Host transcriptional response to SARS‐CoV‐2 infection in COVID‐19 patients

The overall transcriptional reduction, irrespective of disease severity (Figure 1C), is well correlated with the phenomenon of fading host cell functionality and prominent viral protein synthesis, and may be associated with interference in host cellular processes and responses.1 The results indicate a diverse transcriptomic profile in response to SARS-CoV-2, in line with the variable prognosis seen in many COVID-19 patients. IFN-mediated activation of the JAK-STAT signaling pathway may play a role in inducing necroptosis (Figure 2B), and is implicated in Acute Respiratory Distress Syndrome (ARDS) development and protection from severe COVID-19 along with OAS1.2,3 Though not a part of this network, all the MHC class 1 and some MHC class 2 genes (HLA-A,B,C,E,F, and HLA-DQB1, DR-B1, DR-B5), involved in T-cell mediated cell death and the antibody-mediated adaptive immune response, were also upregulated along with RFX5, that binds to MHC-II promoters. The effect on GABAergic interneurons in the olfactory bulb, connecting sensory neurons in the olfactory epithelium, might increase the potential for neurological complications observed in COVID-19 patients.7 Further studies are underway to delineate the implications for neuronal infectivity via the olfactory and respiratory tracts and the nasopharyngeal compartment,6 which are predominantly epithelial cells.