Host caveolin-1 facilitates Zika virus infection via promoting viral RNA replication.
Journal of cell science(2024)
摘要
Zika virus (ZIKV) has gained notoriety in recent years without targeted therapies or vaccines available so far. Caveolin-1 (Cav-1) in host cells plays crucial functions in the invasion of many viruses. However, its specific involvement in ZIKV infection has remained unclear. Here, we reveal that depleting Cav-1 leads to a substantial reduction in ZIKV RNA levels, protein expression, and viral particle production, indicating that ZIKV exploits Cav-1 for its infection. By dissecting each stage of the viral life cycle, we unveiled that, unlike its invasion role in many other viruses, Cav-1 depletion selectively impairs ZIKV replication, resulting in altered replication dynamics and reduced strand-specific RNA levels, concurrently without affecting viral entry, maturation and release. These results reveal an unforeseen function of Cav-1 in facilitating ZIKV replication, that provides new insights into the intricate interaction between Cav-1 and ZIKV and underscores Cav-1 as a potential candidate for anti-ZIKV approaches.
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