Back

Virus-induced vesicular acidification enhances HIV immune evasion.

Yaple-Maresh, M. E.; Flores, G. G.; Zimmerman, G. E.; Gomez-Rivera, F.; Collins, K. L.

2024-12-18 cell biology
10.1101/2024.12.17.628989 bioRxiv
Show abstract

To block endocytic viral entry, cells typically acidify endosomes via upregulated expression of the short isoform of human nuclear receptor 7 (NCOA7) which boosts vacuolar ATPase (V-ATPase) activity. In our study, primary T cells infected with HIV-1 triggered endosomal acidification, yet NCOA7 levels were only modestly altered. Instead, we observed a pronounced depletion of the 50 kDa form of the sodium/hydrogen exchanger 6 (NHE6). Remarkably, NHE6 overexpression or treating cells with low-dose concanamycin A, a V-ATPase inhibitor, selectively neutralized endosomal pH. This neutralization impaired Nef-driven MHC-I downmodulation by our wildtype HIV reporter virus. Mechanistically, NHE6 overexpression disrupted Nef-mediated MHC-I loss by reducing recruitment of Nef to recycling endosome (Rab11+) compartments and blocking Nef interactions with {beta}-COP, and ARF-1. Together, these findings reveal NHE6 as a critical regulator of endosomal pH and HIV immune evasion.

Published in iScience (predicted rank #8) · training set

Matching journals

The top 6 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.