The effects of aging pose an additional challenge for people with HIV due to the neurological and psychological consequences that persist despite antiretroviral therapy. At the Conference on Retroviruses and Opportunistic Infections (CROI) held Feb. 22-25, 2026, in Denver, the scientific community examined how the virus affects the brain, how the reservoir is established in the CNS, and which genetic, immunological or treatment-related factors influence cognitive health.

Antiretroviral therapies against HIV have been in use for more than 30 years and have enabled people living with HIV to maintain undetectable viral levels. Many of them are aging in good health. However, others present symptoms of cognitive decline. HIV can reach the brain and establish a reservoir there. Yet, it is still unknown what this reservoir is like, which cells are affected, and which comorbidities are typical of aging or are associated with the virus.

SLAMF6 is an immune cell receptor whose function was not clear. Does it activate or inhibit cells? The results so far have been contradictory. Now, scientists at the Institut de Recherches Cliniques de Montréal have unveiled evidence that SLAMF6, a protein of the SLAM family that binds to copies of itself, is regulated by interactions between molecules of the same receptor within the same cell.

Parkinson’s disease is a neurodegenerative disorder that affects movement, and tremor is one of its signatures. But it is a much more wide-ranging disorder, and patients experience problems with cognitive and emotional processes as well. SCAN, the somato-cognitive action network identified in 2023, could reshape the definition of PD. Treating this circuit can improve outcomes.

The variety of organoids that can be developed in vitro is enabling major advances. Depending on the type of tissues and the research goals, these small 3D cell-based structures that mimic real tissue offer certain advantages over animal models. Scientists at the University of Padova in Italy have created human neuromuscular organoids to reproduce cancer-induced muscle cachexia, a condition that murine models do not accurately replicate.

A circuit formed by tumor, immune and nervous systems triggers cancer cachexia and anorexia, the excessive loss of weight, muscle and fat experienced in some cancer types. A new study is the first showing these three actors of a triangle interaction that initiates and feeds the process.

The malfunction of lymphatic drainage that occurs in lymphedema leads to excessive cholesterol accumulation in the affected skin and lymphatic vessels, causing inflammation and fibrosis. However, surgery and the chemical reduction of accumulated cholesterol with cyclodextrin reduce inflammation and regenerate lymphatic vessels. Cholesterol is a potential therapeutic target for treating lymphedema, according to this study published on Feb. 11, 2026, in Nature by Veronique Angeli and her colleagues.

Hepatocellular carcinoma (HCC) is the most common form of primary liver cancer, representing approximately 75-85% of all cases. Often considered preventable, primary liver cancer ranks as the sixth most frequently diagnosed cancer and the third leading cause of cancer deaths worldwide. Through a multi-institutional effort, researchers have identified activated ATF6α as a driver of HCC that suppresses immune defenses, predicts response to immune checkpoint therapy, and represents a potential target for intervention.

The neural and neuroimmune mechanisms behind myocardial infarction-triggered cardiac events, immune responses and activation of the nervous system remain largely unexplored. The heart and the brain talk to each other in what is known as cardioception. This communication between the two organs is orchestrated through neurons of the vagus nerve or the dorsal root ganglia, among others. Researchers from the University of California, San Diego have now shown that the dynamics of these interactions may play a crucial role in modulating inflammation, repair and cardiac functioning.

Liver fibrosis in the course of metabolic dysfunction-associated steatohepatitis could be significantly reduced using CAR T-cells generated in vivo. Scientists at the Icahn School of Medicine at Mount Sinai have developed an experimental cell therapy that eliminates only one type of liver cell, the stellate cells that express fibroblast activation protein alpha. This strategy not only reduced fibrosis but also reversed liver damage.