SARS-CoV-2 and influenza viruses: Strategies to cope with coinfection and bioinformatics perspective

Abstract

Almost a century after the devastating pandemic of the Spanish flu, humankind is facing the relatively comparable global outbreak of COVID-19. COVID-19 is an infectious disease caused by SARS-CoV-2 with an unprecedented transmission pattern. In the face of the recent repercussions of COVID-19, many have argued that the clinical experience with influenza through the last century may have tremendous implications in the containment of this newly emerged viral disease. During the last 2 years, from the emergence of COVID-19, tremendous advances have been made in diagnosing and treating coinfections. Several approved vaccines are available now for the primary prevention of COVID-19 and specific treatments exist to alleviate symptoms. The present review article aims to discuss the pathophysiology, diagnosis, and treatment of SARS-CoV-2 and influenza A virus coinfection while delivering a bioinformatics-based insight into this subject matter.

Keywords: COVID-19; SARS-CoV-2; bioinformatics perspective; coinfection; influenza.

Figure 1

The schematic overview of present article

Figure 2

SARS‐CoV‐2 and influenza coinfection of lung epithelial cells based on bioinformatics modeling. SARS‐CoV‐2 showed a significantly slower growth rate than that of other strains. It was reported that other virus strains readily suppress the SARS‐CoV‐2 replication. It is possible that several strains, as well as the influenza virus, may target ACE2 molecules, and thus, result in suppression of SARS‐CoV‐2 by downregulating ACE2. Because it has been suggested that the ACE2 plays a fundamental role in SARS‐CoV‐2 replication.