In an interview with Sumi Sukanya Dutta, dr Gangandeep Kang, executive director, translational health science and technology institute, and Dr Shahid Jameel, CEO, Wellcome trust DBT India alliance, share
their insight on COVID-19 and its implications. excerpts:
How is COVID 19 outbreak different from H1N1 pandemic, both epidemiologically and in terms of our responses?
Dr Kang: COVID19 spreads at least as fast as H1N1, but causes greater mortality. At this moment, we estimate that of 100 people infected, one may die. The original estimate was 3 out of 100, but as we understand more about how many are infected, the rate of mortality may go down further. A lot depends on the quality of healthcare. So some countries like Germany are seeing low mortality. In seasonal influenza, which is what H1N1 has become, the mortality is 1 in 1,000 infected or less.
Dr Jameel: There are two ways to compare COVID-19 with swine flu. One is severity i.e. how many confirmed cases died. The other is transmission rate or R 0 (R naught), which tells how many persons on average can be infected by someone already infected. In the 2009 swine flu pandemic, every country reported cases. WHO estimated that 11-21%of the world population, i.e. 700 million to 1.4 billion people were infected with an estimated 1,50,000 to 5,75,000 deaths, a fatality rate of about 0.02%.
As there is no COVID-19 population screening test yet, we don’t yet know how many people are infected. What we do know is that by today there are over 10,51,635 confirmed cases and 56,985 deaths reported from 208 countries. But, one must also understand that this is not the same as population fatality rate. Public health experts estimate that COVID-19 will eventually have a mortality rate of about 0.5%, i.e. about 20 to 25 times higher than swine flu. The R 0 for swine flu was estimated to be 1.75; that for COVID-19 is estimated to be 2-2.5.
When comparing the two most recent pandemics, it appears that COVID-19 is more severe and transmissible than swine flu.
How is SARS CoV 2 different from other coronaviruses?
Dr Kang: Seasonal coronaviruses cause upper respiratory infection or cold. MERS, SARS and SARS-CoV2 affect the lower respiratory tract as well, and result in much greater respiratory distress. SARS-CoV2 differs from MERS and SARS in spreading much more easily.
Dr Jameel: SARS-CoV-2 belongs to a family of viruses, six Of these, two were associated with severe respiratory disease —SARS and MERS, with about 10% and 25% mortality. The others are endemic and associated with seasonal infections very similar to a mild flu with very little mortality. At a genetic level, SARS-CoV-2 is about 80% identical to SARS virus and only about 50% identical to MERS virus. The closest relatives of SARS-CoV-2 appear to be two bat coronaviruses identified in eastern China in early 2018 — bat-SLCoVZC45 and bat-SL-CoVZXC21. They share 96% similarity.
Many, including doctors, have said that since H1N1 did not make as big an impact on India as it did on many other countries in terms of fatalities. Can the same be anticipated about novel coronavirus?
Dr Kang: No. H1N1 infected a significant proportion of India but was a much milder virus. Many infected people did not know they were infected, and if they had symptoms, they were generally less severe even though a small proportion developed a severe disease and died. There may also have been some immunity from the previous circulation of H1N1, which older people would have some protection from. With SARS-CoV2, the whole world has not seen this virus. So, all — including Indians — are susceptible. If there is any resistance, it will have a genetic basis, and determine how the body responds to infection. As far as I know today, we have not yet had any studies reporting such resistance.
Dr Jameel: In 2009, India reported 10,193 confirmed cases and 1035 deaths due to swine flu. i.e., a case fatality rate of about 10%. From India, there are no figures available on how many people in the population were finally infected. If we assume that only 1 in 10 was detected, the cases go up to ~100,000 and the fatality rate falls to ~1%. From these numbers, it would be wrong to say that India was not affected. I also don’t subscribe to the view that exposure to other infections prevents this one. If there is data, I’ll believe it. But I have not seen any.
There is an interesting perspective on how initial viral load (a person exposed to infection) determines the clinical course of COVID-19 in individuals. Can you explain what that means?
Dr Kang: There are two things to understand — infectious dose and viral shedding. The infectious dose is how many viruses are needed to cause an infection. So, 1 virus in a droplet or 100 viruses may not be enough, but 1,000 will cause an infection in most people who breathe in that many. So, 1,000 is the infectious dose. Viral shedding is how many viruses an infected person sheds and this is determined by viral load, or the amount of viruses in a measured amount. Higher viral load means the person will be more infectious. This can be different for different people and also changes with time. We know now that people are most infectious two days before they have symptoms and when they have symptoms because they are shedding more.
Dr Jameel: This is not unique to COVID-19 alone. It is true for most infections – viral, bacterial or other. If the initial dose is high, the virus has a better chance of finding target cells in the human or animal host, invading them and producing more viruses, during which process cells and tissues are injured. The body itself produces an immune response, which can go haywire if the infection load is high, leading to tissue damage. Together, these cause disease. Let us assume that a single virus particle has only a 0.1% chance of finding a target cell. If there were 10 particles, there would be a 1% chance of a hit. If there were 100 particles a 10% chance, and 1,000 particles would have a 100% chance. These are assumptions just to explain the point. I am not saying it is true for COVID-19.
From pure epidemiology point of view, which earlier outbreak can COVID- 19 be compared to and why?
Dr Kang: Closest is probably the 1918 influenza outbreak— respiratory spread which determined how quickly the virus travelled. Mortality is much lower than 1918, as we have much better knowledge and tools for healthcare. And with the rapidity of developing drugs and vaccines, we have methods of treatment and prevention that are being worked on furiously around the world. I have great faith in scientists. Remember we made HIV/AIDS from a death sentence to chronic disease.
Dr Jameel: It would be improper to compare because the world has not remained static. There is better technology to tackle infections and disease, and better information networks to spread awareness. But there are also more global travel networks, supply chains, environmental degradation, climate change, etc that speed up the evolution of new viruses. Every outbreak is unique. The focus should be on keeping preparedness levels high t h rough research and surveillance.