COVID-19 is commonly compared or even confused with the flu. Professor Martin Michaelis and Dr Mark Wass of the School of Biosciences explain why comparisons between these different diseases, which are caused by different viruses, are not helpful and often misleading:
‘COVID-19 is often referred to as “just another flu” or even a “lesser flu”. However, there are fundamental differences between COVID-19 and flu, which are different diseases caused by different viruses. The flu, also known as influenza, is caused by influenza viruses. In contrast, COVID-19 is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which differs from influenza viruses in its structure and composition, in the way it replicates, in the range of cells that it can infect, and in the disease that it causes.
Mortality rates
‘Seasonal influenza epidemics are estimated to cause between 100,000 to 650,000 deaths each year. In contrast, COVID-19 has already caused more than one million confirmed deaths, although the pandemic is globally still not over its first peak. The actual number of COVID-19 fatalities is likely to be substantially higher due to underreporting. Hence, the health impact of COVID-19 is far greater than that of seasonal flu.
‘Novel influenza viruses can cause pandemics that spread further than seasonal epidemics and can expand beyond the typical flu season. In the 20th and 21st century, influenza pandemic deaths tolls ranged from less than 0.5 million (the Swine Flu pandemic, 2009) to 17-100 million (the Spanish Flu, 1918-1920) cases.
‘COVID-19 has already caused mortality at the level of the Asian Flu (1957/58) and the Hong Kong Flu (1968/69), both being estimated to have caused one to four million deaths. In contrast to these two flu pandemics, the impact of COVID-19 has been reduced by containment measures and lockdowns. Without these measures, the COVID-19 pandemic would have already killed significantly more people.
‘A recent study performed in Manaus, Brazil, suggested that 66% of the population had been infected by SARS-CoV-2 during the first peak. If 66% of the world population became infected, and considering that between 0.2% and 0.9% of SARS-CoV-2-infected individuals are estimated to die, this equates to 10-46 million deaths globally. Hence, the number of deaths expected from an unhindered spread of COVID-19 exceeds those of most influenza pandemics. Countries like the UK, with a high proportion of individuals over 60, would be disproportionately affected by a COVID-19 spread unhindered by containment measures.
Immunity
‘Influenza viruses are known to cause long-term immunity. Infection with an influenza virus strain typically results in life-long protection against that strain and cross-protection against a range of related strains. Despite this strong protective immune response, herd immunity has not been reached against seasonal influenza viruses, as they evolve to escape pre-existing immunity.
‘In contrast, SARS-CoV-2 does not appear to induce lasting immunity in the same way as influenza viruses. Re-infection of patients with SARS-CoV-2 have been recorded.
‘Very early results from antibody therapies suggest that SARS-CoV-2 can mutate and escape antibody recognition. Thus, it is unlikely that an unhindered SARS-CoV-2 spread would result in the desired herd immunity to end the pandemic. Influenza viruses still circulate in populations despite availability of anti-influenza drugs and influenza vaccines.
Long-term damage
‘Finally, SARS-CoV-2 seems to be able to infect more tissue and cell types than influenza viruses and to cause more harm to a wider variety of organs. A substantial fraction of COVID-19 survivors experience long-term problems and organ damage, which is expected to result in a level of secondary mortality that is not seen in influenza survivors.
‘Ultimately, COVID-19 is not a lesser flu, but a novel and dangerous disease. Equating COVID-19 with flu only provides a false sense of safety at a time when we must be vigilant.’
Professor Michaelis and Dr Wass run a joint computational/ wet laboratory. Dr Wass is a computational biologist with expertise in structural biology and big data analysis. Prof Michaelis’ research is focused on the identification and investigation of drugs and their mechanisms of action, with a focus on cancer and viruses. With regard to viruses, Prof Michaelis and Dr Wass work on virus-host cell interactions and antiviral drug targets. In the cancer field, they investigate drug resistance in cancer. In collaboration with Professor Jindrich Cinatl (Goethe-University, Frankfurt am Main), they manage and develop the Resistant Cancer Cell Line (RCCL) Collection, a unique collection of 2,000 cancer cell lines with acquired resistance to anti-cancer drugs. They are also interested in meta-research that investigates research practices in the life sciences.
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