Medicine:HIV remission

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Short description: HIV functional cure without medication

HIV remission is a clinical state in which an individual diagnosed with human immunodeficiency virus (HIV) maintains plasma viral loads below the limit of detection without the ongoing administration of antiretroviral therapy (ART).[1] In the context of HIV/AIDS research, remission is frequently distinguished from a "sterilizing cure," which requires the total elimination of the virus from all anatomical compartments.[2] Instead, remission is often characterized as a "functional cure",[3] wherein the host immune system or external interventions suppress viral replication and prevent disease progression in the absence of medication.[4]

The primary barrier to achieving durable remission is the latent HIV reservoir. During the early stages of infection, the virus establishes a persistent pool of integrated proviral DNA within long-lived resting CD4+ T cells and other cellular reservoirs.[5] While ART effectively arrests active replication, it has no impact on these dormant cells. Consequently, the cessation of treatment typically results in a viral rebound (the rapid re-emergence of detectable viremia) as the latent virus reactivates.[6]

Mechanisms and clinical pathways

Historically, instances of sustained HIV remission have emerged through three distinct pathways involving genetic resistance, intensive clinical intervention, or exceptional host immune responses.

1. Hematopoietic stem cell transplantation

The most robust examples of HIV remission have occurred in patients undergoing allogeneic hematopoietic stem cell transplantation (HSCT) to treat underlying hematologic malignancies. This pathway relies on two primary biological mechanisms:

  • CCR5-Δ32 Mutation: Documentation of the "Berlin", "London (Adam Castillejo)", and "Düsseldorf" patients centers on the use of donors homozygous for the CCR5-Δ32 allele. This genetic mutation results in the phenotypic absence of the CCR5 co-receptor on the surface of CD4+ T cells, rendering the host's new immune system largely resistant to infection by R5-tropic HIV strains.[7]
  • Graft-versus-host effect: Evidence suggests that the replacement of the recipient's original immune system by donor-derived cells facilitates the depletion of the pre-existing viral reservoir through immunologic clearance.[8]

2. Post-treatment control

Post-treatment controllers (PTCs) are individuals who initiate antiretroviral therapy (ART) during the acute phase of infection and subsequently maintain undetectable viral loads following a supervised analytical treatment interruption (ATI). Unlike patients who delay treatment, early-intervention individuals may preserve critical immune functions and limit the initial seeding and diversity of the latent reservoir. This reduction in the viral pool allows for secondary control mechanisms to stabilize viremia levels without ongoing medication.[9]

3. Natural viral suppression

A small fraction of the HIV-positive population, estimated at less than 1%, exhibits the ability to control viral replication naturally. These individuals are categorized based on their clinical presentation:

  • Elite Controllers: This group maintains undetectable viral loads for decades in the absence of ART. The phenotype is strongly associated with specific human leukocyte antigen (HLA) class I alleles, most notably HLA-B27 and HLA-B57.[10] These alleles facilitate a highly efficient cytotoxic T lymphocyte (CTL) response capable of targeting conserved regions of the viral proteome, effectively suppressing replication through superior antigen presentation.[11]

See also

  • Management of HIV/AIDS
  • Undetectable = Untransmittable
  • Timeline of HIV/AIDS

References

  1. ↑ Etemad, Behzad; Esmaeilzadeh, Elmira; Li, Jonathan Z. (2019). "Learning From the Exceptions: HIV Remission in Post-treatment Controllers". Frontiers in Immunology 10. doi:10.3389/fimmu.2019.01749. PMID 31396237. 
  2. ↑ Turk, Gabriela; Seiger, Kyra; Lian, Xiaodong; Sun, Weiwei; Parsons, Elizabeth M.; Gao, Ce; Rassadkina, Yelizaveta; Polo, Maria Laura et al. (1 January 2022). "A Possible Sterilizing Cure of HIV-1 Infection Without Stem Cell Transplantation". Annals of Internal Medicine 175 (1): 95–100. doi:10.7326/L21-0297. ISSN 0003-4819. PMID 34781719. PMC 9215120. https://pure.johnshopkins.edu/en/publications/a-possible-sterilizing-cure-of-hiv-1-infection-without-stem-cell-/. Retrieved 15 April 2026. 
  3. ↑ Cohen, Jon (1 December 2025). "How some treatments can lead to a 'functional cure' for HIV". https://www.science.org/content/article/how-some-treatments-can-lead-functional-cure-hiv. 
  4. ↑ Highleyman, Liz (25 February 2026). "Dual immune modulators delay, but don't prevent, HIV rebound after stopping antiretrovirals" (in en). aidsmap.com. Aidsmap. https://www.aidsmap.com/news/feb-2026/dual-immune-modulators-delay-dont-prevent-hiv-rebound-after-stopping-antiretrovirals. 
  5. ↑ Cohn, Lillian B.; Chomont, Nicolas; Deeks, Steven G. (April 2020). "The Biology of the HIV-1 Latent Reservoir and Implications for Cure Strategies". Cell Host & Microbe 27 (4): 519–530. doi:10.1016/j.chom.2020.03.014. PMID 32272077. 
  6. ↑ Cevaal, Paula M.; Kan, Stanislav; Fisher, Bridget M.; Moso, Michael A.; Tan, Abigail; Liu, Haiyin; Ali, Abdalla; Tanaka, Kiho et al. (29 May 2025). "Efficient mRNA delivery to resting T cells to reverse HIV latency". Nature Communications 16 (1): 4979. doi:10.1038/s41467-025-60001-2. ISSN 2041-1723. PMID 40442114. Bibcode: 2025NatCo..16.4979C. 
  7. ↑ Gometz, Emma (13 April 2026). "Person functionally cured of HIV after bone marrow transplant from sibling". Scientific American. https://www.scientificamerican.com/article/person-functionally-cured-of-hiv-after-bone-marrow-transplant-from-sibling/. 
  8. ↑ Nield, David (13 April 2026). "Sibling Stem Cell Transplant Leads to Rare HIV Remission in 'Oslo Patient'". ScienceAlert. https://www.sciencealert.com/sibling-stem-cell-transplant-leads-to-rare-hiv-remission-in-oslo-patient. 
  9. ↑ Webb, Nicholas E.; Gorman, Matthew J.; Parker, Lily J.; Jung, Wonyeong; Yuan, Dansu; Li, Jonathan Z.; Alter, Galit; Julg, Boris (23 December 2025). "The functional antibody landscape in HIV post-treatment controllers is heterogeneous". Journal of Virology 99 (12). doi:10.1128/jvi.01790-25. PMID 41313002. 
  10. ↑ Descours, Benjamin; Avettand-Fenoel, Veronique; Blanc, Catherine; Samri, Assia; Mélard, Adeline; Supervie, Virginie; Theodorou, Ioannis; Carcelain, Guislaine et al. (15 May 2012). "Immune Responses Driven by Protective Human Leukocyte Antigen Alleles From Long-term Nonprogressors Are Associated With Low HIV Reservoir in Central Memory CD4 T Cells" (in en). Clinical Infectious Diseases 54 (10): 1495–1503. doi:10.1093/cid/cis188. ISSN 1058-4838. PMID 22441653. https://academic.oup.com/cid/article-abstract/54/10/1495/350560. Retrieved 15 April 2026. 
  11. ↑ "Understanding resistance in HIV controller patients: how their antiviral CD4+ T cells are protected from infection" (in en-gb). 16 April 2024. https://www.pasteur.fr/en/research-journal/news/understanding-resistance-hiv-controller-patients-how-their-antiviral-cd4-t-cells-are-protected. 



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