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An antiviral drug used to treatCOVID-19may be driving the virus that causes the disease to evolve , a unexampled study propose .
But is this concern , or particularly surprising ? Not at this tip , and not really , experts told Live Science .
Molnupiravir, pictured above, is an antiviral drug that works by preventing SARS-CoV-2, the virus that causes COVID-19, from replicating.
Scientists analyzed more than 15 million SARS - CoV-2 genomes — genetic material from the computer virus that causes COVID-19 — and see thatmolnupiravirinduces a " mutational key signature " that , if the computer virus is n’t totally obliterated by a course of study of the drug , can be transmitted to other people . Molnupirivar works by causing mutation in the SARS - CoV-2 genome that forbid the computer virus from replicating .
" antecedently people had get up the mutagenic essence of molnupiravir on viruses as a theoretical risk , " study jumper cable authorTheo Sanderson , a research worker at the Francis Crick Institute in London , told Live Science in an electronic mail . " Our employment earn this more concrete because we have found that molnupiravir can give ascension to extensively - mutated viruses that stay catching , " he said . What ’s more , some of the mutations that cropped up repeatedly seem to be ace that could help the virus evade theimmune system , he add together .
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Molnupiravir, pictured above, is approved to treat COVID-19 in many countries worldwide, including in the U.S.
The authors of the study , issue Monday ( Sept. 25 ) in the journalNature , found that after molnupiravir ’s rollout , this mutational signature was common in countries that wide used the drug , such as theU.S.andU.K.However , countries where molnupiravir is not licensed , such asCanada , had few exercise of these signatures .
The findings could assist regulators to assess the risks and benefits of using the drug , but experts told Live Science that many questions remain unreciprocated .
" We should not be concerned with mutations themselves , but rather whether they admit the virus to adapt to infect or transmit better , " saidVaughn Cooper , a prof of microbiology and molecular genetic science at the University of Pittsburgh who was not involved in the inquiry . " In this case , we see comparatively petty grounds that molnupiravir is fuel more adaptations to escape prior resistance or spay infectiousness , " Cooper told Live Science in an email .
Indeed , Sanderson said from this data point alone , it is unmanageable to quantify how common it is for molnupiravir - deduct lineages of SARS - CoV-2 to distribute between hoi polloi . That ’s because , if a single sample of the virus with this molnupiravir signature show up in a database but does n’t have any tightlipped relatives , scientists ca n’t well tell if it came from someone treated with the drug or another individual infected further down the line .
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The study also did n’t turn to the potential risks and benefits of using molnupiravir for individual patients , Sanderson read . This will be of import to realise , especially for those with weakened immune systems , he said . These patients have ahigher risk of exposure of sustain COVID-19 infectionsthat give the virus more chance to break up up lots of mutations .
succeeding molding report could help predict whether the drug could influence the risk of newvariants of concernemerging — another doubt that the current subject field did n’t explore , Sanderson added .
" We have yet to see grounds of more primed succession arise from molnupiravir " — have in mind viruses that can more easily spread and multiply — " but this work certainly provides intermission for mentation and should consider heavily in considerations around succeeding use of the drug , necessitate at the very least mitigations of the peril of this outcome , alongside real mankind data on the effectuality of the drug,“Aris Katzourakis , a prof of evolution and genomics at the University of Oxford who was not involved in the research , recount Live Science in an e-mail .
Mitigation strategies could let in selective prescribing and monitoring chronically infect affected role for evidence of viral evolution , but these safeguard would need to be balance against patients ' clinical needs and the availability of alternative treatment , he said .
This article is for informational purposes only and is not meant to put up aesculapian advice .
