HIV-1 Tat Shown to Undermine Cell Defenses, Boosting TB in Preclinical Study

Researchers describe a preclinical mechanism for HIV-linked tuberculosis vulnerability, suggesting autophagy restoration as a possible approach.

Overview

A CNRS-led team published peer-reviewed findings in PLOS Pathogens on September 18, 2025, identifying HIV-1 Tat as a driver of increased tuberculosis susceptibility.
Experiments in human cells and zebrafish larvae found Tat inhibits clathrin-mediated endocytosis and autophagy, enabling Mycobacterium tuberculosis to multiply inside host cells.
The study reports the same Tat-driven inhibition favors the intracellular proliferation of Toxoplasma.
The authors note Tat is currently difficult to target and propose exploring therapies that restore autophagy to improve host defense.
WHO data cited by the researchers show tuberculosis causes one in three deaths among people with HIV and that HIV increases TB risk by 15 to 30 times.