Journal
CELL HOST & MICROBE
Volume 15, Issue 2, Pages 239-247Publisher
CELL PRESS
DOI: 10.1016/j.chom.2014.01.006
Keywords
-
Categories
Funding
- MRC [U105170648, G0700815]
- BBSRC [BB/J004324/1]
- Academy of Medical Sciences
- Academy of Medical Sciences (AMS) [AMS-SGCL1-Beale] Funding Source: researchfish
- Biotechnology and Biological Sciences Research Council [BBS/E/D/20241864] Funding Source: researchfish
- Medical Research Council [G0700815, MC_U105170648] Funding Source: researchfish
- BBSRC [BBS/E/D/20241864] Funding Source: UKRI
- MRC [G0700815, MC_U105170648] Funding Source: UKRI
Ask authors/readers for more resources
Autophagy recycles cellular components and defends cells against intracellular pathogens. While viruses must evade autophagocytic destruction, some viruses can also subvert autophagy for their own benefit. The ability of influenza A virus (IAV) to evade autophagy depends on the Matrix 2 (M2) ion-channel protein. We show that the cytoplasmic tail of IAV M2 interacts directly with the essential autophagy protein LC3 and promotes LC3 relocalization to the unexpected destination of the plasma membrane. LC3 binding is mediated by a highly conserved LC3-interacting region (LIR) in M2. The M2 LIR is required for LC3 redistribution to the plasma membrane in virus-infected cells. Mutations in M2 that abolish LC3 binding interfere with filamentous budding and reduce virion stability. IAV therefore subverts autophagy by mimicking a host short linear protein-protein interaction motif. This strategy may facilitate transmission of infection between organisms by enhancing the stability of viral progeny.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available