Viruses are Bastards
This is long. VERY long. It also lacks citations, which were in there but I have not managed to get BibTex citations back into the new blog structure. I’ll work on this this week. To comment, please comment on the fediverse post (search for https://medic.cafe/@mikka/109658494762289336 on your instance), comments will show up below this.
Viruses are assholes. Once you peer down that raster electron microscope, you’ll find, that most anything else you see, has its beneficial members. Bacteria in our gut make life as we know it possible. The same is true for fungi. Bread? Beer? Kimchi? Sauerkraut? Unthinkable without yeasts.
Viruses, on the other hand, are by and large not-nice. That’s not to say they’re all bad and have never done anything nice for us. 8% of our genome is derived from retroviruses that, at some point, probably killed most of a population and left the remainder better off. Endogenization, the integration of viral DNA into our own, is probably responsible for us being us.
Viruses can also be plague-ending. It is hypothesised, that mankind survived some of the greater challenges to its move from small clusters of disjointed packs to a more social form of interaction by either being infected with, and building immune responses, to a weaker version of a bad viral strain, or by becoming hosts to viral infections that preferentially infected bacteria and protozoa that would have, otherwise, killed the host.
But, yeah, viruses kill more than they save. Which, evolutionary, should speak against them. Killing your host works for some pathogens, Rabies comes to mind, if the route is oral. But especially respiratory viruses need their hosts to live and breathe. That they’re still around is not so much a testament to human survivability but to viral resilience and spread mechanics.
In other words: unlike other pathogens, once a virus has arrived, it remains and makes itself a home.
There’s a way out (sometimes): vaccination. Smallpox was successfully eradicated when Edward Jenner realised that a weaker version of the virus, cowpox, conferred an immunity against the eviler strain, smallpox. In fact, the word “vaccination” comes from lat. “vacca” (cow). Another virus that was eradicated is Rinderpest, a bovine viral disease affecting ruminants. It is close to the measles virus and was combated, successfully, via a live attenuated vaccine in 2000, with no cases known since 2009.
Other viruses, such as the measles virus itself or rubella, could be effectively eradicated if vaccines were more widely available in developing countries and if vaccine hesitancy wasn’t a thing.
What all those viruses have in common, though, is a long pre-prodrome (“incubation period”). Viruses use the symptoms of their infection to spread. Fecal-oral viruses use diarrhoea or polyuria, respiratory viruses use coughs and sneezes, and so on. Hepatitis A, for example, is fecal-oral, and causes diarrhoea. Hepatitis C is blood borne and causes bleeding.
I say “causes” but that’s of course wrong. The virus is an unthinking, unliving, piece of DNA or RNA, only replicating because it uses the host’s own mechanisms. And the mechanism for spread in living things is, usually, that living thing’s innate immune system. So, in a sense, it’s not the virus that kills and spreads, it’s our own inherent immune system. That’s not always true. Some viruses explode their host cells so rapidly and vehemently, they cause symptoms themselves. But their impact is, even in those cases, much less injurious than that of the innate immune system.
To put this in terms we’ve used a lot and, sadly, interchangeably in the past 1100 days: SARS-CoV-2 is the virus. Its presence in the human body causes the innate immune system to react. This reaction is called COVID-19. So we’re not “getting COVID-19.” We’re “developing COVID-19” from an infection with the SARS-CoV-2 Virus. This becomes very(!) important at the end of this very long piece.
But nature has a way to fix that. Instead of one immune system, we have two. The innate immune system is that first responder. It is, in a way, the “bouncer” inside us. Consisting of barriers such as skin or mucosa, that keep pathogens out, cilia that move pathogens back out once they got in, and huge cells that gobble up everything they see that does not look “right” (the so-called Macrophages, Greek for “big eater”), it’s the immune response version of a toddler with a bag of hand grenades and flame thrower. Sure, the enemy gets decimated, but the environmental damage is great, and the destruction tangible.
That’s where the second immune system, the adaptive one, comes in. Where the innate system is a toddler with a flame thrower, this one is the special forces sniper with a long range scope. Trained specifically to identify and eliminate one treat, it lays in wait until the enemy shows its presence, and … whack. Little to no collateral damage.
