OBJECTIVE: To quantify HIV-RNA in plasma, in lymphoid tissue and proviral DNA in peripheral blood mononuclear cells and to relate these to immunological markers among patients with plasma viral load counts of </= 200 HIV-RNA copies/mL. METHODS: A prospective study of one hundred and three patients was undertaken with an inclusion criteria of plasma viral load of </= 200 copies/mL. The patients had advanced HIV infection; 25% had developed AIDS. Patients were seen every 6 months for a period of 2 years. RESULTS: The median plasma viral load was < 20 copies/mL with no increase during follow-up. Thirty-one per cent had plasma viral load of </= 20 copies/mL at all visits, 44% had >/= 1 measurement with 21-200 and 25% had >/= 1 sample with plasma HIV-RNA > 200 copies/mL. Lymphoid tissue viral load was low at enrolment and declined further during follow-up. Baseline HIV-DNA and immunoglobulin (IgA) differed significantly between the plasma viral load rebound groups (P < 0.05). CONCLUSION: In this cohort, selected solely on the basis of having a plasma viral load of </= 200 copies/mL, we found stable or declining viral loads in the measured compartments during 2 years of follow-up. Baseline HIV-DNA and IgA levels were higher among patients with less complete virological suppression relative to patients with persistently undetectable plasma HIV-RNA. Hence, a high cellular level of HIV-DNA and high plasma IgA may predict subsequent development of low-grade viraemia.
OBJECTIVE: To quantify HIV-RNA in plasma, in lymphoid tissue and proviral DNA in peripheral blood mononuclear cells and to relate these to immunological markers among patients with plasma viral load counts of </= 200 HIV-RNA copies/mL. METHODS: A prospective study of one hundred and three patients was undertaken with an inclusion criteria of plasma viral load of </= 200 copies/mL. The patients had advanced HIV infection; 25% had developed AIDS. Patients were seen every 6 months for a period of 2 years. RESULTS: The median plasma viral load was < 20 copies/mL with no increase during follow-up. Thirty-one per cent had plasma viral load of </= 20 copies/mL at all visits, 44% had >/= 1 measurement with 21-200 and 25% had >/= 1 sample with plasma HIV-RNA > 200 copies/mL. Lymphoid tissue viral load was low at enrolment and declined further during follow-up. Baseline HIV-DNA and immunoglobulin (IgA) differed significantly between the plasma viral load rebound groups (P < 0.05). CONCLUSION: In this cohort, selected solely on the basis of having a plasma viral load of </= 200 copies/mL, we found stable or declining viral loads in the measured compartments during 2 years of follow-up. Baseline HIV-DNA and IgA levels were higher among patients with less complete virological suppression relative to patients with persistently undetectable plasma HIV-RNA. Hence, a high cellular level of HIV-DNA and high plasma IgA may predict subsequent development of low-grade viraemia.
Authors: S Resino; I Galán; A Pérez; J A León; E Seoane; D Gurbindo; M Angeles Muñoz-Fernandez Journal: Clin Exp Immunol Date: 2004-09 Impact factor: 4.330
Authors: Emmanouil Papasavvas; Jay R Kostman; Brian Thiel; Maxwell Pistilli; Agnieszka Mackiewicz; Andrea Foulkes; Robert Gross; Kimberly A Jordan; Douglas F Nixon; Robert Grant; Jean-Francois Poulin; Joseph M McCune; Karam Mounzer; Luis J Montaner Journal: J Clin Immunol Date: 2006-01 Impact factor: 8.542