Journal of acquired immune deficiency syndromes (1999) · 2009
Early control of HIV-1 infection in long-term nonprogressors followed since diagnosis in the ANRS SEROCO/HEMOCO cohort.
СтатьяМногоцентровое исследованиеПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Madec Yoann, Boufassa Faroudy, Avettand-Fenoel Veronique, Hendou Samia, Melard Adeline, Boucherit Soraya, Surzyn Janina, Meyer Laurence, Rouzioux Christine, ANRS SEROCO/HEMOCO Study Group
Аннотация
BACKGROUND: To clarify early correlates and natural history of HIV long-term nonprogressors (LTNPs) since HIV diagnosis.
METHODS: Patients enrolled in the French ANRS SEROCO/HEMOCO cohort with CD4 count >500 cells/mm3 at HIV diagnosis. LTNP status was defined as being asymptomatic, antiretroviral free, and with CD4 cell count >500 cells/mm3 for >8 years after HIV diagnosis. In LTNPs, we modeled the biological markers' progression through a joint model. Factors associated with loss of LTNP status were identified through a Cox model.
RESULTS: Sixty (9%) of 664 patients were identified as LTNPs during follow-up. At enrollment, HIV RNA was <or=2.6 log copies/mL in 24% of LTNPs and HIV DNA was <or=1.85 log copies/10 peripheral blood mononuclear cells (PBMCs) in 31% vs. 3% and 8% in others. In LTNPs, HIV RNA and HIV DNA levels increased by 0.04 log copies/mL per year and 0.07 log copies/10(6) PBMCs per year during the first 8 years after diagnosis. LTNP status was lost in 36 subjects; baseline HIV DNA >1.85 log copies/10(6) PBMCs and high HIV DNA increase were associated with an increased risk of losing LTNP status [adjusted hazard ratio: 2.8 (1.2-6.8) and 2.2 (1.0-4.8), respectively].
CONCLUSIONS: LTNP status is established in the first years of HIV infection, low HIV DNA level at enrollment and slow increase of HIV DNA being associated with maintained LTNP status.
METHODS: Patients enrolled in the French ANRS SEROCO/HEMOCO cohort with CD4 count >500 cells/mm3 at HIV diagnosis. LTNP status was defined as being asymptomatic, antiretroviral free, and with CD4 cell count >500 cells/mm3 for >8 years after HIV diagnosis. In LTNPs, we modeled the biological markers' progression through a joint model. Factors associated with loss of LTNP status were identified through a Cox model.
RESULTS: Sixty (9%) of 664 patients were identified as LTNPs during follow-up. At enrollment, HIV RNA was <or=2.6 log copies/mL in 24% of LTNPs and HIV DNA was <or=1.85 log copies/10 peripheral blood mononuclear cells (PBMCs) in 31% vs. 3% and 8% in others. In LTNPs, HIV RNA and HIV DNA levels increased by 0.04 log copies/mL per year and 0.07 log copies/10(6) PBMCs per year during the first 8 years after diagnosis. LTNP status was lost in 36 subjects; baseline HIV DNA >1.85 log copies/10(6) PBMCs and high HIV DNA increase were associated with an increased risk of losing LTNP status [adjusted hazard ratio: 2.8 (1.2-6.8) and 2.2 (1.0-4.8), respectively].
CONCLUSIONS: LTNP status is established in the first years of HIV infection, low HIV DNA level at enrollment and slow increase of HIV DNA being associated with maintained LTNP status.