A new British study suggests that the CCP virus has a greater chance of mutating during chronic infection. One of the study’s leaders says the virus may be “outwitting our vaccine with mutations.”
In an unedited manuscript pre-published Friday (Feb. 5) in the journal Nature, a team of researchers at Cambridge University said they found serial mutations in treating patients with defective immune systems.
The team sequenced a patient’s viral genome 23 times over 101 days while he was being treated for an infection with a Chinese communist virus, a disease commonly known as novel coronavirus, or COVID-19.
The patient, now deceased, was an elderly man in his 70s whose immune system was “severely compromised.
The team saw a “dramatic shift” in the virus population after the patient was given two doses of recovery serum (plasma containing antibodies extracted from the blood of a recovered CCP-infected patient).
According to a Cambridge University press release, one of the variants that emerged (and once dominated) contained two worrisome mutations.
One is the D796H variant, which appears to reduce the sensitivity of antibodies in plasma. This is a typical viral variant so that it can evade immune pressure.
The other is the ΔH69/ΔV70 amino acid deletion of part of the surface membrane spike protein in the variant, a variant that doubles the infectivity of the virus.
The university writes, “This is a typical pattern of viral mutation, in which escape mutations follow or accompany compensatory mutations.”
The ΔH69/ΔV70 amino acid deletion variant has been detected several times, including in the so-called British variant VUI 202012/01 and the cluster-5 variant found in Danish mink and humans. But this is the first Time researchers have observed its presence in patients.
The team found that while the dominant variant “initially appeared to disappear, it reappeared when a third course of remdesivir and recovery plasma treatment was administered.”
Commenting on the study, Cambridge University professor Ravi Gupta, who led the study, said, “What we’re seeing is essentially competition between different variants of the virus, which we think is being driven by plasma therapy for recovering patients.”
He said the findings raise a “worrisome possibility.”
“Considering that both the vaccine and the treatment target the surface membrane spike protein, a variant of which we see in patients, our study raises the worrying possibility that the virus is mutating, possibly to outwit and outcompete our vaccine.”
Gupta added, “This effect is unlikely to occur in patients with normal immune system function, because better immune control may reduce viral diversity. But it points to a problem we need to be aware of when treating immunocompromised patients, namely that in such cases, viral replication time is prolonged and the chances of viral mutation are greater.”
In this regard, Dr. Julian Tang, a virologist at the University of Leicester, also revealed that a similar phenomenon was found in a 45-year-old immunocompromised patient who received different treatments.
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