Abstract

Novel coronavirus infection (COVID-19) caused by SARS-CoV-2 has some specific clinical and immunopathogenic properties. SARS-CoV-2 is a single-stranded RNA virus that belongs to the Coronaviridae family, the Betacoronavirus genus. COVID-19 can be asymptomatic, the most common clinical manifestation of this disease is viral pneumonia. The development of acute respiratory distress syndrome is noted in less than 5% of cases. The entry gates of this virus are the epithelium of the upper respiratory tract and epithelial cells (epitheliocytes) of the gastrointestinal tract. When the virus enters the human respiratory tract, mucociliary clearance is inhibited and epithelial cells die, allowing the virus to enter the peripheral blood with subsequent damage to target organs (lungs, digestive tract, heart, kidneys). An important pathogenic characteristic of SARS-CoV-2 infection, especially with severe disease, is an excessive immune system response with massive release of cytokines, which causes acute respiratory distress syndrome. Clinical and experimental studies have shown that SARS-CoV-2 can be significantly more sensitive to type I interferons (IFN-I), than other coronaviruses. IFN-I deficiency is thought to play a key role in the pathogenesis of COVID-19, and several studies have shown that delayed IFN-I signaling is associated with sustained viral replication and serious complications. The use of interferon-based medicines (IFN-I) for the treatment and prevention of COVID-19 appears to be quite important to study attentively. This paper presents an original regimen of recombinant interferon alpha-2b-based medicine (Grippferon®, nasal drops and spray) for the medication-assisted post-exposure prevention of COVID-19 in healthcare specialists, working in the pediatric infectious disease hospital. The effectiveness and safety of this medication regimen for the COVID-19 prevention was shown. Key words: medication-assisted prevention, COVID-19, post-exposure protection of healthcare workers, recombinant interferon alpha-2b, Grippferon

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