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the production of these antibodies<br />

by B-lymphocytes. So, the need for<br />

a genetic base for the treatment of<br />

COVID-19 is not only obvious, but also<br />

imperative.<br />

COVID Human Genetic Effort<br />

Even at the time of the onset of the<br />

COVID-19 pandemic, researcher Jean-<br />

Laurent Casanova and his team set<br />

up an international consortium, COVID<br />

Human Genetic Effort, to identify the<br />

genetic and immunological factors<br />

that could explain the occurrence<br />

of severe forms of the disease by<br />

focusing on patients with the severe<br />

forms. By targeting their research on a<br />

specific mechanism of immunity - the<br />

type-I interferon (IFN) pathway, the<br />

researchers could highlight genetic<br />

abnormalities in certain patients that<br />

reduced the production of the type-I<br />

interferon (3-4% of severe forms). In<br />

other patients, they identified that<br />

it was the history and prevalence of<br />

autoimmune diseases that blocked<br />

the action of type-I interferon (10-11%<br />

of severe forms). All these discoveries<br />

would thus explain severe forms of<br />

COVID-19, which covered about 15%<br />

of the total patient population. The<br />

analysis of a control sample of 1,227<br />

healthy people also facilitated an<br />

evaluation of the prevalence of autoantibodies<br />

against type-I interferon<br />

at 0.33% in the general population, a<br />

prevalence 15 times lower than that<br />

observed in patients with severe<br />

forms. These results suggest that the<br />

general population should be<br />

screened for these antibodies and<br />

it can have a huge benefit in the<br />

treatment regime.<br />

The Franco-American laboratory of<br />

Jean-Laurent Casanova and Laurent<br />

Abel has already identified a hundred<br />

genetic diseases that may explain<br />

susceptibility to infections. While some<br />

people recover more or less easily from<br />

infections such as herpes, influenza,<br />

tuberculosis and hepatitis A, others<br />

develop serious clinical forms that can<br />

even be fatal. This is because they<br />

carry an alteration in a gene involved<br />

<strong>December</strong> <strong>2020</strong> / FUTURE MEDICINE / 67

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