COVID Transmissions for 4-7-2022
Is SARS-CoV-2 even the most common coronavirus anymore?
Greetings from an undisclosed location in my apartment. Welcome to COVID Transmissions.
It has been 842 days since the first documented human case of COVID-19. In 842, Byzantine Emperor Theophilos died of dysentery, and passed the throne to his 2 year-old son (his mother ruled as regent). One of many moments where disease has shaped history.
Today we will discuss a few topics in COVID-19; “new” symptoms being recognized by the UK government, a story about interactions between SARS-CoV-2 and genes involved in cancer, and then lastly evidence that SARS-CoV-2 is no longer the most common coronavirus in the US. All that content is free.
In the paid Other Viruses section, we’ll talk about hepatitis C virus, a blood-borne pathogen, and where it might have emerged from.
Have a great weekend!
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Now, let’s talk COVID.
UK adds new symptoms to watch for in the BA.2 environment
The New York Times reports that the UK has expanded its list of symptoms to be watchful for in suspecting COVID-19: https://www.nytimes.com/2022/04/05/world/europe/britain-nhs-covid-symptoms.html
Specifically, the list now includes fatigue/exhaustion and nausea. Something that is pointed out in the article is that previously, the UK’s National Health Service (NHS) had a really limited list of potential symptoms and had been criticized for this. Meanwhile, the change coming during the BA.2 surge in that country may make these additions seem as though they are being driven by a change in the virus.
However, fatigue and nausea are common nonspecific symptoms of many viral illnesses. I have heard reports of both in the context of COVID-19 going back to early 2020 when the main information I had on symptomatology came from Chinese people who I know on social media. So, I would not take this information as evidence of some fundamental change in SARS-CoV-2. Rather, perhaps we can consider that finally, the NHS’s experience with a range of cases has become so extensive that their evidence base is coming to include less-specific symptoms such as these.
Interaction of SARS-CoV-2 elements with cancer-related genes
I recently saw a certain online personality raising concern that SARS-CoV-2 could cause cancer, on the basis of a paper that suggested there are possible direct interactions between SARS-CoV-2 gene products and the products of 4 genes that are involved in cancer, as well as indirect interactions with products of 92 genes involved in cancer.
That paper is here, a preprint that has not been peer reviewed: https://www.biorxiv.org/content/10.1101/2022.04.04.487020v1
I’m writing about this to quiet the alarmism. Firstly, many viruses interact with genes that are involved in cancer. This is because the same immune pathways that shut down viruses are also responsible for culling cells that could potentially become cancerous. This is not new information, and there are many viruses that interact with these types of pathways without causing any kind of cancer. In fact, sometimes these virus-host interactions have made the interacting viruses attractive targets for what are called “oncolytic therapies,” wherein a virus is used to target and destroy cancer cells.
What’s important here is that many viruses kill the cells they infect, and consistently. SARS-CoV-2 is one of those viruses. Sometimes this happens because the virus triggers a pathway that tells the cell something is wrong, and the cell is programmed to destroy itself under those circumstances. Sometimes this happens because the virus throws the cell so far out of whack that it gets destroyed. It can happen a lot of different ways.
Cancer, meanwhile, develops by gradual mutation of body cells to the point where they do not respond by dying when they are presented with problems that would lead other cells down the path of programmed cell death. That’s not all it takes to yield cancer, but it’s a big part of it. The sensors and alarms that would normally detect cell stress, virus infection, and more are all things that viruses have trouble with also.
Furthermore, some of the cell machinery that can be repurposed in useful ways by cancer can also be repurposed in useful ways by viruses. So of course evolution to exploit similar pathways would occur both in cancers and in viruses. There is nothing surprising about this, and it has been documented many times for many viruses.
At the end of the day none of this rules out a possible cancer-causing mechanism for SARS-CoV-2, but certainly none of this rules it in, either. The best argument that this is meaningless for cancer-causing activity is one I’ve already stated: viruses kill cells, and cancer emerges gradually.
