Studying how platelets relate to the HIV reservoir and poor immune recovery
Examines blood samples from adults with HIV to study platelets and the virus.
Plain-language title generated from the registry record
Registry title: Platelets Target the Circulating HIV Reservoir: Implications for Immunological Failure
Key facts
- Where
- Tourcoing, FranceSee the site
AI summary: who the study is looking for
From the trial's eligibility criteria. Machine-read from the registry text on this page, so it can be wrong. The registry text below and the trial team decide who can take part.
The trial is looking for adults living with HIV whose viral load has been undetectable for more than 2 years. Participants give blood samples.
- Age
- 18 years or older
- Sex
- All sexes can join.
- Disease stage
- HIV with an undetectable viral load for more than 2 years. People with CD4+ T cell counts above or below 500 cells/µL are included in separate groups.
- Biomarker or test result
- Undetectable HIV viral load for more than 2 years.
Main reasons for not taking part
- Cannot give free and informed consent
- Pregnant or breastfeeding women
- People under guardianship, curatorship, or a protection mandate
Read by machine on 12 November 2026.
Where in France
- Centre Hospitalier de TourcoingTourcoing, FranceContact: Jean-Jacques Vitagliano, PhDTaking people
Questions to ask the study team
- How often do I need to come in, and for how long each time?
- Are travel costs paid?
- Can I keep my own doctor?
- What happens if I want to stop?
Contact the study team: see the registry record → Contacts and Locations
Print a page for my doctorTrial details
- Who runs it
- Tourcoing Hospital
- Trial code
- NCT07745530
- Record updated
- 17 September 2026
- Original description
HIV/AIDS is a chronic disease that is difficult to eradicate because the virus persists as proviral DNA integrated into the host cells. Despite antiretroviral therapy, proviral DNA persists in lymphoid and myeloid reservoirs, whether circulating (memory CD4+ T cells) or tissue-based (macrophages). HIV reservoirs are highly heterogeneous, making it difficult to identify a specific biomarker or cell profile for a given reservoir. A distinctive feature of HIV reservoirs may be the selective interaction between reservoir cells and platelets. The presence of HIV in platelets could impact disease progression, particularly by triggering the reversal of HIV latency and leading to residual viral production. The frequency of platelets containing circulating virus in the blood is approximately 0.1% of the total platelet volume. Although seemingly negligible, this would represent a daily input of 10⁸ platelets harboring the virus. Furthermore, patients whose platelets contain HIV are primarily those with persistent immunological failure, known as "immunological non-responders" (InR).Read full original descriptionShow less
PLAQUAGE - Platelets Target the Circulating HIV Reservoir: Implications for Immunological Failure
HIV/AIDS is a chronic disease that is difficult to eradicate because the virus persists as proviral DNA integrated into the host cells. Despite antiretroviral therapy, proviral DNA persists in lymphoid and myeloid reservoirs, whether circulating (memory CD4+ T cells) or tissue-based (macrophages). HIV reservoirs are highly heterogeneous, making it difficult to identify a specific biomarker or cell profile for a given reservoir. A distinctive feature of HIV reservoirs may be the selective interaction between reservoir cells and platelets. The presence of HIV in platelets could impact disease progression, particularly by triggering the reversal of HIV latency and leading to residual viral production. The frequency of platelets containing circulating virus in the blood is approximately 0.1% of the total platelet volume. Although seemingly negligible, this would represent a daily input of 10⁸ platelets harboring the virus. Furthermore, patients whose platelets contain HIV are primarily those with persistent immunological failure, known as "immunological non-responders" (InR).
The regulation of the size (number and frequency) of the HIV reservoir by platelets is not known. However, HIV-containing platelets form more conjugates with CD4+ T cells than HIV-free platelets. While HIV-containing platelets do not productively infect cells, they induce metabolic dysfunction in CD4+ T cells (aerobic glycolysis). Increased aerobic glycolysis is a hallmark of T cell activation and senescence.
This suggests an interconnection between the presence of the virus in platelets, the size of the reservoir, and immune dysfunction in HIV.
Inclusion: Adult patients living with HIV with an undetectable viral load for more than 2 years; Beneficiary of a social security scheme or rightful claimant; Patients able to read and understand the information sheet; Having signed the consent form.
Exclusion: being unable to give free and informed consent; pregnant or breastfeeding woman; being under guardianship, curatorship, or a protection mandate.