- Lal, Kerri G;
- Kim, Dohoon;
- Costanzo, Margaret C;
- Creegan, Matthew;
- Leeansyah, Edwin;
- Dias, Joana;
- Paquin-Proulx, Dominic;
- Eller, Leigh Anne;
- Schuetz, Alexandra;
- Phuang-ngern, Yuwadee;
- Krebs, Shelly J;
- Slike, Bonnie M;
- Kibuuka, Hannah;
- Maganga, Lucas;
- Nitayaphan, Sorachai;
- Kosgei, Josphat;
- Sacdalan, Carlo;
- Ananworanich, Jintanat;
- Bolton, Diane L;
- Michael, Nelson L;
- Shacklett, Barbara L;
- Robb, Merlin L;
- Eller, Michael A;
- Sandberg, Johan K
Mucosa-associated invariant T (MAIT) cell loss in chronic HIV-1 infection is a significant insult to antimicrobial immune defenses. Here we investigate the response of MAIT cells during acute HIV-1 infection utilizing the RV217 cohort with paired longitudinal pre- and post-infection samples. MAIT cells are activated and expand in blood and mucosa coincident with peak HIV-1 viremia, in a manner associated with emerging microbial translocation. This is followed by a phase with elevated function as viral replication is controlled to a set-point level, and later by their functional decline at the onset of chronic infection. Interestingly, enhanced innate-like pathways and characteristics develop progressively in MAIT cells during infection, in parallel with TCR repertoire alterations. These findings delineate the dynamic MAIT cell response to acute HIV-1 infection, and show how the MAIT compartment initially responds and expands with enhanced function, followed by progressive reprogramming away from TCR-dependent antibacterial responses towards innate-like functionality.