Molnupiravir causes transmissible mutations in SARS-CoV-2
Ok, so I told you masks don’t work to prevent respiratory virus infection and transmission, and now the latest Cochrane review has confirmed that they don’t work.
Aaaaand, I told you that neither influenza vaccines nor COVID-19 vaccines prevent infection with, or transmission of, the viruses associated with them, and now Dr Anthony ‘I Am the Science’ Fauci himself has confirmed that neither they, nor any other vaccines for respiratory diseases caused by viruses that replicate predominantly in the respiratory mucosa, prevent infection or transmission.
Let’s try for three for three.
I told you back in May 2022 that Merck’s antiviral drug molnupiravir (sold under the brand name Lagevrio) generated mutated versions of SARS-CoV-2 that were shed in recipients’ nose and throat secretions, and could potentially lead to new, transmissible variants of unknown virulence. Our fearless drug regulator, the Therapeutic Goods Administration (TGA), airily dismissed the significance of this finding on the say-so of an unnamed ‘independent expert’:
“The likelihood of mutations resulting in a more virulent strain of SARS-CoV-2 from treatment with molnupiravir over the long-term has not been assessed. It is less likely, but unproven, that virus mutation induced by molnupiravir will increase virulence of SARS-CoV-2.”
Australian Public Assessment Report for Molnupiravir, p. 39
As a result of the TGA’s provisional approval of molnupiravir, over 380 000 prescriptions for this twenty year old drug which has never been used before due to concerns about its mutagenicity, had been issued in Australia by December 2022. Australian health authorities are still heavily pushing its use despite evidence of higher death rates in people treated with molnupiravir compared to placebo, and despite the National Clinical Evidence Taskforce in the UK recommending against it:
And now, an international team of researchers has produced compelling evidence that versions of SARS-CoV-2 with mutations consistent with the pattern induced by molnupiravir are showing up in global sequence databases, and that these viral variants are transmissible.
To make sense of the new paper, which has not yet been peer reviewed but was considered significant enough to garner a write-up in Nature – one of the world’s most prestigious scientific journals – we need to do a quick review of molnupiravir’s mechanism of action.
As explained in The great molnupiravir swindle,
“It works by creating errors in the virus’s genetic code, known as mutagenesis. Each time the virus replicates in the presence of molnupiravir, more and more errors accumulate, eventually building up to an ‘error catastrophe’ that stops the virus from functioning.”
The great molnupiravir swindle
(The authors of the new paper dispute the notion of ‘error catastrophe’, and I’ve included their argument as a footnote for those interested in the finer points of this argument.
The mutations produced in the viral genetic code by molnupiravir are not random. Instead, they result in very specific substitutions in the four-letter nucleotide ‘alphabet’ that spells out the viral genetic code.
Briefly, in RNA viruses including SARS-CoV-2, the genetic code is comprised of specific sequences of uracil (U), cytosine (C), adenine (A) and guanine (G). During the ‘reading’ of the genetic code that results in protein formation, A and U always pair with each other, while C and G pair with each other. Each three-nucleotide sequence (known as a ‘codon’) represents an amino acid, and the order in which the nucleotides appear dictates the order in which amino acids are strung together to form a protein. (There’s a good summary of this process here for those who want to delve deeper.)
Molnupiravir results in substitution of adenine for guanine (a G-to-A mutation) and uracil for cytosine (a C-to-U mutation). This ‘mispelling’ of the viral code results in masses of mutant virions, most of which are non-viable – that is, they’re unable to do what viruses do to survive, which is to highjack the host cell’s protein-making apparatus in order to make more copies of themselves. However, some of these mutants are viable, and their signature mutations showed up in samples taken from participants in a clinical trial of molnupiravir. These same signature mutations can also be identified and tracked using the global viral sequencing databases GISAID and INSDC.
And that’s exactly what the international team of researchers who wrote this recent paper did.
They examined a mutation-annotated phylogenetic tree, which is a method for visually representing the relationships between the genetic sequences of various samples of SARS-CoV-2 that are uploaded to these global databases (see the example below), and identified branches with multiple G-to-A and C-to-U substitutions, consistent with molnupiravir-driven mutation.
Their analysis identified six key facts:
In summary, mutations consistent with molnupiravir’s known mechanism of action, and of the same types that were found in the nasopharyngeal secretions of people who took the drug in a clinical trial, have shown up in global sequencing databases, since molnupiravir began to be prescribed, in the countries which are using it, in the age group for which it is approved, and in patterns which indicate that it is generating transmissible variants with high mutation rates.
When it comes to the implication of their findings, the study authors take a cautious approach. They point out that they have not proved that the use of molnupiravir is driving the mutations that they identified, nor that these mutations are intrinsically more dangerous or transmissible. They call for “public health authorities in countries showing these patterns [to] perform investigations to determine if these sequences or clusters can indeed be directly linked back to use of molnupiravir.”
However, as coauthor Theo Sanderson, a computational biologist at the Francis Crick Institute in London, stressed,
“I would say that our work closes down the possibility that these [molnupiravir-mutated] viruses can never be transmitted.”
COVID drug drives viral mutations — and now some want to halt its use
Rustem Ismagilov, a quantitative bioscientist at the California Institute of Technology in Pasadena who was not involved in the study, stressed that it “underscores the need to quickly measure any risk that molnupiravir poses in terms of sparking new variants, and to weigh them against the drug’s benefits”, adding
“If we are playing Russian roulette, we’d better know our odds.”
COVID drug drives viral mutations — and now some want to halt its use
All I can say is, good luck with that one. I’d lay odds on hell freezing over before any study on the adverse effects of molnupiravir secures funding.
Given molnupiravir’s lack of clinical benefit, the unanswered questions about its capacity to trigger cancer, and these latest findings that point to the strong possibility that it is driving variants with high mutation rates, any sane health authority would drop it like a hot brick. But the TGA continues to insist that it “meet[s] the high safety, efficacy and quality standards required for use in Australia.” One wonders how bad a drug has to be to not meet those standards. (Or perhaps the disqualifying criteria are actual safety and effectiveness, as with hydroxychloroquine and ivermectin.)
Get the appWhat can we ordinary folk do in the face of the complete regulatory capture that is driving unsafe, ineffective and inadequately tested products into the mouths and arms of Australians?
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