LAMR1 restricts Zika virus infection by attenuating the envelope protein ubiquitination. Issue 1 (1st January 2021)

• Record Type: Journal Article
• Authors: Hu, Dingwen; Wang, Yingchong; Li, Aixin; Li, Qin; Wu, Caifeng; Shereen, Muhammad Adnan; Huang, Shanyu; Wu, Kailang; Zhu, Ying; Wang, Wenbiao; Wu, Jianguo
• Is Part Of: Virulence. Volume 12:Issue 1(2021)
• Page Start: 1795
• Page End: 1807
• Publication Date: 2021-01-01
• Subjects: Laminin receptor 1, LAMR1 -- Zika virus, ZIKV -- E protein -- ubiquitination -- eukaryotic translation initiation factor 3 subunit 5, EIF3S5; Virulence (Microbiology) -- Periodicals; Bacterial diseases -- Periodicals; Molecular microbiology -- Periodicals; 579.05
• DOI: 10.1080/21505594.2021.1948261
• Languages: English
• ISSNs: 2150-5608

Abstract

ABSTRACT: Zika virus (ZIKV) infection can cause severe neurological disorders, including Guillain–Barre syndrome and meningoencephalitis in adults and microcephaly in fetuses. Here, we reveal that laminin receptor 1 (LAMR1) is a novel host resistance factor against ZIKV infection. Mechanistically, we found that LAMR1 binds to ZIKV envelope (E) protein via its intracellular region and attenuates E protein ubiquitination through recruiting the deubiquitinase eukaryotic translation initiation factor 3 subunit 5 (EIF3S5). We further found that the conserved G282 residue of E protein is essential for its interaction with LAMR1. Moreover, a G282A substitution abolished the binding of E protein to LAMR1 and inhibited LAMR1-mediated E protein deubiquitination. Together, our results indicated that LAMR1 represses ZIKV infection through binding to E protein and attenuating its ubiquitination.