The Omicron variant, which South African and other scientists say may not be deadly, may have emerged from a patient with HIV/AIDS and a prolonged Covid-19 infection, researchers who are tracking the new coronavirus variant believe. This, however, may not be the first time that such mutations have occurred.
Several cases through the two years of the pandemic caused by the China-origin virus have shown that prolonged infection, which allows the virus to replicate for a longer duration, along with a compromised immune response, leads to immunity-defying mutations. These are mutations that antibodies that the human body generates fail to fight effectively.
The biology of a virus’s mutations
Mutations are changes in the pattern of the protein that makes the virus, a submicroscopic infectious agent (or pathogen) that replicates only inside the living cells of an organism. Sometimes these changes in the genetic codes can change a protein in the virus that effectively improves one of its functions, such as its infectiousness or the severity of the disease.
When infected, a host cell is forced to produce rapidly thousands of copies of the original virus. When not inside an infected cell or in the process of infecting a cell, viruses exist in the form of independent particles, or virions, consisting of
- the genetic material, that is, long molecules of DNA or RNA that encode the structure of the proteins by which the virus acts;
- a protein coat, the capsid, which surrounds and protects the genetic material; and in some cases
- an outside envelope of lipids.
The shapes of these virus particles range from simple helical and icosahedral forms to more complex structures. Most virus species have virions too small to be seen with an optical microscope, as they are one-hundredth the size of most bacteria.
A study published in the journal Nature in February, for example, showed data from one immunocompromised patient who died after 102 days of being Covid-positive.
By sequencing samples taken on 23 different days over a span of 102 days, a team from the University of Cambridge in the UK showed that mutations that spread more easily and/or can escape antibodies can emerge in immunocompromised patients who stay Covid positive for prolonged periods.
In this case, the septuagenarian patient was undergoing chemotherapy for lymphoma, which is cancer that begins in cells of the lymph system or the body’s disease-fighting network.
The patient was initially treated with two courses of remdesivir over 57 days, but the medication failed.
The patient was then administered convalescent plasma, which at the time of the study was still an experimental therapy with the potential to treat Covid-19. The team observed that after the plasma therapy had begun, the virus started mutating more rapidly.
Scientists say it is likely that both chemotherapy and underlying lymphoma contributed to the combined immunodeficiency of B and T cells — white blood cells that play a key role in the body’s immune response.
What Harvard scientists say
Last year, in a letter published in The New England Journal of Medicine (NEJM), scientists from Harvard Medical School described the case of an immunosuppressed Covid positive patient who was treated with a mix of anticoagulants, steroids, and antivirals.
During 152 days of persistent SARS-CoV-2 infection in the patient, the team identified as many as 12 mutation spikes in the spike protein, some of which were linked to immune evasion.
Based on several such reports reported through the pandemic, scientists from several institutions in the US had written in an article published in the NEJM, noting that there is a need to identify whether certain forms of immunosuppression are associated with an increased risk of giving rise to immune escape mutations, such as specific cancers or therapies, prolonged use of glucocorticoids, long-term chemotherapy, or radiotherapy.
“Similarly, organ transplant recipients and those with untreated or poorly controlled human immunodeficiency virus infection may also have prolonged SARS-CoV-2 infection and could constitute a reservoir of divergent escape variants that can spread in the general community,” the scientists said.
They explained that prolonged viral replication along with inadequate immune response facilitates the emergence of immune escape mutations.
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