Key result
Inhibition of CVB1-induced medium-sized extracellular vesicle production with calpeptin or CAPNS1 siRNA knockdown limited the spread of Coxsackievirus B1 in HeLa cells.
Why the study?
Details of nonlytic virus transmission of CVB1 remained unclear.
CVB1 utilizes a nonlytic extracellular vesicle-to-cell mechanism for viral transmission, which can be inhibited by blocking EV release.
Supports nonlytic CVB1 spread via mEVs in vitro; leaves open in vivo relevance for myocarditis pathogenesis.
Like most non-enveloped viruses, CVB1 mainly uses cell lysis to spread. Details of a nonlytic virus transmission remain unclear. Extracellular Vesicles (EVs) transfer biomolecules between cells. We show that CVB1 entry into HeLa cells results in apoptosis and release of CVB1-induced ‘medium-sized’ EVs (CVB1 i -mEVs). These mEVs (100–300 nm) harbour CVB1 as shown by immunoblotting with anti-CVB1-antibody; viral capsids were detected by transmission electron microscopy and RT-PCR revealed CVB1 RNA. The percentage of mEVs released from CVB1-infected HeLa cells harbouring virus was estimated from TEM at 34 %. Inhibition of CVB1 i -mEV production, with calpeptin or siRNA knockdown of CAPNS1 in HeLa cells limited spread of CVB1 suggesting these vesicles disseminate CVB1 virions to new host cells by a nonlytic EV-to-cell mechanism. This was confirmed by detecting CVB1 virions inside HeLa cells after co-culture with CVB1 i -mEVs; EV release may also prevent apoptosis of infected cells whilst spreading apoptosis to secondary sites of infection.
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Jorfi et al. (2023) studied Coxsackievirus B1 infection. Calpeptin or CAPNS1 siRNA knockdown vs. Untreated or control siRNA was evaluated on Viral transmission and extracellular vesicle release. Inhibition of CVB1-induced medium-sized extracellular vesicle production with calpeptin or CAPNS1 siRNA knockdown limited the spread of Coxsackievirus B1 in HeLa cells.
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