But training specialists takes time. If the enemy was not encountered before, a curious Hunger Games like dance begins: Macrophages (and others such as their little cousins, the dendritic cell) murder invaders and then, like the toddler they are, proudly drag parts of the eliminated threat actor back to their mothers. Or, in this case, the lymph nodes, where young specialist recruits wait to be trained. The dance is simple: each specialist recruit can assemble randomly a set of tools to combat this invader. If the tools work, the specialist is either sent out to kill, becomes parent to many more specialists with the same tool, or becomes a memory cell that will remember the right tool for the job for a more or less long time.
If the specialist fails, it is eliminated, lysed into its components and reused to make a new specialist.
To leave this morbid metaphor, learning new pathogens takes time. Time that, in some cases, we don’t have. Viruses that cause violent innate immune responses and integrate into the host’s own tissue (such as all Herpes Viruses, more about that in a second) are still able to maim or even kill before such training happened. And many viruses will have, by that time, used the innate immune systems’ response to spread. That’s bad.
So back to vaccinations. Vaccinations preempt that training phase above, often without causing much of the innate immune response. And even if they do, the training material we inject or give per mouth is capable of training but not of replicating or leaving the body and infecting others.
However, and that’s the rub: even a learned immune system takes time to engage. The specialists who were made memory cells take days to replicate into an amount sufficient to kill the virus. The good news is, that once this happens, body-internal signalling as well as the reduction in pathogen load, tells the innate immune system to pipe it down. We take the flame thrower from the toddler. With that, we reduce both spread and mortality.
But back to the respiratory virus thing. Remember that word, up there? Prodrome? Pre-Prodrome, also known as “incubation period” is the time from infection to symptoms. In some cases, like Hepatitis C, this can be weeks to months. In Measles it’s still 11 to 12 days. Same for Smallpox (7 to 19 days).
That’s enough time to build up that adaptive immune system again. Not enough time to learn from scratch, but if a vaccine or a prior infection caused our bodies to learn the intricacies and build memory cells, the response is faster than the development of symptoms. Or, in other words, the two acute things about viral infection: spread and the mortality from our own innate immune systems’ response, are prevented.
In SARS-CoV-2, that incubation period is below three days in all strains and between one and 2.8 days depending on strain, up to seven days in two strains that do not circulate anymore, and even 12 days in a strain that basically offed itself by taking so long.
Sex, age, morbidities, or prior infection have no impact on this. 2.8 days after infection you’re infectious and you’ll be having symptoms (often so mild you won’t even notice them, which is dangerous since you’re still infectious and don’t know to isolate).
A weakened innate immune system, funnily enough, can help here. By taking itself longer to respond, or responding much less violently, a tired toddler in other words, it reduces symptoms and spread. In the long run, however, that’s no good.
So what does this mean for us?
It means that, even with a prior infection or vaccination, we’ll get infected again if we’re exposed to the virus. And we’ll be infectious, no matter what. If we’re vaccinated or had a prior infection, that will end faster, with less symptoms (which, we remember, are mostly caused by the innate immune system, not the adaptive). So we’re, on a time axis, less infectious.
But we simply don’t have enough time to respond to the infection before it becomes symptomatic.
The lockdown measures taken in the first months and years of the pandemic, along with vaccinations and masks, had a profound impact on the damages that could have been. There is no doubt and no denying (though some less than savoury and less than educated people try), that they prevented a much, much, worse outcome. Especially the health care sector, swamped as it was with SARS-CoV-2 cases, was shielded from a much worse outcome. If you think what we experienced was bad (and it was), just think how it’d have been without those measures.
But they also led to another, law of unintended consequences and all, side of things: SARS-CoV-2 is extremely infectious. It takes very little to become infected, so little in fact, that studies in China and Spain showed that room air with no discernible viral presence could still lead to infection in some people. And “some people” is enough for a virus to spread. There’s a reason more than 75% of all SARS-CoV-2 infections happen at home or in close acquaintance quarters.
