DEFA1B inhibits ZIKV replication and retards cell cycle progression through interaction with ORC1.

ABSTRACT:

Aims

Zika virus (ZIKV) infection causes a public health concern because of its potential association with the development of microcephaly. During viral infections, the host innate immune response is mounted quickly to produce some endogenous functional molecules to limit virus replication and spread. Exosomes contain molecules from their cell of origin following virus infection and can enter recipient cells for intercellular communication. Here, we aim to clarify whether ZIKV-induced exosomes can regulate viral pathogenicity by transferring specific RNAs.

Main methods

In this study, exosomes were isolated from the supernatants of A549 cells with or without ZIKV infection. Human transcriptome array (HTA) was performed to analyze the profiling of RNAs wrapped in exosomes. Then

SUBMITTER: Li S 

PROVIDER: S-EPMC7567675 | biostudies-literature | 2020 Dec

REPOSITORIES: biostudies-literature