Research Projects

The COVID-19 pandemic has led to the development of therapeutics to control the spread of highly pathogenic human coronaviruses. A recent study from the PI's laboratory has found the therapeutic potential of a host gap junction protein connexin 43 (Cx43) against MHV-A59, highlighting the importance of Cx43 expression at the cell surface to reduce MHV infectivity and spread. The study aims to investigate the mechanism behind altered Cx43 expression, using the MHV-A59-induced disease as a model for viral-induced demyelination, which mimics the pathological hallmarks of human neurological disease Multiple sclerosis. The proposed proposal explores the regulation of Cx43 expression by the balance between pro-inflammatory (TNF-alpha) and anti-inflammatory (TGF-beta1 and IL-10) signaling pathways, using the established MHV-induced model. The researchers aim to further dissect the downstream signaling of TNFalpha-TGFbeta1 and IL-10 in controlling Cx43 expression and modulate these cytokines or their downstream pathways to develop a cytokine-based therapy to stabilize Cx43 expression in the CNs, potentially reducing acute stage beta-CoV infectivity and spread and reducing chronic stage demyelination.