SARS-CoV-2 changes the classic trait of virus that becomes endemic: Shahid Jameel

Shahid Jameel, former head of the Indian SARS-CoV-2 Genomics Consortium, talks to DTE about how a virus mutates, COVID-19 pathway, concerns about re-infection

The new coronavirus pandemic (COVID-19) is ready to enter its third year. That new variant of concern, Omicron, which has already spread to at least 70 countries in less than a month, has triggered renewed fear across the globe.

With over 270 million cases and over 5.3 million deaths globally, no country has been spared. Vaccine efficacy has also been questioned, and preliminary reports show a reduced neutralization of the mutated virus.

What have we learned about the SARS-CoV-2 virus and its mutations so far?

Dr. Shahid Jameel, eminent virologist and former head of the Indian SARS-CoV-2 Genomics Consortium (INSACOG), speaks to Down to earth on how a virus mutates, the pathway of COVID-19, concerns about re-infection in the face of declining immunity and vaccine efficacy.

Taran Deol (TD): How does a virus behave traditionally?

Shahid Jameel (SJ): What happens when some genetic material multiplies? Our cell divides in two, the deoxyribonucleic acid (DNA) present in it also makes a copy of itself so that each cell gets the same information.

Viruses are the same. When any genetic material is copied, it is copied by enzymes, whether it is the genetic material in our cell or by a virus, and enzymes often make mistakes. Our cells have other enzymes that can detect this defect and correct it. Viruses do not have this proofreading mechanism.

There is also a difference between viruses that have DNA as their genetic material and those that have ribonucleic acid. The former depends on the enzymes present in our cells to multiply. Therefore, they can benefit from the proofreading mechanisms.

When an RNA virus multiplies, it uses its own enzymes and therefore cannot correct the errors.

Mutations occur randomly due to copying errors. These errors accumulate. And although these errors occur randomly, which mutant virus is selected depends on other factors. The only mutations we see are those that provide some selective benefit to the virus.

TD: Does SARS-CoV-2 follow this trajectory? When does it become endemic?

SJ: It is not possible to predict when COVID-19 will become endemic. It depends on how much capacity this virus has to mutate and even that is very difficult to predict.

I think the virus is changing in the direction of becoming more transmissible and less serious, and it’s a classic feature of viruses that go from epidemic to endemic.

Omicron is more transferable than Delta, and according to initial data, it is also less serious. It is on the verge of becoming endemic, but when it will happen can not be predicted.

Whether another variant will emerge and replace Omicron on its way to becoming endemic is a possibility but cannot be predicted.

TD: With COVID-19 heading into its third year, it will be the longest-running pandemic since the outbreak of the Spanish flu in 1918. What have we understood about it so far?

SJ: I want to make two comparisons. SARS-CoV-1 and SARS-CoV-2 are from the same family of viruses, but have manifested themselves very differently.

The main difference is that while SARS-CoV-1 was transmitted from one person to another when the person showed symptoms, SARS-CoV-2 spread even before symptoms began to show.

This is for me the crucial difference why SARS-CoV-2 has spread so much while SARS-CoV-1 did not, even though the latter was more lethal.

The Spanish flu in 1918 was caused by a virus with a genome size smaller than the COVID-19 virus. The influenza virus has about 15,000 bases, while the coronavirus has about 30,000, which means that it has a greater capacity to mutate.

Just the mutation space on the virus tells us that coronavirus has a much greater ability to change than an influenza virus in normal times.

Coronavirus is probably in the flu category. We often need boosters until this virus becomes so entrenched in the population that everyone has been exposed to it. And if the virus changes a little bit, we need either boosters every few years, or it will infect us mildly.

COVID-19 will also become a cold-causing virus, but it has not been done yet. New varieties will emerge, local peaks will continue to happen. As more and more people are vaccinated, the duration between these peaks will increase and the extent will decrease.

This is how this virus becomes endemic.

Read: COVID-19 is already endemic, lack of data plagues understanding of vaccine efficacy: Gagandeep Kang

TD: The World Health Organization (WHO) has warned of risks of re-infection with Omicron, this comes against the background of declining immunity.

