Eight influenza virus cellular manipulations which can boost concurrent SARS-CoV-2 infections to severe outcomes

Viral pathogens in the lungs can cause severe outcomes, including acute lung injury and acute respiratory distress syndrome. Dangerous respiratory pathogens include some influenza A and B viruses, and the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Unfortunately, concurrent infections of influenza virus and SARS-CoV-2 increase severe outcome probabilities. Influenza viruses have eight cellular manipulations which can assist concurrent SARS-CoV-2 viral infections. The eight cellular manipulations include: (1) viral protein binding with cellular sensors to block antiviral transcription factors and cytokine expressions, (2) viral protein binding with cell proteins to impair cellular pre-messenger ribonucleic acid splicing, (3) increased ribonucleic acid virus replication through the phosphatidylinositol 3-kinase/Akt (protein kinase B) pathway, (4) regulatory ribonucleic acids to manipulate cellular sensors and pathways to suppress antiviral defenses, (5) exosomes to transmit influenza virus to uninfected cells to weaken cellular defenses before SARS-CoV-2 infection, (6) increased cellular cholesterol and lipids to improve virion synthesis stability, quality and virion infectivity, (7) increased cellular autophagy, benefiting influenza virus and SARS-CoV-2 replications and (8) adrenal gland stimulation to produce glucocorticoids, which suppress immune cells, including reduced synthesis of cytokines, chemokines and adhesion molecules. Concurrent infections by one of the influenza viruses and SARS-CoV-2 will increase the probability of severe outcomes, and with sufficient synergy potentially enable the recurrence of tragic pandemics.