What is it about?

We report a patient with multiple sclerosis who acquired HIV while receiving fingolimod, a drug used to treat this neurodegenerative disease. Viral levels at HIV diagnosis were lower than expected, and after three years of antiretroviral treatment, no replication‑competent viruses were detected. This situation is very different from patients with HIV treated only with ART in which reservoirs and competent viruses are detected. This suggest that fingolimod is tackling the viral reservoirs. Actually, we confimed that fingolimod was associated with enhanced antiviral activity, reduced expression of HIV receptors, and decreased cellular susceptibility to infection. Overall, our results suggest that drugs of the fingolimod family may limit HIV infection and reservoir formation.

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Why is it important?

We describe the first case of a person who acquired HIV during fingolimod treatment for multiple sclerosis. This case report provides the first human in vivo evidence that fingolimod potently restricts HIV infection and limits the seeding of the viral reservoir, reaching an undetectable intact HIV reservoir after three years on ART raising the possibility of a (functional cure). Our work also explored HIV expression by transcription quantifications, showing a surprisingly low expression and induciblitiy of HIV in the fingolimod-treated patient. This finding helps to resolve the translational gap between promising in vitro data and inconclusive studies on non-human primates, confirming the antiviral effects of this drug in a clinical setting.

Perspectives

Our results positions fingolimod, as a novel therapeutic approach to be explored in HIV cure strategies aimed at reducing or controlling the latent and transcriptionally active reservoir.

Elisa Moraga
AIDS and HIV Infection Group, Fundació de Recerca Clínic Barcelona- Institut d’Investigacions Biomèdiques August Pi i Sunyer (FRCB-IDIBAPS), Barcelona, Spain

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This page is a summary of: Fingolimod increases cellular resistance to HIV-1 infection and limits viral reservoir size in peripheral CD4+ T-cells, PLoS Pathogens, June 2026, PLOS,
DOI: 10.1371/journal.ppat.1014266.
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