A three-part treatment given shortly after infection prevented a HIV-like virus from returning in infant monkeys after therapy stopped, according to research from Oregon Health & Science University, published in Nature Microbiology.
The findings do not show that HIV can be cured in human newborns. They do provide an important early indication that rapid, combined treatment could stop the virus from forming the hidden reservoirs that make HIV so difficult to eliminate.
The study used infant rhesus macaques exposed to simian-human immunodeficiency virus, known as SHIV. This virus is used in primate research because it mimics key aspects of human immunodeficiency virus infection, including its effects on the immune system and its capacity to persist in the body.
Modern antiretroviral therapy, or ART, has transformed HIV care. Taken consistently, ART can suppress the virus to undetectable levels, preserve immune function and prevent HIV from progressing to acquired immunodeficiency syndrome, or AIDS. Sustained viral suppression also prevents sexual transmission of HIV.
However, ART does not remove HIV entirely. The virus can remain dormant inside infected immune cells, creating viral reservoirs. These reservoirs may not be visible in standard blood tests. If ART is stopped, the inactive virus can restart replication and return to detectable levels. This rebound remains one of the biggest barriers to a cure.
The tudy examined whether treatment delivered in the first days after infection could prevent those reservoirs from becoming permanent. Scientists tested a combination of daily ART, two broadly neutralising antibodies and leronlimab, an experimental monoclonal antibody.
Each component has a separate role. ART blocks the virus from copying itself inside cells. Broadly neutralising antibodies, often called bNAbs, can recognise and neutralise many forms of HIV-like viruses. They may also help direct immune responses towards infected cells. Leronlimab blocks CCR5, a receptor on immune cells that many strains of HIV use to gain entry. Blocking CCR5 may limit the virus’s ability to infect fresh target cells.
The strategy was designed to attack infection at several points at once: restricting viral replication, neutralising virus outside cells and reducing the opportunity for further cellular infection.
Researchers studied 55 male and female infant rhesus macaques. At around one month old, the animals were exposed to SHIV. The team then compared seven treatment strategies, including single therapies, two-part combinations and the full three-part regimen.
The most striking findings came from eight macaques that received all three treatments starting 72 hours after exposure. The virus was already detectable in the animals’ blood when treatment began. This is significant because it shows that the intervention was not purely preventative. Infection had already started.
These macaques received one dose of two broadly neutralising antibodies, nine weekly doses of leronlimab and daily ART for 27 weeks. At the end of this period, ART was stopped. Researchers then monitored the animals closely for signs that SHIV had returned.
None of the eight macaques experienced viral rebound.
The team carried out further tests to assess whether the virus had truly been eliminated or was merely being controlled by the immune system. They depleted the macaques’ CD8 T cells, immune cells that are important in controlling viral infections. If hidden SHIV had remained, weakening this immune response might have allowed it to reappear.
No rebound was detected.
More than six months after treatment ended, researchers found no viral DNA in blood samples. At 84 weeks after SHIV exposure, they also found no detectable virus in tissue samples. In contrast, the virus returned in animals that received individual treatments or two-part regimens, including ART alone and ART combined with broadly neutralising antibodies.
The comparison suggests that the full combination was necessary to achieve the strongest effect. ART lowered viral replication. Antibodies may have neutralised circulating virus and improved clearance of infected cells. CCR5 blockade may have prevented the virus from entering new immune cells. Together, the treatments may have reduced the chance for SHIV to establish long-lasting reservoirs.
The findings are especially notable because they come from a non-human primate study. Rhesus macaques remain one of the most valuable models for HIV research. Their immune systems are not identical to those of people, yet studies in primates have helped shape understanding of HIV transmission, immune responses and antiretroviral treatment.
Still, the results must be interpreted carefully. Success in infant macaques does not guarantee success in newborns. SHIV is not HIV, even though it is designed to resemble it. Human HIV is genetically diverse, and a treatment effective against a research virus may not work in the same way against every circulating strain.
Timing may be one of the greatest challenges. Treatment began within three days of exposure. In clinical practice, it may be difficult to know exactly when an infant acquired HIV. Infection can occur during pregnancy, labour, delivery or breastfeeding. Some babies may be identified as high risk immediately. Others may not receive a diagnosis until weeks or months later, when a larger reservoir may already have formed.
The treatment package also raises practical and safety questions. ART is already used in infants, with age-appropriate dosing and close medical supervision. Broadly neutralising antibodies and leronlimab have not been established as a standard combination for newborns. Human research would need to establish safe doses, treatment schedules, possible drug interactions and long-term effects.
Access would matter as well. A regimen involving specialised antibodies, frequent monitoring and rapid testing may be difficult to deliver in settings with limited health-care resources. This is particularly important because the greatest global burden of paediatric HIV is found in countries where access to advanced medicines and laboratory testing can be uneven.
If the approach eventually reaches human trials, it may first be considered for newborns with a known high risk of acquiring HIV. These could include babies born to people living with HIV who did not receive effective ART during pregnancy or who had unsuppressed viral levels near delivery. In such situations, clinicians may be able to begin intensified treatment immediately while diagnostic testing is under way.
Several questions need answers before any clinical use. Researchers must determine whether the treatment remains effective if started later than 72 hours after exposure. They must establish how long therapy would need to continue. They also need to confirm that no virus remains in difficult-to-sample tissues, such as the gut, lymph nodes and brain.
The study adds to a wider body of research suggesting that very early HIV treatment can sometimes limit reservoir formation. Rare cases of prolonged HIV remission have been reported in children who began ART shortly after birth. Such outcomes have not been reliable or common. Most people with HIV experience viral rebound when ART is interrupted, even after years of successful treatment.
The new research offers a more specific explanation for why early treatment may need support from other approaches. ART controls replication, yet it may not be enough to prevent every infected cell from becoming a reservoir. Combining ART with antibodies and a drug that blocks viral entry could provide a stronger early barrier.
This reflects an established principle in HIV medicine: combination treatment works better than relying on one mechanism. Standard ART already uses several medicines because the virus can adapt rapidly. The new approach applies combination therapy to a different goal, not simply long-term suppression, but preventing persistent infection from becoming established.
A safe method to clear HIV after exposure would be a major advance. Lifelong ART is highly effective, though it requires continuous access to medicine, regular health care and sustained adherence. For children and families, eliminating the need for lifelong treatment would have enormous medical and social value.
That possibility remains experimental. The evidence comes from eight treated macaques, not human clinical trials. Researchers will need carefully designed studies to test safety and effectiveness in newborns. Participants would require frequent, sensitive testing and long-term follow-up after treatment is stopped.
For now, immediate HIV testing and prompt ART remain essential for babies with confirmed infection or substantial exposure risk. ART can protect immune health, prevent AIDS and greatly improve long-term outcomes.
The findings provide cautious optimism. In infant monkeys, treatment with ART, broadly neutralising antibodies and CCR5 blockade prevented SHIV from returning after therapy ended, even after scientists reduced an important part of the immune response.
It is not a cure for HIV in people. It is, however, a meaningful step towards understanding whether a narrow window soon after infection could one day be used to prevent HIV from becoming lifelong.
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