HIV: Two people suppressed the virus for years while pausing medication

A growing number of cases show that some people with HIV can avoid becoming ill even while pausing their medication, as virus levels in their blood remain low

Two people with HIV who were able to stop taking medication for several years without becoming ill from the virus offer clues for future strategies to suppress the infection.

But both eventually had to restart taking medication, showing the current limitations of such approaches, says Tae-Wook Chun of the National Institutes of Health (NIH) in Maryland.

People with HIV can avoid becoming ill by taking lifelong medicines that stop the virus from multiplying, but copies of the virus remain in their immune memory cells throughout the body. This means that for most, if they stop medication, the virus starts multiplying again and levels in the blood rebound, requiring a return to drug therapy.

A few individuals who pause their HIV medication don’t see their blood virus levels quickly rebound, but it is unclear why. They are sometimes called “post-treatment controllers”. The phenomenon seems to happen more often in people who begin anti-HIV drug treatment in the first few weeks after infection, perhaps because the virus doesn’t have a chance to become established in so many of their immune cells.

The latest study looks at two people who both began early anti-HIV treatment and later stopped their medication as part of an NIH trial of a therapeutic vaccine to treat HIV infections, although they received a placebo version of the vaccine. When the virus didn’t restart multiplying at the end of the six-month trial, the men chose to stay off their medication and continue having frequent blood tests, even though they had been told they had the placebo.

The pair were able to continue without anti-HIV medication for 3.5 and four years, but different immune mechanisms seemed to be responsible in each case.

There are two main arms of the immune system: antibodies and T-cells. Until now, it was thought that T-cells, which directly kill virus-infected human cells, were more important for post-treatment controllers. But Chun and his colleagues found that while T-cells were responsible in one man, antibodies were suppressing virus multiplication in the other. “He had an amazing antibody response that probably completely contained viral replication,” says Chun.

This second man had to restart medication because he became infected with another HIV infection, which was resistant to his antibodies. HIV viruses are highly variable and there are many genetic subtypes circulating.

The first man, who was being protected by T-cells, saw three relatively small rises in the level of virus in his blood followed by spontaneous falls. After three years he chose to restart medication without telling his doctors, which they discovered through a regular blood test.

The findings show that researchers looking at post-treatment controllers need to frequently test people’s blood samples, both for new HIV infections and for evidence of HIV drugs even if they aren’t being officially provided, says Chun.

“Any case of spontaneous control of HIV in the absence of [antiviral] therapy is worth being reported. It will add to the body of information we have,” says Javier Martínez-Picado at the IrsiCaixa AIDS Research Institute in Badalona, Spain.

Martínez-Picado’s team has been studying the only three people thought to have been cleared of an HIV infection, which happened because they developed cancer that needed a bone marrow transplant. They received bone marrow from people who had a natural mutation that gives their immune cells some resistance to the virus.

Journal reference: Nature Medicine, DOI: 10.1038/s41591-021-01503-6

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