Coxsackievirus B3 is a major etiological factor for myocarditis (infection of the heart) and virus-induced heart failure, for which effective therapy is lacking. There is increasing evidence that aberrant accumulation of protein aggregates and damaged organelles contribute to heart failure; however, the underlying molecular mechanism remains poorly characterized.
Dr. Honglin Luo and her team studied how coxsackievirus B3 disrupts a cellular degradation pathway (called autophagy), leading to impaired protein homeostasis. They discovered that coxsackievirus B3 directly targets sequestosome 1 and CALCOCO2, two autophagy adaptor proteins that normally act to eliminate protein aggregates and damaged organelles. These two proteins differentially regulate viral replication before succumbing to degradation by viral proteases. This study provides novel mechanistic insights between virus infections and impaired protein homeostasis as a consequence of disrupted autophagy.
By improving our understanding of viral infection mechanisms, Dr. Luo and her group of researchers can strategize future therapeutic targets for treating coxsackievirus B3 infections.
Read the full study here.