With it being that infectious, we essentially eradicated all strains, very often before we noticed it, that took more to spread: the ones that were deterred by masks, the ones that didn’t make it to being infective fast enough and got caught by that adaptive immune response. And with it being so mutagenic, meaning it mutates faster and more than other viruses (largely this is a function of easy spread and wide distribution, not so much a direct mutagenic ability), more virulent and less easily caught strains emerged and became the norm.
No where is this as visible as in China today. After years of brutal lockdowns, that caused very real human and economic harm, forced testing (we recall the shocking videos of goons clad in hazmat suits dragging people from their homes or beating and tasing them into testing stations), and many more measures to effect a “Zero Covid” state, all it took was a loosening of the measures and new strains, probably circulating in smaller communities for months, spread like wildfire. China still has mandatory testing and mask mandates even in social, private, functions. Yet, the virus “found a way” around. That is, if we attribute consciousness to a piece of RNA. Which we should not.
For us this means three things:
The virus is here to stay. Like any other virus (and, remember, I promised a bit of waxing on Herpes at the end), the question of its eradicability is based on its incubation period. Measles, Polio, Smallpox, or the Rinderpest (a measles virus, we recall), can be eradicated. Vaccines protect pretty well against infection with or the transmission of Hepatitis B (90 day incubation period). Vaccines don’t protect against being infected with or infecting others with SARS-CoV-2.
Ok, ok, there’s an exception to this. Those specialists, they don’t just go away over night. After they have been activated, they stick around for a while. During that time, about three to six months in the case of SARS-CoV-2, any hapless virus making its way into the body will face the might of SEAL Team Over 9000 and stand no chance. So, in a way, strain adapted vaccinations every six months might help tremendously.
It also means, that we can’t rest on old measures. The virus will find a way around them. Masks and lockdowns worked, and mask mandates should not be senselessly discarded, but that’s not what an ever evolving viral profile needs to be combated alone. Vaccinations save lives, reduce spread, and take strains off the health care system.
But, and this is number three: infections will happen. Everyone, masked or not, lockdown or not, vaccinated or not, will become infected and will infect others. Infections can cause, not only in the unvaccinated or people with metabolic or other morbidities, long sequelae (long term effects).
So the measure today is not to rest on the laurels of yesteryear but to realise that there won’t ever be a Zero Covid. And that now, research into the prevention, diagnosis, and treatment of Post-Infective Syndrome must be the new focus.
This isn’t fatalism. It’s not throwing our hands up and giving up. It’s going back to the first few paragraphs: two things in SARS-CoV-2 are problems: developing COVID-19 and long term sequelae.
If we can’t prevent infections, we can do more. We can still rely on barriers (masks, testing, stay at home, less large scale events). This does not prevent infections, but it might stretch the gaps between infections from once a year to maybe once every other year. That’s, over the lifetime of a human being, a lot.
If infections happen, we have to have good means to combat the effects of COVID-19. This means a continuous development of tools and medications (think Tamiflu for SARS-CoV-2), as well as working screening to detect developing COVID-19 symptoms. Here, for example, technology like Quantified Flu, can help. It detects minute changes in body temperature, using popular technologies like the Apple Watch or Oura Rings. A warning that something might be “in the bush” could lead to earlier detection of infections and appropriate measures.
Speaking of earlier detection. Some companies are working on more sensitive and more specific tests that can be done at home without all the hassle of nasal swabs, adding buffer, etc. A simple strip, licked once, that shows infections with a high sensitivity (yet, as of now, pretty low specificity, leading to too many false positives).
Infections can cause a host of long term symptoms. 7.5% of all infected adults had sequelae for up to six months after resolution. Over one percent had even longer persistent issues. The biggest challenge here is to differentiate between sequelae unique to SARS-CoV-2 and those generally known as “Post-Infective Syndrome,” a host of post-infective symptoms that occur in most viral and some bacterial infections and generally resolve over time. But even here, the number of those infected SARS-CoV-2 puts another demand on science to finally take PIS seriously, despite the funny acronym, and research diagnoses and care.
A Tangent that is almost longer than the article
Which brings us to that “I’ll talk about Herpes for a second” part. Indulge an aging warrior for a second, because to him this isn’t new.
In fact, there’s a virus we all should know, but few do. And even fewer take it seriously.
