your hands often, with soap and water, for at least 20 seconds.
- If soap and water isn’t available, use an alcohol-based hand sanitizer with at least 60% alcohol.
- Stay home when you are sick and minimize contact with others until you are well.
- Cover your cough or sneeze with a tissue, then throw the tissue in the trash.
- Practice social distancing to keep at least 6 feet between you and anyone else to reduce the likelihood of community transmission of the virus
Even if the WHO convinced every viroid of SARS-CoV-2 to shed its protein coat tomorrow and walk into the sea, remember that doesn’t mean the immunocompromised and the vulnerable within our communities will get to stop suddenly worrying about their worlds being turned upside down thanks to what may become a not-so-simple case of con crud. As COVID-19 comes and will eventually go, remember con cruds of all types will remain threats to those with compromised immune systems. Hopefully understanding a bit more about viruses and immunity will help you to remember in every year to come that you have an obligation to be mindful and to protect not just yourself, but the communities that support and sustain us all.
Kelly Lagor is a scientist by day and science fiction writer by night. Her fiction and nonfiction have appeared in various places and she tweets and blogs about all kinds of nonsense @klagor and at kellylagor.com.
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