The first concerning variant has come to be known as B.1.1.7. It was first reported in the UK late last year but has now been detected in at least 60 countries, according to the World Health Organization. Report after report has demonstrated that this strain spreads person to person more readily than the original strain.
B.1.1.7 is not the only strain that appears to have this capability. California experts, for example, have recently described an unrelated variant, dubbed CAL.20C, which is also thought to be highly transmissible and may be responsible for much of the dramatic increase in cases there.
And surely there will be others -- this is how all viruses behave. They replicate many times over but each copy is a not-quite-perfect replica of the original. These mistakes, in the eyes of scientists, are called mutations and can accumulate quickly. Eventually, an environmental pressure is imposed on the countless slightly mismatched copies and a new "more fit" viral mutated strain will emerge. It's evolution 101: if one viral strain can get from here to there faster or more efficiently than the other strains, it will infect the next person and the next person and the next person before the other variants can get near the anyone. And presto -- it is king of the hill.
The control of a more contagious strain seems to me to be straightforward and effective: even more attention to the now-familiar "mask, social distance and avoid crowds" approach for many more months as the population is systematically vaccinated.
In addition to increased contagiousness, two other alarming possibilities have been suggested for various new strains: greater lethality and the possibility of reduced vaccine effectiveness.
Before sinking into despair however, it is important to remember that early information from labs and news agencies, though crucial to keep the public on their toes, is far short of established truth. The judgment of these observations by sober peer review has not yet taken place. We have seen only pre-prints and analyses of several pre-prints at once, but no officially refereed medical journal publications.
Recall the recent hydroxychloroquine era of bad feeling when rumors and carnival barker claims ran far ahead of boring but incisive published scientific reports that showed the drug does not have clinical value in treating Covid-19. As is the case with hydroxychloroquine, we must mind the gap in time between clickbait headlines and scientific publication.
Giving the newness of the reports, it is not surprising that the issue of increased lethality with some strains is far from settled. The most compelling argument has been laid out by experts in the UK who have reviewed their experience with the B.1.1.7 strain. According to UK medical experts, the variant may be as much as 30% more lethal, leading the US CDC to actively review the data.
Patrick Vallance, the chief UK health adviser, has described the potential impact clearly: "for every 1,000 60-year-olds infected with the new strain, perhaps 13 or 14 might be expected to die, compared with 10 in 1,000 for the original strain." A small statistical difference perhaps but at the scale of millions of cases, a possible public health calamity.
But unlike the claim of increased transmissibility, the jury is still out on this one. Vallance has noted that the data is "not yet strong" and the UK group presenting the data already has expressed their substantial uncertainty. Per their report, there is a "realistic possibility" that B.1.1.7 is more lethal than the original Covid-19 strain -- and they chose this wording carefully. They define a "realistic possibility" as having a 40% to 50% likelihood (aka a coin toss) of eventually being proven true. This range is set in contrast to "likely or probable" (55% to 75%) or "highly likely" (80% to 90%). In other words -- it is maybe true that the B.1.1.7 may be more lethal. Right now, that's all that can be said.
The final concern is perhaps the most chilling: two preliminary, non-peer reviewed reports, each from South Africa have explored why, however rarely, some patients develop two sequential infections from two distinct strains, suggesting the immunity developed from the first infection was insufficient to protect against a second strain.
In one study, newer strains of the virus were combined with a lab-produced monoclonal antibody that was known to be effective in controlling a strain of the original "Spring 2020" virus. Researchers found that, in the test tube, these same monoclonal antibodies that protect against the original virus strain failed to control some of the newer viral strains. This suggests that such these antibodies -- part of the antibody repertoire induced by current vaccines -- might be ineffective at warding off infection from variant strains.
The other experiment also was a lab-based, not clinical, observation. In this one, a different group of researchers found six patients who had survived actual Covid-19 infection from early strains of the virus. They took samples of these patients' blood, skimmed off the antibody portion and then exposed the antibody to new virus strains found in South Africa. The old antibody did not handle the new virus as briskly as expected.
This work is extremely important but also extremely preliminary: not peer-reviewed, small sample sized, lab-based observations only. We would be wrong to ignore the findings -- but even more foolish to take the conclusions as definitive evidence of trouble. Especially since there are no reports of vaccinated persons developing disease from a new strain. The current amount of vaccine-induced antibody seems sufficient. That said, the current vaccines will likely need to be updated eventually to better protect against the ever-evolving virus.
And perhaps most important of all, antibody is only one part of the complex mechanics of human immunity. Other types of immune response, such as that delivered by the T-cell lymphocyte, may well be functioning at full capacity even against the various newcomers.
It was inevitable that the evolving information throughout the pandemic was, is and will remain confusing. In addition to the intrusion of politically motivated mischief is the simple fact that we developed technology that has outstripped our ability to understand, really, just what the test results mean. Yes, we have sophisticated neutralizing antibody tests and phylogenetic trees constructed from whole genome sequencing and complex artificial intelligence-based models to simulate possible population dynamics -- but we don't fully know what's going on. Information is all around us but has no clear truth to build upon. Or as the poet said, "water water everywhere / nor any drop to drink."
But this is how progress always looks when it unfolds in real time. Giant steps forward are tidied up for entry into history books. Fleming invented penicillin! Salk invented the polio vaccine! Steve Jobs invented the personal computer! Missteps and screw ups, chaos and panic, high anxiety and deep fear are all whited out from the official version so that the flow of progress appears smooth and steady.
Live events though, can be miserable to experience, no matter how happy the eventual ending. And the unsettlingly high pitch of confusion that characterizes the Covid-19 pandemic right now demonstrates that countless brilliant, cantankerous, sometimes loopy scientific minds are working on the problem. In other words, the noise you hear right now is the surest sign that real progress is being made.
"Opinion" - Google News
January 29, 2021 at 09:06AM
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What do we really know about the new Covid-19 variants? - CNN
"Opinion" - Google News
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