Scientists at Institut Pasteur have gained new insights into how some people control HIV-1 replication after interruption of antiretroviral treatment (ART). The investigators found a fingerprint involved in long-term viral remission.

The extent of the damage that will be caused if the U.S. overseas aid program, the President’s Emergency Plan for AIDS Relief (PEPFAR), is axed or has its funding cut, is laid out in an expert analysis published in The Lancet April 8, which estimates nearly 500,000 children could die from AIDS-related causes by 2030, while 1 million children will be infected with the virus.

The availability of effective antiretroviral therapy has lowered the risk, and the severity, of neural sequelae of HIV infection. “Early in the HIV pandemic, approximately 15% of people with HIV had dementia and or encephalitis,” Howard Fox told his audience. “Fortunately, with treatment, the prevalence of these severe disorders has been greatly lowered. But there is persistence of what are called more minor disorders – which are not minor if you have them.”

It was previously demonstrated that the HIV-1 integrase (IN)-interacting host factor INI1/SMARCB1 binds to HIV-1 IN through its Rpt1 domain of INI1 (INI1-Rpt1) and plays a key role in assembly and particle production.

At the 2025 meeting of the Conference on Retroviruses and Opportunistic Infections (CROI) it was the best of times, it was the worst of times. On the first full day of the conference, reports from the first HIV cure trial conducted in Africa, the RIO trial and others showed that perhaps, a broadly useful cure is on the horizon.

At the 2025 meeting of the Conference on Retroviruses and Opportunistic Infections (CROI) it was the best of times, it was the worst of times. On the first full day of the conference, reports from the first HIV cure trial conducted in Africa, the RIO trial and others showed that perhaps, a broadly useful cure is on the horizon.

The development of an effective HIV vaccine remains an urgent public health need due to the high genetic variability and rapid mutation rates of the virus, which limit the generation of broadly neutralizing antibodies.