Abstract
BackgroundBy persisting in infected cells for a long period of time, proviral HIV-1 DNA can represent an alternative viral marker to RNA viral load during the follow-up of HIV-1 infected individuals. In the present study sequential blood samples of 10 patients under antiretroviral treatment from 1997 with two NRTIs, who refused to continue any antiviral regimen, were analyzed for 16 – 24 weeks to study the possible relationship between DNA and RNA viral load.MethodsThe amount of proviral DNA was quantified by SYBR green real-time PCR in peripheral blood mononuclear cells from a selected group of ten patients with different levels of plasmatic viremia (RNA viral load).ResultsVariable levels of proviral DNA were found without any significant correlation between proviral load and plasma HIV-1 RNA levels. Results obtained showed an increase or a rebound in viral DNA in most patients, suggesting that the absence of therapy reflects an increase and/or a persistence of cells containing viral DNA.ConclusionEven though plasma HIV RNA levels remain the basic parameter to monitor the intensity of viral replication, the results obtained seem to indicate that DNA levels could represent an adjunct prognostic marker in monitoring HIV-1 infected subjects.
Highlights
By persisting in infected cells for a long period of time, proviral HIV-1 DNA can represent an alternative viral marker to RNA viral load during the follow-up of HIV-1 infected individuals
Therapy interruption determined a significant increase in RNA viral load in all HIV-1 seropositive patients enrolled in the study
We quantified proviral DNA load in peripheral blood mononuclear cells (PBMC) isolated from patients' whole blood sequential samples at fixed times after therapy suspension
Summary
By persisting in infected cells for a long period of time, proviral HIV-1 DNA can represent an alternative viral marker to RNA viral load during the follow-up of HIV-1 infected individuals. Many papers have clearly demonstrated that HIV-1 RNA plasma viral load quantitative determination is a pivotal parameter to monitor viral replication and the effectiveness of HAART therapy [1,2,3,4,5]. Quantitative analysis of proviral DNA in HAART-treated patients showed opposite results: on one hand, the decline in DNA load seemed to indicate the long term impact and effectiveness of retroviral treatment [9,10,11,12], on the other DNA levels remained stable over several years in PI ART naïve patients [2,13].
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