TRIM22 suppresses Zika virus replication by targeting NS1 and NS3 for proteasomal degradation.

ABSTRACT:

Background

Recognition of viral invasion by innate antiviral immune system triggers activation of the type I interferon (IFN-I) and proinflammatory signaling pathways. Subsequently, IFN-I induction regulates expression of a group of genes known as IFN-I-stimulated genes (ISGs) to block viral infection. The tripartite motif containing 22 (TRIM22) is an ISG with strong antiviral functions.

Results

Here we have shown that the TRIM22 has been strongly upregulated both transcriptionally and translationally upon Zika virus (ZIKV) infection. ZIKV infection is associated with a wide range of clinical manifestations in human from mild to severe symptoms including abnormal fetal brain development. We found that the antiviral function of TRIM22 plays a crucial role in counterattacking

SUBMITTER: Zu S 

PROVIDER: S-EPMC9429444 | biostudies-literature | 2022 Aug

REPOSITORIES: biostudies-literature