Alarm set off by French Nobel Laureate Luc Montaigner’s claim that the jabs could create virus variants.
Antibody dependent enhancement (ADE), when antibodies to an infection can sometimes aggravate infection or trigger a respiratory disease, is something that vaccine developers must watch out for. However, there is no scientific case that such ADE may actually trigger newer virus variants, says experts.
The controversy was triggered by a much-shared article in the last few days, that claimed the French 2008 Nobel Laureate, Luc Montaigner, 89, to have said vaccination in a pandemic was lethal and there was an association between rising vaccinations and death rates. While it emerged that he did not explicitly say so, he did say that vaccinations were an “enormous mistake” as they were creating “the variants”.
The interview is in French and a translation is available on the website of the RAIR Foundation, which describes itself as an “activist grassroots” organisation to “to combat threats from Islamic supremacists, radical leftists and their allies”.
In an excerpt from the interview, Montaigner, who in 2008 was co-winner of the Nobel Prize in Medicine for discovering the Human Immunodeficiency Virus (HIV), says that, “It is the antibodies produced by the virus that enable an infection to become stronger. It’s what we call Antibody Dependent Enhancement (ADE), which means antibodies favour a certain infection. The antibody attaches to the virus, from that moment it has the receptors, the antibodies, we have them in the macrophage (a white blood cell that consumes infectious cells).”
Gagandeep Kang, microbiologist at Christian Medical Centre, Vellore, in a series of tweets on Wednesday, laid out why Montaigner’s assertions were incorrect.
Vaccination was a method to teach the immune system to trigger the antibodies and specialised immune-system cells in case of a future infection by an actual virus. There were both neutralising and non-neutralising antibodies produced.
In some individuals with a defective immune system, a viral infection could trigger a long bout of viral replication that could produce variants able to avoid the immune-system generated cells. While relatively few of them could escape immunity, some could spread through populations, multiply and be more resilient to vaccines as evidenced by B.1.351 (South Africa variant) and B.1.617.2 (India variant) though two doses of vaccine continued to be effective against them. “The only way to decrease variants is not to stop vaccination, but to increase it to stop virus circulation and replication,” she said.
ADE was identified as a “potential problem” in vaccine development, said Dr. Kang and an example of it was in the case of infection with the virus causing a dengue infection. There were four types of dengue virus and an infection or vaccination against one could trigger enhanced disease if someone were subsequently infected with a type to which there weren’t enough neutralising antibodies produced. “All (Sars cov2) vaccines were being evaluated to see that they made high amounts of neutralising antibodies. And they are,” said Dr. Kang.
However, it was important to continue studying long-term protection and immune response in vaccine breakthrough cases (infection after vaccination) to understand what was happening with immunity and safety. But so far there wasn’t any (concerning) signal, she added.
In an earlier interview with The Hindu, Vineeta Bal, immunologist and professor at the Indian Institute of Science Education and Research, Pune had said that neutralising antibodies were “good antibodies” but that didn’t make non-neutralising ones automatically bad until proved. “Their utility may be limited. Some antibodies on binding to their targets lead to ADE [Antibody Dependent Enhancement of viral infection] and they can be labelled as ‘dangerous’ or ‘bad’ in your parlance. But in an immune individual amongst a large number of antibodies, such ADE causing antibodies are pretty much impossible to identify.”
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