According to science.org, two independent research groups have identified a specific class of immune cells as crucial for achieving a “functional cure” for HIV, where patients can stop antiretroviral drugs (ARVs) for many months or even years. The studies, published in Nature and Nature on World AIDS Day, focused on patients in experimental trials involving broadly neutralizing antibodies (bNAbs). In one trial led by the Ragon Institute, between 14% and 22% of participants controlled their infection for at least 2 months after antibody treatment, with one person maintaining control for over 7 years. A separate UCSF study gave 10 patients bNAbs plus an experimental vaccine and a reservoir-reducing drug, finding that seven had prolonged viral control, including one participant who went without drugs for 4 months. Both teams pinpointed “stemmy” precursor CD8 memory T cells as the key biomarker for this long-term control.
The Relay Race Against the Virus
Here’s the thing about HIV treatment: ARVs are amazing, but they’re a lifelong sentence. The virus hides in reservoirs, and if you stop the pills, it almost always comes roaring back in weeks. So a “functional cure” isn’t about eradicating every last bit of HIV DNA. It’s about training your immune system to be a permanent, effective security guard that keeps the virus in a box after you stop the drugs. That’s the holy grail these researchers are chasing.
And they think they’ve found the specific security guard that matters most. These “stemmy” CD8 cells have a unique, self-renewing quality. In the patients who successfully controlled HIV, these precursor cells were ready to rapidly clone themselves into an army of “killer T cells” when they sensed the virus trying to make a comeback. David Collins from the Ragon Institute uses a great analogy: it’s like a relay race. The bNAb treatment slows down the returning HIV, giving these stemmy T cells a “running start” to mature and mobilize. Without that head start? The virus, a “really fast runner,” wins every time.
More Than Just One Piece
But is it really that simple? Of course not. Immunologist Michel Nussenzweig, who co-authored both papers, is careful to say these stemmy CD8 cells are likely just one part of a broader immune response. The UCSF study suggests a “vaccinal effect” is also at play, where the bNAb-virus complex itself stimulates other immune defenses. And in a preprint, Nussenzweig’s team found that a patient’s own, naturally occurring antibodies also seem to help in achieving long-term control.
So we’re looking at a complex immunological orchestra, not a solo act. But identifying the first-chair violinist is a massive deal. As Sharon Lewin from the Peter Doherty Institute put it, the field “urgently needs” insights like this to push forward. Now researchers have a clear target: how do we safely stimulate the production and activity of these specific stemmy CD8 cells in everyone with HIV?
What This Means For Patients
For someone like Tom Perrault, the San Francisco participant in the UCSF study, this isn’t just academic. He’s been on effective ARVs for 25 years, but he worries about the long-term, low-grade inflammation they don’t stop. “Taking the pills is not an automatic panacea and everything is sunshine and lollipops,” he says. That’s the real-world stakes. A functional cure could mean freedom from a daily pharmaceutical regimen and potentially a healthier long-term outlook.
The path from this biomarker discovery to a widely available therapy is long. It will require more trials, more fine-tuning of combination therapies (antibodies, vaccines, reservoir shocks), and a deep understanding of why only some people’s immune systems play along. But for the first time, scientists have a strikingly clear signal in the noise. They know which immune soldiers to look for and, more importantly, which ones they need to recruit. That’s a fundamental shift. After decades of suppression, the conversation is finally, tangibly, turning toward durable control.
