Cons, Crud, and Coronavirus

The world is a different place today than it was a month ago, as world governments scramble to gain the upper hand against the still-growing coronavirus pandemic. We are in a state of collective limbo, watching helplessly as the number of worldwide cases climb towards two million, and dramas around testing, personal protective equipment, and critical medical supplies continue to unfold. It’s hard to not anxiously wonder if life will ever feel normal again. It’s hard to not worry about what the world will look like on the other side. It’s hard to not despair.

With calls for social distancing to help reduce the rate of transmission, “flatten the curve,” and relieve the serious burden on our medical institutions, 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 purpose—from professional to academic to artistic communities, on local to regional to global scales. As we continue to isolate for the foreseeable future, we need to remember we are doing this not only to protect ourselves, but those larger communities, and through them, our collective futures. We are all in this together.

It is no surprise the worldwide lockdown was preceded by the canceling of large meetings. 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 Flu1 at the 2009 Penny Arcade Expo in Seattle. The stress, lack of sleep, poor diet, increased inebriant consumption, and disruption of exercise routines all conspire to weaken the immune systems of even the healthiest attendees, while the ability to regularly wash your hands is impaired, increasing the risk of pathogen infections; all the while being surrounded by large numbers of people who traveled from all over the world to hang out together in a confined space.

With the COVID-19 situation continuing to evolve, it’s understandable to feel apprehensive about 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 higher pressure as they scramble to feed a public anxious for a glimmer of hope that will mark the end of this crisis, misinformation continues to find 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 news out of a sense of both professional curiosity and personal vigilance. As a member of a vulnerable population in a state where I have been mandated to stay indoors2 and practice social distancing3, 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, including hate crimes and other stigmatizations of Asians and Asian-run businesses. Novel diseases have always sparked particularly visceral public reactions—see the AIDS epidemic of the 90s4, 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 cold5, 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 influenza6, 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 touch one of the mucous membranes on our face. Coronaviruses7 cause diseases in humans that range in severity from a few strains that cause the common cold, to the SARS-CoV8 virus, which killed 11% of the over 8,000 people it infected in a 2002 outbreak originating in China, to the MERS-CoV9 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 accurate10, 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 Chinese scientists reacted quickly and publicly11, 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 study12 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, which was also the case with the 2002 SARS-CoV virus, but a recent paper13 in the journal Science indicates the SARS-CoV-2 virus is also being spread by the asymptomatic. This is why such an abundance of caution is being taken—five days is a long time to walk around unaware you are spreading a dangerous disease. As such, worldwide quarantine efforts were enacted to keep those who are infected but asymptomatic away from others.

The second critical difference is that while the mortality rate among diagnosed cases is lower than for SARS-CoV, it is still dangerously high. Let me put things 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 season14 of 0.06%. By contrast, COVID-19 so far has a higher mortality rate than the 1918 H1N1 Spanish Flu15 (Spanish Flu – 2.5% vs. 6.2% with COVID-19 as of April 12th, 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 demographic similar to the seasonal flu—the immunocompromised and those with complicating conditions16. Furthermore, young and healthy individuals should not assume they are immune to COVID-19 complications—hospitalization and fatality rates are still much higher17 for all populations than for the seasonal flu. Because it is spreading so easily18 and puts at-risk populations19 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 spread20 of the disease to prevent already overtaxed healthcare systems21 from becoming even more overwhelmed, leading to further loss of life.

These are unprecedented times. But perhaps in the long run some good will come out of it. Perhaps by exposing  the inherent weakness of individualist political philosophies and a blind beliefs in capitalism, we can begin to take steps towards a world in which we begin to act like the global community that we are—one in which we can depend on one another not only for our collective survival, but for better future in which compassion and mutual aid is a central piece. For now, we must focus on the smaller steps, resisting the urge to buy into emotionally charged, secondhand information that promises false hope, and remain vigilant. We must remember that our decisions may have unintended and potentially lethal consequences.

Here are links to the current recommendations from the CDC22 and the WHO23 for the public:

  • 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
  • Wear a mask in public to reduce the potential for asymptomatic spread of the virus through breathing and talking

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, and the sort of vigilance you’re exhibiting now is the same vigilance they have had to exhibit every day of their lives. Hopefully understanding a bit more about viruses and immunity will help you to remember you have an obligation to be mindful to protect not just yourself, but the communities that support and sustain us all.



[1] “PAX Swine Flu Outbreak Soars to Nearly 100 Cases of ‘H1Nerd1′” by Gus Matrapa. Wired. September 9, 2009.

[2] ” California Governor Calls For Closure Of All Bars, Wineries To Combat Coronavirus Spread” by Associated Press, KPBS Staff. KPBS. March 16, 2020.

[3]  “Self-Quarantine? Isolation? Social Distancing? What They Mean And When To Do Them” by Julie Appleby. NPR. March 16, 2020.

[4] ” LGBTQ History Month: The early days of America’s AIDS crisis” by Tim Fitzsimons. NBC News. October 15, 2018.

[5]  “Common Colds: Protect Yourself and Others.” Centers for Disease Control and Prevention, Centers for Disease Control and Prevention, 11 Feb. 2019,

[6] “Influenza (Flu).” Centers for Disease Control and Prevention, Centers for Disease Control and Prevention, 10 Apr. 2020,

[7] “Coronavirus.” World Health Organization, World Health Organization,

[8] “Severe Acute Respiratory Syndrome (SARS).” World Health Organization, World Health Organization, 23 July 2015,

[9] “Middle East Respiratory Syndrome Coronavirus (MERS-CoV).” World Health Organization, World Health Organization, 10 Mar. 2020,

[10] “Mystery deepens over animal source of coronavirus” by David Cyranoski. Nature. February 26, 2020.

[11] “China’s response to a novel coronavirus stands in stark contrast to the 2002 SARS outbreak response” by John Nkengasong. Nature. January 27, 2020.

[12]  Lauer SA, Grantz KH, Bi Q, et al. “The Incubation Period of Coronavirus Disease 2019 (COVID-19) From Publicly Reported Confirmed Cases: Estimation and Application.” Ann Intern Med. 2020; [Epub ahead of print 10 March 2020]. doi:

[13] Li, Ruiyun, et al. “Substantial Undocumented Infection Facilitates the Rapid Dissemination of Novel Coronavirus (SARS-CoV2).” Science, American Association for the Advancement of Science, 16 Mar. 2020,

[14] “2019-2020 U.S. Flu Season: Preliminary Burden Estimates.” Centers for Disease Control and Prevention, 10 Apr. 2020,

[15] “1918 Pandemic (H1N1 Virus).” Centers for Disease Control and Prevention, Centers for Disease Control and Prevention, 20 Mar. 2019,

[16] Wu, Zunyou. “The Coronavirus Disease 2019 (COVID-19) Outbreak in China-Summary of a China CDC Report.” JAMA, American Medical Association, 7 Apr. 2020,

[17] “Global Covid-19 Case Fatality Rates.” CEBM,

[18] “Johns Hopkins Coronavirus Resource Center.” Johns Hopkins Coronavirus Resource Center,

[19] Centers for Disease Control and Prevention,

[20] Godoy, Maria. “Flattening A Pandemic’s Curve: Why Staying Home Now Can Save Lives.”  NPR, 13 Mar. 2020,

[21] Centers for Disease Control and Prevention,

[22] Centers for Disease Control and Prevention, Centers for Disease Control and Prevention,

[23] “Advice for Public.” World Health Organization, World Health Organization,


Kelly Lagor

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

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