Omicron: four insights from this week.

We've learned tons already. Scientists will learn even more from this experience so that in the future, there will be less uncertainty.

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In this installment of Inside Medicine, I’m sharing a collection of timely talking points; insights and analyses regarding the Covid-19 Omicron variant.

Over the last week or so, I appeared on several television networks to discuss various aspects of Omicron, what we know, and what we are learning. While I usually am given a sense of the topics before going on live television, sometimes the anchors go in unexpected directions. Sometimes they don't ask key questions I anticipated. The result is, sometimes I say things I had not planned on saying, and sometimes I don’t get to say important things I had meant to work in.

So, I thought I’d share some of these talking points with you here. In the four clips below (from CNN with Anderson Cooper, BBC News with Nada Tawfik, CBSN with Lana Zak, and Yahoo! Finance with Akiko Fujita, Jared Blikre, and Anjalee Khemlani), I managed to discuss some of the following talking points, but some of them didn’t quite make it on air. Without further ado, here are my Omicron talking points for the week of November 29-December 5, 2021, with key points in bold:

1. Scientists are getting better at reading the genetic sequence of a virus and predicting how it will behave based just on that information. But that technological know-how has a long way to go before we can accurately prognosticate whether a brand new Covid-19 variant like Omicron will be more contagious or make people sicker. There are two analogies I've been mulling over that I think capture the situation.

a. Weather. Over many years, meteorologists have improved in their ability to track radar and satellite images and forecast how serious a storm may end up being several days later. Similarly, geneticists are getting better at looking at mutations in a virus variant and estimating how its behaviors may differ from earlier versions as a result of those changes.

b. Architecture. Seasoned experts can look at design plans on a piece of paper or a screen and tell us whether that building will be safe once built. Other experts can opine on how well the space will serve its intended function. By analogy, scientists are now looking at mutations identified in new variants and are learning how to interpret whether that virus might be more contagious, or if it might evade vaccine- or infection-derived immunity.

We’ve never studied a virus so intensely as we are studying SARS-CoV-2, so I expect rapid progress in this realm. While we should expect an endless parade of worrying new variants to emerge at some clip for the foreseeable future, I believe the windows of uncertainty will become shorter, and answers will come sooner and sooner. With each go-round, scientists will get better at knowing whether a new variant is a genuine threat, based on the genetic information we can now obtain almost immediately.

2. Evolution favors a virus that has mutated to become more contagious. If a new mutation that a virus acquires while replicating in our bodies makes that virus easier to spread or more likely to evade our immune system's existing immunity to it, the viral particle that contains that particular mutation will outcompete other particles and proliferate. If the advantage is great enough, it can eventually take over an entire region. For example, if you have two variants that are approximately equally contagious, around 50% of cases in a region will be each variant if the first cases occurred around the same time. But if one is substantially more contagious, it will soon drown the other variant out. Delta did exactly this last summer. We do not yet know whether Omicron will do the same. This is the classic example of "survival of the fittest."

3. Evolution does not favor a virus that has mutated to cause worse disease or death more frequently. Viruses, including coronaviruses, do not actually benefit from making us sicker. In fact, at the extreme, if a virus killed its host within minutes of invading it, that virus would die out because it would not have a chance to use our bodies to replicate and spread to another host. One of the great evolutionary advantages a respiratory virus can have is the ability to spread from one host to the next before the first person has developed symptoms. Why? Because when we acquire an infection, the symptoms we experience actually serve several purposes. The main purpose is to fight off the infectious pathogen. Fever, cough, sneezing, and nasal congestion may be bothersome, but they are actually immune adaptations, albeit inefficient ones. When we experience cold and flu-like symptoms, that is a telltale sign that our bodies are fighting off an invader, literally trying to eliminate or expel it. But nasty symptoms have another evolutionary function: they serve as a kind of warning to those around us, as if saying, “Stay away from me, because I am probably contagious with some nasty virus.” Viruses that become highly contagious before symptoms appear exploit those usual assumptions. Generally, we assume when we encounter a person without any outward signs of illness, they're probably not carrying some communicable disease we might catch. So, we lower our guard. The smartest experts I know believe that SARS-CoV-2 “superspreading” occurs when a person who is asymptomatic (or has just the slightest inkling of early symptoms) encounters a high number of people in a small, poorly ventilated space.

4. Is Omicron deadlier than previous variants? Does it cause infections in people who have already had Covid-19 or been vaccinated (and even boosted) against it? So far, we have been relying on anecdotes. Soon, carefully collected data will be available and made public. Then we will know for sure. Until then, we have to be careful not to jump to conclusions. We've begun to suspect that reinfections will be more common with Omicron. But what can we make of the early clinical anecdotes we've heard? For example, hospitals in South Africa have started sharing detailed albeit informal information on what they’ve been seeing. The news is good, for now. Most of the significant cases have been found among the unvaccinated. But the overall numbers may still be too small to be reliable. As we know, the case fatality rate for Covid-19 can range from far under 0.1% in some young people, to well over 5-10% in some older and sicker populations. So it would take many, many cases for the numbers of good and bad outcomes to start to mean anything, statistically. The talking point I kept returning to this week was that “anecdotes are asymmetric.” What I mean by that is this: if I heard that the first 25 Omicron patients that a hospital treated were all vaccinated or boosted, and they were all on ventilators fighting for their lives in the intensive care unit, I would be very concerned. Based on the usual averages, a sudden early influx of patients like this would be highly worrisome. (In general, we see a wide array of Covid-19 patients, from barely symptomatic to actively dying.) On the other hand, so far, the lack of “bad outcomes” in the anecdotes we’ve heard could simply reflect “business as usual” for Covid-19. If Omicron is “another Delta” that would still be terrible news—even though at this point, given the hype, it will be a relief if we learn that Omicron does not cause worse disease or that does not evade the protection against severe illness, long-term suffering, hospitalization, and death that vaccines have brilliantly provided so far.

Here are four segments from the past week:

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