SJ: When everyone talks about immunity, they are actually talking about antibodies. But immunity is more than antibodies.

When our body reacts to a foreign body like a virus, it is raises two kinds of immunity. One is called antibody-based immunity, which protects against infection. The second is called T-cell-based immunity, which kills infected cells and protects them from disease.

After an infection or vaccination, the level of antibodies will decrease over time. However, a memory response develops that causes the body to produce antibodies and T cells when it becomes infected with a virus it remembers.

It is very easy to look at antibodies, it is much harder to look at the T cell responses, and these responses still come downstream. By saying that immunity is declining, people believe that over time, more and more of us will get a symptomatic infection. But that does not mean that more of us will get the disease.

If the goal is to protect people from serious illness and not re-infection, it is very possible. What is acceptable in each country or region will depend on its health care system.

TD: What about booster doses? It raises not only clinical but also ethical questions.

SJ: Gives boosters at this point in a country like India really puts the cart before the horse. India has only fully vaccinated about 38 percent of its population.

So to say that you need to allow boosters means that you are taking these doses away from people who have only been given one dose or none.

Our priority should be to get the second dose for people who already have one dose and two doses for people who do not have any. But that does not mean we should not talk about boosters. We need to plan and find out who gets boosters, which vaccines to use as boosters, and when to administer them.

Read: ‘COVID-19 wave not separate device, comes periodically’

TD: What are India’s options for a booster dose?

SJ: Currently, four vaccines have been approved in India – Covishield (90 percent in circulation), Covaxin, Sputnik V and Zydus Cadila. Our capacity to make Covishield is high. Our capacity to manufacture Covaxin is reasonable and increasing.

A person receiving two doses of Covishield will not benefit much from the third dose of Covishield due to the nature of the vaccine.

Covishield is made using a virus that causes the common cold in chimpanzees, which is used to make COVID-19 virus spike protein. So once you have given two doses of Covishield, you not only increase the immune response to the nail protein, you also increase the immune response to all the chimpanzee proteins in the vehicle virus, which is greater in number.

So if you keep giving that vaccine, you are probably increasing the reactions to the chimpanzee virus proteins and not the COVID-19 virus tip protein.

The Sputnik V vaccine also uses a similar adenovirus.

Hyderabad-based Biological E’s Corbevax and Serum Institute of India’s Covovax – both of which are protein-based vaccines – are India’s best bidder for a booster shot. They can be produced in large quantities and are perfect for booster doses.

In people who received Covishield, for example, a protein vaccine will selectively only increase the peak response. Between the two companies, they can make about 1.5-2 billion doses annually.

Phase 3 trials have been performed for both vaccines and data are with the regulator. We will have lots of vaccines to give as boosters and maybe even give as primary vaccines if they are approved.

TD: We have already experienced six contagious crises since the beginning of this century. What do you think a post-COVID-19 world would be like? Do you see more contagious threats on the way?

SJ: It seems that infectious diseases are occurring more frequently now than they used to. Part of that may be because of our ability to detect their appearance better than we used to.

But I do not think it’s just that. We play with the environment. Most infectious diseases start from animals, and when the virus breaks out in humans, they cause diseases.

As we increase the interaction between wild animals, domestic animals and humans, these viruses will continue to jump. When deforestation, we give it the opportunity. Much of the deforestation is done to clear land for agriculture and for human habitation, and that brings the forest closer to humans and livestock.

The Nipah virus in Malaysia jumped from a bat into a pig that was on a farm next to a forest. The forest had been cleared for palm plantation. Bats began to roam on fruit trees in the plantation, their excrement and half-eaten fruits being eaten by infected pigs. The virus then spread to humans.

Several diseases are spread by mosquitoes. When temperatures rise due to global warming, mosquitoes can survive at higher latitudes and can therefore spread disease to a larger population.

It is estimated that by 2080, more than 1 billion people, primarily in northern Europe, will have their first exposure to a mosquito-borne disease.

These examples underscore the important role that ecological practices play.

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