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The majority of SARS-CoV-2-infected individuals remain paucisymptomatic, contrasting with a minority of infected individuals in danger of death. Here, we speculate that the robust disease resistance of most individuals is due to a swift production of type I interferon (IFNα/β), presumably sufficient to lower the viremia. A minority of infected individuals with a preexisting chronic inflammatory state fail to mount this early efficient response, leading to a delayed harmful inflammatory response. To improve the epidemiological scenario, we propose combining: i) the development of efficient antivirals administered early enough to assist in the production of endogenous IFNα/β; ii) potentiating early IFN responses; iii) administering anti-inflammatory treatments when needed, but not too early to interfere with endogenous antiviral responses.
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Combining Antivirals and Immunomodulators to Fight COVID-19
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