Spreading Omicron May Be Safer

Here is a Wall Street Journal Opinion article by Vivek Ramaswamy and Apoorva Ramaswamy titled "
Slow the Spread? Speeding It May Be Safer".

I suspect these guys are right.  If so, it provides another example of the incompetence, or worse, of Government and a whole bunch of other organizations and people.

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The Omicron variant is spreading across the globe, but so far the strain appears to be less deadly than its predecessors. That’s good news, but here’s a risk that policy makers in every country should appreciate: Policies designed to slow the spread of Omicron may end up creating a supervariant that is more infectious, more virulent and more resistant to vaccines. That would be a man-made disaster.
To minimize that risk, policy makers must tolerate the rapid spread of milder variants. This will require difficult trade-offs, but it will save lives in the long run. We should end mask mandates and social distancing in most settings not because they don’t slow the spread—the usual argument against such measures—but because they probably do.

To understand why, first consider an important scientific distinction, between antigenic drift and antigenic shift. Antigens are molecules—such as the spike protein of SARS-CoV-2—that an immune system detects as foreign. The host immune system then mounts a response.

“Antigenic drift” describes the process by which single-point mutations (small genetic errors) randomly occur during the viral replication process. The result is minor alterations to antigens such as the spike protein. If a point mutation makes the virus less likely to survive, that variant gradually dies off. But if the mutation confers an incremental survival advantage—say, the ability to spread more quickly from one cell to another—then that strain becomes more likely to spread through the population.

Antigenic drift is a gradual, varying process: A single-point mutation alters one peptide, or building block, of a larger protein. Hosts with immunity against a prior strain generally enjoy at least partial immunity against “drifted” variants. This is called “cross-protection.”

Each time an immune host is exposed to a slightly different antigenic variant, the host can tweak its immune response without becoming severely ill. And the more similar the new strain is to the last version the person fought off, the less risky that strain will be to the host.

By contrast, “antigenic shift” refers to a discontinuous quantum leap from one antigen (or set of antigens) to a very different antigen (or set of antigens). New viral strains—such as those that jump from one species to another—tend to emerge from antigenic shift. The biological causes of antigenic shift are often different from those of antigenic drift. For example, the physical swap of whole sections of the genome leads to more significant changes to viral genes than those caused by individual point mutations.

But there’s a sorites paradox: How many unique point mutations collectively constitute an antigenic shift, especially when human hosts are deprived of opportunities to update their immune response to “drifted” variants?

Vaccinated and naturally immune people can revamp their immune response to new viral strains created by antigenic drift. Yet social distancing and masking increase the risk of vaccine-resistant strains from antigenic shift by minimizing opportunities for the vaccinated and naturally immune to tailor their immune responses through periodic exposures to incrementally “drifted” variants.

This is a familiar notion in virology. Take the rise of severe shingles cases over the past decade, partly a result of the widespread use of the chickenpox vaccine. Shingles and chickenpox are caused by the same virus. Before widespread use of the chickenpox vaccine, parents regularly updated their own immunity by getting exposed to chickenpox from their children, or from other adults who were exposed by children. But now that most children are vaccinated against chickenpox and don’t contract it, older adults suffer from more severe cases of shingles.

The absolute risk of a more virulent strain of SARS-CoV-2 is low. That’s because viruses “care” more about propagating themselves than about killing the host: Most viruses evolve to become more infectious and less virulent. But this is only a rule of thumb, not a biological law. Like any trend, we should expect a distribution of outcomes around the modal one—and the more iterations you allow, the more likely you are to get an unlikely outcome. Enforcing social-distancing policies amid widespread vaccination makes the emergence of a vaccine-resistant superstrain more likely.

Why not prepare for this outcome simply by developing new vaccines against novel strains more quickly? Because even mRNA vaccines can’t be developed fast enough to outrun a vaccine-resistant supervariant. On Dec. 8, Pfizer committed to delivering its first batch of new vaccines that cover the Omicron variant within 100 days. Yet by mid-March, a significant percentage of the U.S. population will have already been infected with Omicron.

Meanwhile, mask mandates and social-distancing measures will have created fertile ground for new variants that evade vaccination even more effectively. Significant antigenic shifts may create new strains that are increasingly difficult to target with vaccines at all. There are no vaccines for many viruses, despite decades of effort to develop them.

Will relaxing restrictions come at the cost of more hospitalizations and deaths as the next variant starts to spread? Perhaps, but it would reduce the risk of a worst-case scenario and greater loss of life in the long run.

The most important step in fighting the Covid-19 pandemic was the distribution of vaccines. With this milestone now achieved, the global response should shift from preventing the spread to minimizing the probability of an antigenic shift. Whether SARS-CoV-2 was made in a lab is the subject of debate, but let’s make sure we don’t manufacture an even more dangerous strain of the virus with misguided policies.