According to the World Health Organisation, tuberculosis accounts for one in three deaths among people living with HIV. In fact, even when receiving effective antiretroviral treatment, HIV-positive individuals are 15 to 30 times more likely to contract tuberculosis than HIV-uninfected people.
In a study to be published in PLOS Pathogens, the CNRS-led research team1 highlights the key role played by Tat2 – a viral protein secreted by HIV-infected cells – in this hyper-vulnerability phenomenon. Studies conducted on human cells and zebrafish larvae revealed that this protein blocks the cell defence mechanism known as autophagy, thereby promoting the survival and multiplication of the bacterium responsible for tuberculosis – Mycobacterium tuberculosis – in target cells3.
These findings shed new light on the synergy between HIV and tuberculosis and pave the way for the development of innovative therapeutic strategies. Although the Tat protein remains difficult to target at present, treatments aimed at restoring the autophagy mechanism could be developed to better protect patients.
- From l'Institut de recherche en infectiologie de Montpellier (CNRS/Université de Montpellier), Laboratory of Pathogens and Host Immunity (CNRS/Inserm/Université de Montpellier), l'Institut de pharmacologie et biologie structurale (CNRS/Université de Toulouse) and l'Institut interdisciplinaire de neurosciences (CNRS/Université de Bordeaux).
- Transactivator of transcription.
- Known as macrophages, these cells belong to the white blood cell group. Their main role is to destroy cellular debris and pathogens throughout the body.