What if I told you, it was highly infective. That many children and almost all adults were exposed to it? That its traces can be found in over 90% of Europeans over 25? And that it had a higher likelihood than SARS-CoV-2 of causing immediate, acute, damages.
More, what if I told you, that that sequelae of this virus not only make SARS-CoV-2 long term effects look like child’s play, they’re probably responsible for most of those SARS-CoV-2 long term effects?
How about this: when you’re infected, which can last from weeks to months, you’re at risk of your spleen exploding. Your platelets may become so reduced, brushing your teeth can cause anemia or worse. You could develop viral hepatitis from it and be at a very real risk of liver cancer or cirrhosis. You could get myocarditis from it. Encephalitis, meningitis, and Guillain-Barré syndrome are also possible and not super rare.
Once you have it, it will remain in your body. It can reactivate at any time, but mostly when another viral infection (like SARS-CoV-2 hits you) and cause all of the above again. In a majority of people hospitalised with COVID-19 that had no other comorbidities (overweight or obese, age, immunocompromised, Type 2 Diabetic), this virus was found to have been reactivated.
In rare cases, this virus can become chronic (0.1-0.3%). These people have swollen lymph nodes, their liver and spleen suffer and may go on strike or self-destruct. They also have constant muscle aches, headaches, anemia, and fatigue.
Oh, it gets worse. This virus causes 50-70% of all childhood cancer in Africa. The deadly Burkitt Lymphoma is caused by it. Only 35% of all patients (all of them young) survive. But even in western countries, all lymphomas, leukemias, and autoimmune disorders have a strong correlation with it. Did I mention nasopharyngeal cancers, or cancers in the back of the nose? Or stomach cancer?
And that’s not to mention that recent studies seem to suggest that Type 1 Diabetes and rheumatoid arthritis are caused by it, as well as IBS and… and this is the kicker… multiple sclerosis seems to be linked to it as well.
The virus is called EBV, Epstein-Barr virus. EBV has a cute name in Germany “the Students Disease” and in English it’s called “Kissing Disease.” Because that’s mainly how it spreads. In earlier days, with parents being less affectionate and the age of romance happening later, it usually hit students after their first romantic encounters. In most people it causes a brief period of fever and stomach aches. In some it causes more. We all know someone who had “Mono” as a kid, which is short for “infectious mononucleosis,” the disease caused by EBV. This virus infects naïve tonsillar B cells, meaning it sheds into the mouth, using an immune system component to do so. That immune system again, eh?
So why did I tell you this? Simple: viral infections are bastards and have killed many million people. The 2009 and 2017 flu pandemics killed many people. EBV kills. Hepatitis kills. That does not minimise the need to care for and against SARS-CoV-2, but outlines that maybe it is time to have a more comprehensive viral prevention and treatment program that lets go of the “barriers protect” as the only paradigm and combines barriers with treatment and other means of prevention.
A good example here is HIV. While there were no other means, barriers (condoms) were the only way. Today, with post- and pre-exposure prophylaxis and antiviral drugs that lower viral load to an undetectable level, we are able to curb the disease. And that does not mean you should stop wearing condoms, but condoms aren’t the only, and not the best, defense anymore.
Health inequities and religious, social, and political resistance stand in the way, so those as well need addressing and working on.
We can’t eradicate most viruses. But we can do what we do best, if we are willing to do the work: respond. And if there is a political, social, and societal will to do so, if there are mechanisms in place that encourage Pharma and research to find those responses, then SARS-CoV-2 and, almost more importantly, EBV or Hepatitis, won’t claim as many lives or ruin as many lifetimes anymore. And that’s a good thing.
For years EBV researchers were the callers in the forest, screaming into a void that something has to be done. It took SARS-CoV-2 to cause world wide visibility of the bastards that are viruses. Rather than contently leaning on masks and lockdowns, let’s use this momentum. Let’s research. Let’s demand research. Let’s end Burkitt Lymphoma and reduce MS to a rare occurrence.
We can do it.
This entry was revised in late 2021 to include new findings and new research.
This entry was revised in early 2023 to be added to the new blog and received a huge overhaul. No changelog remains, but I’ll restart that now. Treat it as a new piece and disregard the older ones.