The rate of development of vaccines against SARS-CoV-2 has been unprecedented. Quite a few vaccines have already been squeezed through the loophole of ‘emergency’ use before adequate mandated clinical trials. Some vaccines are based on the adenovirus, modified to carry the spike protein of SARS-CoV-2 as antigen. Some are based on the modified messenger RNA encoding the spike protein and some are inactivated virus. More are in the pipeline.
The world is sighing with relief and people who are vaccinated are feeling invincible and immortal. But wait, not so fast. SARS-CoV-2 is an RNA virus. There is limited proof-reading of the genetic code while the virus is replicating. So, with each generation, there is variation in the genetic material. Already, there are distinct well-recognised strains going around. The vaccines that are used now may have limited effectiveness against these new strains.
To take the analogy of the strategy for reducing the chances of drug resistance among microbes, where multiple drugs hit the pathogen from different directions (as with TB, leprosy, HIV etc.), one could think of a cocktail of COVID vaccines. Instead of a vaccine that only uses the spike protein of SARS-CoV-2 as antigen, we could use a vaccine that has more than one antigen.
“But that would mean going back to the drawing board to examine technical feasibility and economics. And, of course, more testing and clinical trials”, says M Asokan, Jawaharlal Nehru Centre for Advanced Scientific Research, Bengaluru.
“There is yet another problem with the vaccines”, points out Udaykumar Ranga, JNCASR. “The first line of defense for respiratory viruses is the production of immunoglobulin A by cells in the respiratory mucosal immune system. These cells have to be constantly alert to a variety of pathogens that enter the respiratory tract. So the turnover of these cells is high. There are no memory cells left behind as in the case of the B cells of the systemic immune system”.
The human body responds to vaccines that are injected by producing immunoglobulin G. And, within a few weeks, the antigens are removed by the coordinated action of various types of immune cells. Yet a few B cells of the immune system, capable of producing antibodies against the specific antigen, remain. These memory cells are recruited at short notice when there is another infection by the same pathogen. But these memory B cells are stored in the bone marrow, spleen and tonsils, not in the upper respiratory tract where SARS-CoV-2 first infects. So the virus can infect and reproduce there and it is only when it spreads to become a systemic infection that memory B cells are recruited. Though the resulting pathology is quickly overcome by the production of adequate antibodies, people who are thus infected can transmit the virus.
The solution is to have vaccines that are inhaled instead of being injected. But, of course, the vaccinations will have to be repeated, because maintaining memory cells in the mucosa of the upper respiratory tract is a challenge.
Under such conditions, it is impossible to envisage herd immunity to break the cycle of infections and transmission, even if we vaccinate all the seven billion plus people living on the planet. Especially since the virus infects some other animals also.
Please remember that it took nearly a century to create a vaccine against the influenza virus. And, each year, a new vaccine has to be brought out to control the strain that is circulating. So don’t start behaving like an immortal if you are immunised against SARS-CoV-2. You may not die of COVID-19, but you can get re-infected. Protect yourself (and protect others who are not yet vaccinated) by following the protocols.
For more details, read the review article on the topic by scientists from JNCASR, scheduled to be published in the 25th April issue of Current Science .
The preprint can be accessed here: Inducing quality immune response to respiratory viruses may not be a simple task
Udham P K
Freelance Science Writer, Pune
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