Dr. Naga Suresh Veerapu , Virologist at the Department of Life Sciences, Shiv Nadar University, saidin an interview that theSARS-CoV-2 virus, in spite of its relatively simple structure, had managed to evolve the ability to jump species, and good science requires that the Indian Council of Medical Research (ICMR) test many more samples.
Coronavirus | Interactive map of confirmed coronavirus cases in India
What’s so unique about the SARS-CoV-2 virus? Given that it shares similarities with other coronaviruses, four of which are responsible for the common cold in India, is it reasonable to expect some protection?
There are large similarities between this virus and the SARS virus [SARS-CoV identified in 2003] in genetic make-up and antigenic regions. There is a strong possibility for cross immunity [when recovery after infection from one virus protects against another strain]. However, these viruses continuously mutate their genomes and can mask their proteins to evade detection [by the immune system] and jump species.
Is there any evidence for cross immunity so far?
There is no evidence so far — unless epidemiologists (those who study disease patterns) contact everyone who has been infected and know if they have previously been infected with SARS-CoV [it won’t be known]. However, there is a lot of difference between common cold, or seasonal flu viruses, and the coronavirus. Seasonal flu viruses are segmented viruses and adept at changing their genetic make-up, and combine the properties of human and animal flu virus. SARS-CoV-2, in contrast, is simpler. It’s a single segment [virus] and despite that, it has managed to adapt and jump species and spread in humans. Genome-wise, there is a 10%-15% difference between the SARS-CoV and SARS-CoV-2. The virus in Italy is of a lineage different from the one in China. Viruses are very flexible.
If there are such differences — and Indians from different countries are bringing in slightly different strains — how effective can a potential vaccine be?
Consider the Hepatitis C virus, that I research on. It has several genotypes. An antiviral that works on one genotype may not be effective on another. Similarly, if it is a live-attenuated (or inactivated strain) vaccine, it may not be effective across all strains of COVID-19. So, vaccines that produce very powerful neutralising antibodies should be more helpful. More than vaccines, it’s best if we can identify some good anti-viral though they, too, sometimes have strain specification. On the whole, however, making antivirals is relatively easier than [making] vaccines.
Do you see any promising antivirals in the making for COVID-19?
I am sure there are some in the making. For the HCV (Hepatitis C virus), it took 20 years to make a direct-acting antiviral because the systems weren’t in place to see if a chemical compound could inhibit viral replication. Now, we have effective antivirals against HCV.
A debate now emerging in India is regarding testing. Is our case load low because we are testing too little, or are there genuinely too few cases? Firstly, How reliable are these diagnostic kits, the most popular being real time PCR (polymerase chain reaction)?
To identify the virus, the kits are designed to look at highly conserved regions of the genome (portions that undergo little change as they are essential to the virus’ constitution) and these must be as concise as possible. It is only on this basis that primers are designed, and real time PCRs are the gold standard for assessing viral infections. But they have their challenges. They are prone to carry-over contamination (that is, if mishandled the particles can jump from one biological sample to another and lead to wrongly attributing the presence of virus when there isn’t any.) This means that the technicians who handle the test have to be very careful, experienced and skilled. You also have to exert proper positive and negative controls.
Are you implying that if we dramatically scaled up tests, and involve labs with varying expertise and experience, there could be a risk of many cases falsely being termed ‘positive’?
That possibility is there. Even very good labs under the best of conditions can make errors. But many of these diagnostics are very safe and robust and are designed to minimise handling errors.
Do you agree with the ICMR’s approach of testing 20 samples a week from 50 labs, or about 1,000 samples, to find evidence of community transmission?
It’s bizarre to limit sample testing to 100 or 1,000 per week. If the number of cases is growing, there should be a step up in the number of samples tested. It is fundamental and [there should be] no second thought about it. There are asymptomatic samples —any case with the hint of a cold/cough ought to be tested and you shouldn’t be waiting for evidence of community transmission. I don’t know [the] government’s thinking but everyone should be tested for infection.
The government’s argument seems to be that testing widely could falsely convince some that they are not carriers and that this could contribute to fear and panic?
That is up to the government on how they want to approach it. But as a strategy, there is no doubt that more testing should be done.
