SARS-CoV-2 may regulate cellular responses through depletion of specific host miRNAs.

Cold viruses have generally been considered fairly innocuous until the appearance of the severe acute respiratory coronavirus 2 (SARS-CoV-2) in 2019 which caused the coronavirus disease 2019 (COVID-19) global pandemic. Two previous viruses foreshadowed that a coronavirus could potentially have devastating consequences in 2002 (severe acute respiratory coronavirus (SARS-CoV)) and in 2012 (middle east respiratory syndrome coronavirus (MERS-CoV)). The question that arises is why these viruses are so different from the relatively harmless cold viruses. Based on an analysis of the current literature and using bioinformatic approaches, we examined the potential human miRNA interactions with the SARS-CoV-2's genome, and compared the miRNA target sites in seven coronavirus genomes that include SARS-CoV-2, MERS-CoV, SARS-CoV, and four non-pathogenic coronaviruses. Here, we discuss the possibility that pathogenic HCoVs including SARS-CoV-2 could modulate host miRNA levels by acting as miRNA sponges to facilitate viral replication and/or to avoid immune responses.