ndians airlifted from Wuhan at a quarantine facility in New Delhi, February 3
Noted scientist Markus Hoffmann works at the infection biology unit of German Primate Center in Göttingen-based Leibniz Institute for Primate Research, one of the world’s most reputed institutions in medical research. He is the lead author of a recent paper titled ‘SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and is Blocked by a Clinically Proven Protease Inhibitor’. The paper is an outcome of collaboration between the Leibniz Institute Charité—Universitätsmedizin Berlin. Hoffman demystifies the findings of the research on SARS-CoV-2 virus, which causes Corona virus 2019 (Covid-19). He adds that the most significant finding of his team is that camostat mesylate, a drug approved for human use in Japan to treat pancreatic inflammation, inhibits SARS-CoV-2 infection of lung cells in cell culture. “We also know that the compound blocks SARS-CoV infection in a rodent model. Therefore, we feel that the suitability of camostat mesylate for treatment of COVID-19 should be evaluated within clinical trials,” he avers. He also talks to Open about other findings of his study. Edited excerpts:
Could you please explain the significance of your finding in layman’s language?
We found out that SARS-CoV-2 uses the same cellular protein like SARS-CoV (which caused the Severe Acute Respiratory Syndrome (SARS), a viral respiratory illness that killed many people in 2003) to attach to lung cells. This protein is called angiotensin converting enzyme 2 (ACE2). Further, we discovered that like the related SARS-CoV and MERS-CoV (which caused the Middle East Respiratory Syndrome (MERS) that was first identified in Saudi Arabia in 2012) SARS-CoV- 2 also exploits the cellular protease TMPRSS2 to activate its envelope protein and thus be able to infect cells. Our most significant finding is that camostat mesylate, a drug approved for human use in Japan to treat pancreatic inflammation, inhibits SARS-CoV-2 infection of lung cells in cell culture. We also know that the compound blocks SARS-CoV infection in a rodent model. Therefore, we feel that the suitability of camostat mesylate for treatment of COVID-19 should be evaluated within clinical trials.
Your study also suggests that that antibody responses raised against SARS-CoV could at least partially protect against SARS-CoV-2 infection. Can you elaborate on this? What kind of drugs can be used for the purpose of likely prevention?
We do not think that antibodies raised against SARS-CoV would cross-protect against SARS-CoV-2. However, it might be possible that residual SARS-CoV-specific antibodies in people who survived SARS during the outbreak in 2002/03 might have the potential to protect from severe courses of COVID-19. Further, one can speculate that vaccine strategies that were developed to combat SARS-CoV can be adapted to SARS-CoV-2, as it is likely that there would be a similar mode of protection by a potential vaccine.
Your paper says that convalescent SARS patients exhibit a neutralising antibody response that can be detected even 24 months after infection. How does it manifest?
Although it is believed that antibody responses against coronaviruses are short-lived, our data suggests that once a person has overcome SARS-CoV-2 infection then there might be protective immune response for at least a year before re-infection might occur. However, this is at present purely speculative.
What are the lessons for the rest of the world from countries such as China, Taiwan, Singapore and Hong Kong that have managed to handle the crisis with a certain degree of success?
I believe that it is important to have the capacity for and to perform thorough testing of probable cases and contacts of infected persons. This is crucial to comprehend the extent of local outbreaks and devise appropriate strategies in order to break up transmission chains and contain or at least slow down the spread of the virus.
What are your thoughts on this latest report that recovered patients are testing positive again for Covid-19?
It is much more likely that one of the negative tests was false-negative or that the concentration of virus has decreased around the detection limit of the test. Therefore, depending on how the sample is taken it can be borderline positive or negative. I think it would be necessary to have negative tests on 2 or 3 successive days to be sure that there is no residual virus.