Cerebrospinal-fluid HIV-1 RNA and drug concentrations after treatment with lamivudine plus zidovudine or stavudine

Foudraine, Norbert A.; Hoetelmans, Richard M. W.; Lange, Joep M. A.; Wolf, Frank de; Benthem, Birgit Hb van; Maas, Jolanda; Keet, I. P. M.; Portegies, Peter

doi:10.1016/s0140-6736(98)07333-4

Cited by 156 publications

(76 citation statements)

References 30 publications

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“…Studies disagree on the correlation between CSF and plasma viral load (BREW et al 1997, ELLIS et al 1997, CINQUE et al 1998, MARTIN et al 1998, FOUDRAINE et al 1998, McARTHUR et al 1997, BOSSI et al 1998, ROBERTSON et al 1998. However, as seen in the present study, this may depend on the characteristics of the study population such as stage of HIV disease, presence of neurological disease, use and type of ARV therapy, CSF parameters and, possibly, other factors not investigated.…”

Section: Christo Et Al 2007 Cecchini Et Al 2009)contrasting

confidence: 51%

“…Some investigators found no correlation between CSF and plasma viral load (BREW et al 1997, ELLIS et al 1997, CINQUE et al 1998, MARTIN et al 1998, FOUDRAINE et al 1998, SCHRAGER et al 1998, ANTINORI et al 2002, while others did (McARTHUR et al 1997, BOSSI et al 1998, ROBERTSON et al 1998, GARCIA et al 1999. The lack of a correlation between the two compartments suggests that the presence of HIV-1 RNA may not simply be due to passive passage of the virus from blood to CSF but rather to intrathecal replication (CINQUE et al 1998, SMITH et al 2009).…”

Section: Introductionmentioning

confidence: 99%

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Analysis of correlation between cerebrospinal fluid and plasma HIV-1 RNA levels in patients with neurological opportunistic diseases

Christo

Greco

Aleixo

et al. 2011

Rev. Inst. Med. trop. S. Paulo

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SUMMARYThe question of whether HIV-1 RNA in cerebrospinal fluid (CSF) is derived from viral replication in the central nervous system or simply reflects the transit of infected lymphocytes from the blood compartment has long been a matter of debate. Some studies found no correlation between CSF and plasma viral load, whereas others did. The lack of a correlation between the two compartments suggests that the presence of HIV-1 RNA is not simply due to the passive passage of the virus from blood to CSF but rather due to intrathecal replication. To evaluate the correlation between plasma and CSF HIV-1 RNA levels and to identify situations in which there is no correlation between the two compartments, seventy patients were prospectively studied. The association between CSF and plasma viral load was evaluated in the total population and in subgroups of patients with similar characteristics. A correlation between the CSF and plasma compartments was observed for patients undergoing highly active antiretroviral therapy (HAART), those with a CD4 T lymphocyte count lower than 200 cells/mm 3 , and those with increased CSF protein content. On the other hand, no correlation was observed for patients without adequate virological control, who had a CD4 count higher than 200 cells/mm 3 and who did not use HAART. The correlation between the two compartments observed in some patients suggests that CSF HIV-1 RNA levels may reflect plasma levels in these subjects. In contrast, the lack of a correlation between the two compartments in patients who were not on HAART and who had normal CSF proteins and a poor virological control possibly indicates compartmentalization of the virus in CSF and, consequently, plasma-independent intrathecal viral replication.

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Section: Christo Et Al 2007 Cecchini Et Al 2009)contrasting

confidence: 51%

Section: Introductionmentioning

confidence: 99%

Analysis of correlation between cerebrospinal fluid and plasma HIV-1 RNA levels in patients with neurological opportunistic diseases

Christo

Greco

Aleixo

et al. 2011

Rev. Inst. Med. trop. S. Paulo

View full text Add to dashboard Cite

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“…Alternatively, the stability of 184M-labeled cells might have resulted from residual replication of wild-type virus regardless of treatment regimen. However, this seems unlikely because lamivudine penetrates well into putative anatomic sanctuaries (53,54) and the fitness difference between 184M and 184V virus in the presence of lamivudine is large (25). Division of latently infected memory cells without viral production, rather than residual replication, could also result in a net gain of some HIV infected cells (42), but this would not explain the regimen dependence of decay rates.…”

