Abstract
Coxsackievirus B3 (CVB3) is an important human pathogen linked to cardiac arrhythmias and acute heart failure. CVB3 infection has been reported to induce the formation of autophagosomes that support the viral replication in host cells. Interestingly, our study shows that the accumulation of autophagosomes during CVB3 infection is caused by a blockage of autophagosome–lysosome fusion rather than the induction of autophagosome biogenesis. Moreover, CVB3 decreases the transcription and translation of syntaxin 17 (STX17), a SNARE (soluble N-ethylmaleimide-sensitive factor activating protein receptor) protein involved in autophagosome–lysosome fusion. Overexpression of STX17 restored the autophagic flux, alleviated the virus-induced lysosomal dysfunction, and decreased the apoptosis induced by CVB3 infection in HeLa cells. Taken together, our results suggest that CVB3 infection impairs the autophagic flux by blocking autophagosome–lysosome fusion. These findings thus point to potential new therapeutic strategies targeting STX17 or autophagosome–lysosome fusion for treating CVB3-associated diseases.
Highlights
Introduction CoxsackievirusB (CVB) belongs to the genus Enterovirus in the family Picornaviridae
After Coxsackievirus B3 (CVB3) infection of HeLa cells at low and high multiplicity of infection (MOI), we observed a marked punctate LC3 distribution, which increased in a dose-dependent manner (Fig. 1a, c)
To confirm the protective effect of syntaxin 17 (STX17) against cell death induced by CVB3 infection, cleaved caspase-3 was detected by western blot analysis, and the results showed that STX17 inhibited the cleavage of caspase-3 in CVB3-infected HeLa cells (Fig. 6e, f)
Summary
Introduction CoxsackievirusB (CVB) belongs to the genus Enterovirus in the family Picornaviridae. CVB are the most common cause of infectious myocarditis, which can lead to dilated cardiomyopathy and cardiac failure resulting in permanent heart damage or death[1] This group of viruses contains some of the most common pathogens affecting children and young adults[2,3,4], which makes it an important study subject for pediatricians. These viruses are a frequent cause of pancreatitis and aseptic meningitis[5,6]. As an important member of the CVB group, coxsackievirus B3
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