Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology · 2007
Control of HIV-1 RNA load after HAART interruption: relationship with CCR5 co-receptor density and proviral DNA load in HIV-infected patients.
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Soriano-Sarabia Natalia, Vallejo Alejandro, Fernández Gerónimo, Genebat Miguel, Gutiérrez Sonia, Muñoz-Fernández Maria Angeles, Leal Manuel
Аннотация
BACKGROUND: CCR5 co-receptor density has been reported to play a role in the level of HIV production. In addition, reports about the relationship between proviral DNA load and plasma HIV load are controversial.
OBJECTIVES: To analyse the role of CCR5 co-receptor density and proviral DNA load in the control of plasma HIV-viral load after HAART interruption, comparing patients whose plasma HIV load was persistently below 4log(10) RNA copies/mL, defined as "HIV controllers", with patients who showed a viral load higher than 4log(10) RNA copies/mL, defined as "non-controllers".
STUDY DESIGN: Proviral DNA load quantification (N=55) and CCR5 co-receptor density (N=29) were determined in HIV-infected patients on prolonged HAART interruption.
RESULTS: Twenty-three percent of our HAART interruption cohort were classified as HIV controllers, while 77% were classified as non-controllers. CCR5 co-receptor density was statistically higher in HIV controllers than in non-controllers, while proviral DNA load was not different between them. CCR5 co-receptor density in activated CD4 cells was independently associated with HIV plasma load after interruption.
CONCLUSIONS: The observation of a higher CCR5 co-receptor expression in HIV controllers suggests that HIV infection leads to the selection of CD4 cells with low CCR5 co-receptor density after HAART interruption.
OBJECTIVES: To analyse the role of CCR5 co-receptor density and proviral DNA load in the control of plasma HIV-viral load after HAART interruption, comparing patients whose plasma HIV load was persistently below 4log(10) RNA copies/mL, defined as "HIV controllers", with patients who showed a viral load higher than 4log(10) RNA copies/mL, defined as "non-controllers".
STUDY DESIGN: Proviral DNA load quantification (N=55) and CCR5 co-receptor density (N=29) were determined in HIV-infected patients on prolonged HAART interruption.
RESULTS: Twenty-three percent of our HAART interruption cohort were classified as HIV controllers, while 77% were classified as non-controllers. CCR5 co-receptor density was statistically higher in HIV controllers than in non-controllers, while proviral DNA load was not different between them. CCR5 co-receptor density in activated CD4 cells was independently associated with HIV plasma load after interruption.
CONCLUSIONS: The observation of a higher CCR5 co-receptor expression in HIV controllers suggests that HIV infection leads to the selection of CD4 cells with low CCR5 co-receptor density after HAART interruption.