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.

Among preterm infants with RDS, there was a significant decrease in the need for invasive ventilation in the NIPPV group as compared with NCPAP group, especially for the infants who received surfactant. However, NIPPV could not decrease the need for invasive ventilation both in the subgroup of infants whose GA ≤ 30 weeks or BW < 1,500 g and the subgroup of infants with BW of >30 weeks or BW > 1,500 g. It is limited to analysis the primary outcome generally. Larger trials of this intervention are needed to assess the difference in this primary outcome and the related complications between both forms of noninvasive respiratory support.

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