ABSTRACT
Understanding how viruses evade innate defenses to efficiently spread in their hosts is crucial in the fight against infections. In our study, we provided new insights on the first step initiating an LC3C (microtubule associated protein 1 light chain 3 gamma)-associated degradative pathway exploited by HIV-1 (human immunodeficiency virus type 1) to overcome the antiviral action of the restriction factor BST2 (bone marrow stromal cell antigen 2)/tetherin. We have uncovered an unsuspected and unconventional function of the autophagy-related protein ATG5 in the recognition and engagement of BST2 molecules trapping viruses at the plasma membrane, and directing them toward this LC3C-associated pathway for degradation. Additionally, we highlighted that HIV-1 uses this LC3C-associated process to attenuate the inflammatory responses triggered by BST2-mediated sensing of viruses.
List of abbreviations
AIDS | = | acquired immunodeficiency syndrome |
ATG5 | = | autophagy related 5 |
ATG12 | = | autophagy related 12 |
ATG14 | = | autophagy related 14 |
BST2/tetherin | = | bone marrow stromal cell antigen 2 |
FIP200/RB1CC1 | = | RB1inducible coiled-coil 1 |
HIV-1 | = | human immunodeficiency virus type 1 |
MAP1LC3C/LC3C | = | microtubule associated protein 1 light chain 3 gamma |
SYK | = | spleen associated tyrosine kinase |
pSYK | = | phosphorylated spleen associated tyrosine kinase |
Vpu | = | Viral Protein U |
Disclosure statement
No potential conflict of interest was reported by the author(s).