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    Gabriele Taylor was my undergraduate philosophy tutor at St Anne’s College, Oxford from 1989-1992. I remember her as an incisive…

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Why is the new variant of the coronavirus more transmissible (if it is)?

Brian Leiter

It's been hard to find a clear answer to this in the media.   The most common surmise I've seen is that the new variant reproduces more in the nose and throat, and so people expel more of it when they sneeze or cough.   But a recent NYT article suggests these as possible explanations:

In a typical coronavirus, the tip of the spike protein is like an ill-fitting puzzle piece. It can latch onto human cells, but the fit is so loose that the virus often falls away and fails to infect the cell.

The N501Y mutation seems to refine the shape of the puzzle piece, allowing a tighter fit and increasing the chance of a successful infection….

One mysterious [additional] mutation in the B.1.1.7 lineage [of the coronavirus] deletes the 69th and 70th amino acids in the spike protein. Experiments have shown that this deletion enables the coronavirus to infect cells more successfully. It’s possible that it changes the shape of the spike protein in a way that makes it harder for antibodies to attach.

I'd be curious to know what other accounts of the mechanism readers have seen.  I'll conclude with observations by longtime reader Dr. David Ozonoff from the Boston University School of Public Health, with whom I've corresponded a bit about this:

I don’t think we know how (or truthfully even whether) the virus is more transmissible. Transmission is very complicated and depends on characteristics of the host (us), the environment (social behavior, season, etc.) and the virus itself. The evidence so far available does suggest increased transmission is very plausible but I don’t believe the evidence is ironclad (but it doesn’t have to be). In this context the exact mechanism (which is what you seem to be seeking) is just speculative and increased viral load is a reasonable speculation. Increased affinity for the ACE-2 receptor and increased infectivity of younger age groups has also been mentioned. I don’t think we can say what the exact mechansm or mechanisms is/are at work here.

UPDATE:  Dr. Ozonoff just sent along this informative new article from the generally excellent STAT.

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3 responses to “Why is the new variant of the coronavirus more transmissible (if it is)?”

  1. Jennifer Hornsby

    In the UK it is generally accepted — thanks both to lab. experiments and to epidemiologists' study of the spread of the new variant* — that the new variant IS more transmissible. Since even the lockdown sceptics believe this, I can't think there's much reason to doubt it.
    * https://cmmid.github.io/topics/covid19/reports/uk-novel-variant/2020_12_23_Transmissibility_and_severity_of_VOC_202012_01_in_England.pdf
    [Admittedly this hasn't yet been peer-reviewed.]

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  2. David Ozonoff

    I agree that increased transmissibility is generally accepted by most knowledgeable observers (including me), but the matter is much more complicated than given credit for. The pre-print cited is pretty clear that the evidence is circumstantial and based largely on modeling:

    "Combining multiple behavioural and epidemiological data sources with mathematical models, we estimated that the novel SARS-CoV-2 variant VOC 202012/01 is more transmissible than existing circulating SARS-CoV-2 viruses.

    Despite these limitations, we found strong evidence that VOC 202012/01 is spreading significantly faster within southeast England than preexisting non-VOC 202012/01 variants. Our modelling analysis suggests this difference can be explained by an overall higher infectiousness of VOC 202012/01—with some evidence that the increase may be particularly marked in children—but not by a shorter latent period or immune escape alone."

    It can be very difficult to disentangle the various estimates of increased transmissibility, what they are based on, and what they mean. Taking account of different ways to estimate whether the variant is more transmissible does indeed strongly suggest increased transmissibility, although how much and in what contexts is not at all clear at this juncture. I don't think the main question is binary (whether to doubt it or not) but rather what exactly it means in a population context. As I suggested in an earlier communication with our blog host, increased transmissibility is more troubling than increased virulence (disease severity) because it grows exponentially. Increased virulence only grows linearly.

    Having said all that, I am not really a doubter. I too accept that B.1.1.7 is more transmissible. I find the evidence very plausible. But just plausible, at this point.

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  3. Jennifer Hornsby

    Thanks. I can only agree that the matter is complicated, and I certainly don’t pretend to know much about the complications.
    You’re saying that what I said was generally agreed is very plausible. That for which there’s very plausible evidence should impinge on public policy, I think, and it's for the best that it should be generally agreed. My disagreements are with people who care not about what's very plausible, who make stuff up, and who repeat claims that have actually been disproved.

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