New variant of coronavirus would have a higher transmissibility 28:33
Editor's Note:
William Haseltine, PhD, is chair of the global health expert group ACCESS Health International.
He is the author of numerous books, including his recently published autobiography, 'My Lifelong Fight Against Disease: From Polio and AIDS to COVID-19'.
The opinions expressed in this comment are yours.
You can read more articles like this at cnne.com/opinion.
(CNN) -
The UK Government has sounded the alarm about a variant strain of SARS-CoV-2, the virus that causes Covid-19, which appears to spread more easily than previous versions.
Although much is still unknown, what we know about this new variant tells us important things about the virus: it can adapt to become more easily transmissible and could become more difficult to neutralize, possibly being able to beat the vaccine to a small extent. .
To date, SARS-CoV-2 has mutated at a fairly constant rate, with only one or two variations per month.
Some variations have caused scientists to pause, sometimes by mutating to become more transmittable and at other times by mutating to become more effective at avoiding detection by our immune systems.
But with this new variant, called B.1,1.7, the virus has acquired 17 mutations while changing the proteins of the virus, according to the Centers for Disease Control and Prevention, which affect four different viral proteins: peak protein, ORF1ab, Orf8 and protein N, the main nucleocapsid.
While the large number of mutations in a variant is concerning, what is perhaps more concerning is how the mutations, taken together, could change how the virus works.
One of the mutations, N501Y, increases the strength with which the spike protein binds to the human ACE2 receptor, which may make it easier for the virus to take root in those infected.
This mutation is probably why this new variant, first isolated in the UK in late September, now accounts for more than 60% of new infections in and around London.
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A second mutation in the spike protein, 69-70del, removes two amino acids, the removal of which may allow the virus to evade some immune responses and, combined with another mutation, may make it more transmissible.
The 69-70del mutation has been found in other variant strains, including the Denmark mink strain, and appears to occur when patients carry the virus for several months under immune pressure, not necessarily from the patient's own immune system but from treatments such as the convalescent plasma that pumps antibodies into the patient's system.
A third mutation, P681H, occurs in what is called the spike protein cleavage site, which is an area known to affect how quickly the virus can enter and kill cells.
Changes in this part of the virus could potentially increase its ability to cause disease, and its lethality, although there is no evidence yet to show that this new variant is more dangerous to humans.
This mutation alone is enough to be disturbing.
The fact that it is combined in this variant strain with another mutation of the Orf8 protein, which can also increase pathogenicity, is cause for alarm.
Mutations affecting the other two proteins, ORF1ab and the N protein, are also suspected to allow the virus to replicate more rapidly and evade the immune system, although much more research is needed to see how each of these 17 mutations affects how the virus works.
Still, we know enough to make some assumptions.
First, SARS-CoV-2 knows how to adapt and adapt quickly, just like the flu virus.
Therefore, we must be prepared for the possibility that the virus will be with us in the long term.
Like a flu shot, a covid shot might not be a one-time affair.
We already know from a recent study published in the
New England Journal of Medicine
that the half-life of neutralizing antibodies in at least one of the vaccines, Moderna's vaccine, decreases relatively rapidly over a three-month period in those who respond most vigorously. and shorter in those with a less vigorous response.
Although the study was small, it questions whether a vaccine that is received today will remain effective for 12 months, 18 months or longer.
B.1,1.7 tells us something new: not only could immunity disappear, but the potency of the vaccine itself can change if the virus changes.
This is not to say that modern medicine cannot keep up with an evolving covid-19 virus, as it does with the flu.
But it may not be as simple or as easy as many had hoped it would be.
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Second, with the 69-70del mutation we may be facing a medical paradox.
In an effort to save the lives of the immunosuppressed who were infected with the virus, healthcare providers sometimes administered multiple rounds of antibody treatments to their patients.
In some cases, patients recovered after a round of treatment only to get sick again and require another dose.
Even in a single patient, immune suppression over a period of weeks and sometimes months gives the virus a multitude of opportunities to learn our best defenses and to mutate to be more effective in evading our immune systems.
Although the administration of antibody treatments can save a human life, a study from the United Kingdom hypothesizes that it could also facilitate the creation of new strains of the virus.
Lastly, the variant suggests that we must immediately begin planning the next generation of covid vaccines to respond more effectively to a changing virus.
That licensed vaccines are already being tested against the new variant should give us some hope.
The companies have expressed confidence that their vaccines could protect against it, and BioNTech noted that its vaccine could be modified to combat the new variant.
Variant of covid-19 would have arrived in the US in November 0:30
Still, it is worth continuing to study targets for alternative vaccines that could be more effective in protecting the population against variants of the virus.
Right now, most vaccines in development target the spike protein.
This includes the Moderna, Novovax, and Johnson & Johnson vaccines, as well as adenovirus-based vaccines such as AstraZeneca's.
These vaccines can work against the current version of the virus, but if we want to anticipate the spread of the disease, we must expand the targets that vaccines are targeting to include other proteins such as the ORF1ab, Orf8 and N proteins or the ORF3b protein, which others have studied.
Other countries have developed vaccines with more traditional methods, using inactivated whole viruses.
This type of vaccine, or other vaccines that target multiple proteins at the same time, may be the best approach to move forward.
I often compare viruses to code-breaking machines, running the numbers until they find a new way to exploit whatever ecological niche they inhabit, trillions of copies of a single virus each changing and adapting to each new challenge.
Sometimes we come across a virus that learns to break through our defenses faster than we can rebuild them.
I am afraid that SARS-CoV-2 could be one of them.