Two more patients appear to have beaten HIV

One patients had a stem cell transplant; the other patient’s recovery appears to be related to a special kinds of cells she possesses:

A 66-year-old man in Southern California and a woman in her 70s in Spain are the latest in a small group of people who appear to have beaten their HIV infections, providing researchers new clues to a possible cure at a time when Covid-19 and other crises are slowing progress against the spreading virus.

Doctors caring for the man said they have not found any human immunodeficiency virus that can replicate in his body since he stopped antiretroviral drug therapy in March 2021 after a transplant of stem cells containing a rare genetic mutation that blocks HIV infection. He was given the transplant for leukemia, for which people with HIV are at increased risk. Details of his case were made public Wednesday and will be presented at a large international AIDS conference in Montreal, which opens Friday.

He is the oldest of five patients thus far who appear to have rid their bodies of HIV after the risky procedure and had been infected the longest, since 1988, offering hope for a growing cohort of aging HIV patients, said Jana Dickter, an infectious disease doctor who cares for the man at City of Hope, a cancer research and treatment center in Duarte, Calif., in the Los Angeles area.

“He saw many of his friends and loved ones become ill and ultimately succumb to the disease and had experienced some stigma associated with having HIV,” she said. His success “opens up the opportunity potentially for older patients to undergo this procedure and go into remission from both their blood cancer and HIV.”

The woman in Spain still has HIV lying dormant in some cells in her body. But the amount is declining, and the virus isn’t replicating even though she stopped antiretroviral therapy more than 15 years ago, said Juan Ambrosioni, one of the doctors caring for her at the Hospital Clinic of the August Pi i Sunyer Biomedical Research Institute in Barcelona.

She was diagnosed with HIV at age 59 shortly after becoming infected, and entered a clinical trial in which she received antiretroviral drugs as well as therapies to boost her immune system. After nine months, the antiretrovirals were stopped, Dr. Ambrosioni said.

Years of research finally revealed how she keeps her HIV naturally under control, he said: she has high levels of two types of immune cells that the virus normally suppresses and that probably help control viral replication, he said. Details of her case will be presented at the same conference. Both patients declined to be identified publicly.

You should be able to read the rest of the article in the Wall Street Journal by Betsy McKay by clicking this link.

It does not appear to be behind a paywall.


Are we finally on the road toward an HIV vaccine?

If I had a dollar for every time I read a headline like that.

But, if we are to believe what writer Jackie Flynn Mogensen reveals in this article, we could be closer than ever:

So, if researchers do manage to create an HIV vaccine that works, it has to clear several complicated hurdles. It will have to A) offer broad protection against an enormous number of variants; B) teach our bodies how to do something we don’t normally do on our own; and C) do this in such a way that offers total immunity. It’s largely because of these challenges that we don’t have an HIV vaccine today, and in part why several major clinical trials for potential vaccines have been unsuccessful; for every strategy we’ve thrown at HIV, the virus has found a way around it.

“It’s the Holy Grail of vaccines,” Haynes says.

The good news is, after spending years learning how HIV works (and enduring repeated clinical failures), many leading HIV researchers I spoke with say they have finally singled out—and tested—the right tool to fight the virus: rare, powerful antibodies known as “broadly neutralizing antibodies,” or bnAbs. Some people produce these antibodies after years of infection.

In general, infection-blocking antibodies work like this: When a virus enters your body, antibodies recognize and attach themselves to proteins on the surface of viruses, preventing those pathogens from entering our cells, and protecting us from getting sick. But because HIV mutates so easily, the virus’ surface can look pretty different between variants, making it difficult for antibodies to keep up. There are, however, a few parts of the virus that don’t change much between variants, like the virus’ “Achilles heel.” Antibodies that attach to those spots are known as broadly neutralizing.

You can read the rest here.

Scanning electron micrograph of HIV-1 (in green) budding from cultured lymphocyte. Multiple round bumps on cell surface represent sites of assembly and budding of virions. (Wikimedia Commons: C. Goldsmith Content Providers)