Can some subsets of T cells be infected by SARS-CoV-2, following expression of CD147 or CD26, especially activated and exhausted memory T cells?
Does SARS-CoV-2 reduce the ratio of full-length wild-type human STING/truncated STING isoforms in antigen presenting cells at early stages of COVID-19?
Does SARS-CoV-2 activate aryl hydrocarbon receptor, like α-coronaviruses do?
In COVID-19, is IFN-β more detrimental than helpful when given to patients already admitted in ICU units?
Do Jak-inhibitors enhance or reduce the replication of SARS-Cov2 in vitro and in vivo together with the α and β IFNs levels?
Is the subdomain within the C terminus domain (CTT) of STING (miniCTT) different in patients with severe COVID-19?
Are GM-CSF+ CD4 T cells capable of prodigious ex vivo IL-6 and IFN-γ production in critically ill COVID-19 patients infected by SARS-CoV-2?
Is IL-6 negative feedback on cGAS-STING activation abolished in severe SARS-Cov infections by inhibition of ULK1 (and autophagy) by the SARS-CoV viruses?
Is this defect increased by concurrent infections by herpes-viruses?
Which mechanisms are mostly responsible for the down-regulation of STING activity in T and B cells, as compared to myeloid immune cells and non-immune cells: trafficking, degradation, miRNA-mediated repression, or post-translational modifications?
Are Tregs even more prone to exhaustion and/or lymphopenia than effector T cells in mouse or humans with gain of function mutations of STING?
Does gain of function and/or activation of some STING-pathways in helper T cells, including Tfh, lead to their premature apoptosis and contribute to the rather short duration of antibodies towards SARS-CoV infections?
Is the functionality of some STING pathways impaired in subsets of memory B and T cells in SAVI syndromes and COVID-19?
Does concurrent EBV and SARS-CoV-2 infections in B cells increase the exhaustion of T lymphocytes by over-activated presenting B cells?
Is miR-576-3p deficient in T cells from severe COVID-19?
