Journal Article DZNE-2026-00266

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png
HIV-1 Vpr is targeted for degradation by autophagy.

 ;  ;  ;  ;

2026
PLoS Lawrence, Kan.

PLoS pathogens 22(3), e1014020 () [10.1371/journal.ppat.1014020]

This record in other databases:    

Please use a persistent id in citations: doi:

Abstract: Autophagy is part of the innate immune arsenal to fight viruses, including HIV-1. We previously reported that HIV-1 Gag is targeted for autophagy-mediated degradation. Here, we identify HIV-1 Vpr, an important virulence factor, as an autophagy target in HIV-1 NL4-3, a lab adapted molecular clone. Notably, Vpr proteins from a collection of transmitted/founder viruses (TFVs) were resistant to autophagy. Based on this observation, we identified residues at positions 37, 45, 77, 83-86, 93-94 in NL4-3 Vpr as responsible for its susceptibility to autophagy. Importantly, differences between NL4-3 and TFV Vpr proteins at these positions impact their interaction with the autophagy receptors NDP52, SQSTM1/p62 and TAX1BP1. By engineering NL4-3 molecular clones harboring either autophagy-sensitive or -resistant vpr, we found that in 2D and 3D in vitro systems virus spread was significantly reduced for the virus carrying autophagy-sensitive Vpr. In conclusion, our study identifies Vpr as a novel autophagy target and suggests that Vpr susceptibility to autophagy impacts HIV-1 spread.

Keyword(s): Autophagy: physiology (MeSH) ; Humans (MeSH) ; vpr Gene Products, Human Immunodeficiency Virus: metabolism (MeSH) ; vpr Gene Products, Human Immunodeficiency Virus: genetics (MeSH) ; HIV-1: metabolism (MeSH) ; HIV-1: genetics (MeSH) ; HIV-1: pathogenicity (MeSH) ; HIV Infections: metabolism (MeSH) ; HIV Infections: virology (MeSH) ; HIV Infections: immunology (MeSH) ; HEK293 Cells (MeSH) ; Proteolysis (MeSH) ; vpr Gene Products, Human Immunodeficiency Virus ; vpr protein, Human immunodeficiency virus 1

Classification:

Contributing Institute(s):
  1. Neurovirology and Neuroinflammation (AG Sparrer)
Research Program(s):
  1. 351 - Brain Function (POF4-351) (POF4-351)

Database coverage:
Medline ; Creative Commons Attribution CC BY (No Version) ; DOAJ ; Article Processing Charges ; BIOSIS Previews ; Biological Abstracts ; Clarivate Analytics Master Journal List ; Current Contents - Life Sciences ; DOAJ Seal ; Ebsco Academic Search ; Essential Science Indicators ; Fees ; IF >= 5 ; JCR ; PubMed Central ; SCOPUS ; Science Citation Index Expanded ; Web of Science Core Collection
Click to display QR Code for this record

The record appears in these collections:
Document types > Articles > Journal Article
Institute Collections > UL DZNE > UL DZNE-AG Sparrer
Documents in Process
Public records
In process

 Record created 2026-03-11, last modified 2026-03-11


Restricted:
Download fulltext PDF Download fulltext PDF (PDFA)
External link:
Download fulltextFulltext by Pubmed Central
Rate this document:

Rate this document:
1
2
3
 
(Not yet reviewed)