A dead cell is dead and won’t become cancerous. Cancer has to emerge gradually. SARS-CoV-2 killing the cells that it infects stops them from becoming cancerous, for certain. So I don’t really see this having wide-ranging implications unless we discover a definitive mechanism by which SARS-CoV-2 can persist in the body without killing cells. Since no one has demonstrated anything like that, I want to push back against claims that these data suggest a possible future where many recovered people end up with cancer.
Instead, I think this is a perfectly fine paper that helps us understand how SARS-CoV-2 interacts with pathways that also regulate cancer, a fact which could be used when considering therapeutics against the virus. There are a lot of failed anti-cancer therapies out there that are safe, but weren’t effective against cancer. If SARS-CoV-2 is using the same cellular machinery, perhaps one of those candidates would make a good antiviral. That’s the takeaway for me, here.
According to one source, SARS-CoV-2 is currently not the most prevalent coronavirus in the US
I recently discovered a new website called Syndromic Trends. It is operated by a company called BIOFIRE Diagnostics, which makes systems for diagnosing illnesses caused by various pathogens.
One of the things that this diagnostic company does is create what is basically an index of respiratory pathogen prevalence. I don’t find their particular metric to be very transparent, and I wish to emphasize this, but essentially by weighting the average prevalence of various pathogens that they test for, at the various sites where their system is used, they are able to estimate the share of overall respiratory illness being caused by specific pathogens within their dataset.
This is not exactly rigorous epidemiology. We have a sample of respiratory illnesses collected at healthcare sites within the US that happen to have chosen to purchase and use a specific diagnostic system. The chances for bias are big here.
However, as something to provide general estimates? I think the recent data are pretty interesting.
Specifically, here is the estimated share of respiratory illness being caused by various coronaviruses:
This is really interesting to see. While I am always skeptical of national data—local is always preferable—and there are potential sources of bias here, the history of this graph follows the history of the US national pattern with regard to SARS-CoV-2 over time. And there are a few lessons we can learn from it.
One, we’re in a period of relative safety. If you felt confident going out last summer, if this is to be believed, we’re in a similar situation now—and probably with a greater share of population immunity. Second, just because we are in a period of relative safety now doesn’t mean we can’t see huge surges later. The highest peak on this graph comes after the first time that SARS-CoV-2 crossed OC43 prevalence by this indexing method. So, when I say “period of relative safety,” I think I might as well be saying “smoke ‘em if you got ‘em.” We can’t predict the future and this doesn’t mean the pandemic is over. But it does suggest that if you’ve taken the right precautions for your individual situation, this is one of the safer times in the pandemic to get out and enjoy yourself. Again, that’s if this is something to be believed. There are many reasons these data could be flawed. But they’re interesting!
When I say you should try to enjoy yoursevles, though, that doesn’t mean being reckless. Keep those masks handy and a close eye on what your local situation is. Keep an eye on ventilation where you are. Keep your vaccinations current.
Part of science is identifying and correcting errors. If you find a mistake, please tell me about it.
Though I can’t correct the emailed version after it has been sent, I do update the online post of the newsletter every time a mistake is brought to my attention.
No corrections since last issue.
What am I doing to cope with the pandemic? This:
Rewriting workplace COVID-19 policy
I talk about work as vaguely as possible here—largely to comply with social media policies set by my employer but also because it is and should be irrelevant—but lately, work and this newsletter have overlapped in a few big, practical questions in front of me:
Can we expect the current lull to hold? For how long?
Is the pandemic coming to an end?
How do we protect people who will still be vulnerable to COVID-19 when the pandemic ends?
I don’t have good answers to these questions yet. I don’t have an answer to “when can the masks come off, really?” But they’re what I’m contemplating at night. I think it is interesting that as COVID-19’s prevalence dips, and more people are able to put it out of their minds, it is even more often on mine.
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Where did hepatitis C virus even come from?
In the RNA virus community, hepatitis C virus (HCV), is a very strange species. It’s a positive-sense RNA virus that infects the liver and spreads largely through intravenous drug use or blood donation, and is specifically a human virus. And in the evolutionary record, it seems to be at least 200 years old, if not up to 1000.1
This begs an immediate question—how can a virus that spreads primarily via modern technologies be so old? Let’s explore.