Severe acute respiratory syndrome coronavirus 2 may exploit human transcription factors involved in retinoic acid and interferon-mediated response: a hypothesis supported by an in silico analysis

The pandemic of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causing disease 2019 (COVID-19), resulting in disease, is a worldwide emergency. Because recently it has been found that SARS-CoV dependent on host transcription factors (TF) to express the viral genes, efforts are required understand molecular interplay between virus and response. By bioinformatic analysis, we investigated human TF can bind SARS-CoV-2 sequence be involved transcription. In particular, analysed key role interferon (IFN) We several could induced by IFN antiviral response, specifically some IFN-stimulated gene factor 3 (ISGF3) unphosphorylated ISGF3, which were promote open reading frame. Moreover, 22 binding sites present only infecting humans but not bat RaTG13. IFN, retinoic acid signalling regulation RNA polymerase II, thus facilitating its own replication cycle. This mechanism, competition, may steal these processes, explaining SARS-CoV-2's disruption IFN-I cells mechanism SARS depletion leading cytokine storm. identified three exclusively Brazilian P.1 variant explain higher severity syndrome. These data shed light dependence from machinery associated with response strengthen our knowledge virus's replicative activity, paving way for new targets drug design therapeutic approaches. • Several (TFBS) Twenty-two TFBS genomic region isolated bats. A strong involvement signaling emerges binds sequence. Two mutations within cause formation mucus hyperproduction pulmonary disorders.