Section: Resultsmentioning

confidence: 99%

Heterogeneous clearance rates of long-lived lymphocytes infected with HIV: Intrinsic stability predicts lifelong persistence

Strain

Günthard

Havlir

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

227

200

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Viral replication and latently infected cellular reservoirs persist in HIV-infected patients achieving undetectable plasma virus levels with potent antiretroviral therapy. We exploited a predictable drug resistance mutation in the HIV reverse transcriptase to label and track cells infected during defined intervals of treatment and to identify cells replenished by ongoing replication. Decay rates of subsets of latently HIV-infected cells paradoxically decreased with time since establishment, reflecting heterogeneous lymphocyte activation and clearance. Residual low-level replication can replenish cellular reservoirs; however, it does not account for prolonged clearance rates in patients without detectable viremia. In patients receiving potent antiretroviral therapy, the latent pool has a heterogeneous and dynamic composition that comprises a progressively increasing proportion of stable lymphocytes. Eradication will not be achieved with complete inhibition of viral replication alone.

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“…In addition, several studies have conclusively shown that HAART can suppress cerebral spinal fluid (CSF) levels of HIV ribonucleic acid (RNA) (Foudraine et al, 1998) and this decline appeared to correlate with the successful reversal of neurological deficit (Ellis et al, 2000;Marra, 1999). However, despite the progress associated with HAART, HIVassociated neurological disease continues to be the major cause of morbidity and mortality in HIV patients, suggesting that HAART does not provide complete protection against neurological damage in HIV/AIDS (Dougherty et al, 2002;Kolson, 2002;Sacktor et al, 2001a).…”

Section: Introductionmentioning

confidence: 99%

HIV-TAT Protein Upregulates Expression of Multidrug Resistance Protein 1 in the Blood–Brain Barrier

Hayashi

Peng

András

et al. 2005

J Cereb Blood Flow Metab

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Central nervous system (CNS) complications of human immunodeficiency virus (HIV) infection remain a serious health risk in HIV/acquired immunodeficiency syndrome despite significant advances in highly active antiretroviral therapy (HAART). Specific drugs used for HAART are substrates for the efflux transport systems, such as the multidrug resistance-associated proteins (MRPs), which are present on brain microvascular endothelial cells (BMEC) and astrocytes, that is, the main cell types that form the blood-brain barrier (BBB). Thus, drugs employed in HAART are actively removed from the CNS and do not efficiently inhibit HIV replication in the brain. To study the potential mechanisms of this process, the aim of the present research was to address the hypothesis that HIV Tat protein can contribute to upregulation of MRP expression at the BBB level. Tat is a protein produced and released by HIV-infected cells, which may play an important role in brain vascular pathology in the course of HIV infection. Among the family of MRPs, exposure to Tat specifically induced MRP1 messenger ribonucleic acid and protein expression both in BMEC and astrocytes. These alterations were accompanied by enhanced MRP1-mediated efflux functions. Furthermore, activation of the mitogen-activated protein kinase signaling cascade was identified as the mechanism involved in Tat-mediated overexpression of MRP1. These results indicate that Tat exposure can lead to alterations of the BBB functions and decrease HAART efficacy in the CNS through overexpression of drug efflux transporters.

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Cerebrospinal-fluid HIV-1 RNA and drug concentrations after treatment with lamivudine plus zidovudine or stavudine

Cited by 156 publications

References 30 publications

Analysis of correlation between cerebrospinal fluid and plasma HIV-1 RNA levels in patients with neurological opportunistic diseases

Analysis of correlation between cerebrospinal fluid and plasma HIV-1 RNA levels in patients with neurological opportunistic diseases

Heterogeneous clearance rates of long-lived lymphocytes infected with HIV: Intrinsic stability predicts lifelong persistence

HIV-TAT Protein Upregulates Expression of Multidrug Resistance Protein 1 in the Blood–Brain Barrier

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