Evaluation of proviral copy number and plasma RNA level as early indicators of progression in HIV-1 infection

Verhofstede, Chris; Reniers, S.; Wanzeele, Filip Van; Plum, Jean

doi:10.1097/00002030-199410000-00008

Cited by 76 publications

(32 citation statements)

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“…Viral RNA levels are 30-fold less in HIV-2 infection compared to HIV-1 infection (29). In contrast, the levels of HIV-2 proviral DNA reported here are similar to those found in studies of HIV-1 infection, in which median levels of HIV-1 proviral DNA ranged from 105 to 400 copies/ 10 6 PBMCs in individuals without AIDS (4,9,34). Levels of proviral DNA, as measured in this study, were not related to CD4 ϩ cell counts ( ϭ Ϫ0.03, P ϭ 0.90).…”

supporting

confidence: 79%

“…The pathogenesis of HIV-1 is closely related to plasma viral load; differences in viral load have been clearly associated with differences in rates of disease progression (23,24,26,32). Levels of proviral DNA in infected cells have also been related to disease, though this appears to be a weaker association than that for plasma RNA (8,9,34).…”

mentioning

confidence: 99%

“…Nearly half of the HIV-2-infected individuals have a nearly quiescent infection, and the paired levels of viral RNA and proviral DNA differ dramatically from those found in HIV-1 infection, where RNA-to-DNA ratios are only rarely less than 1.0 and are above 10.0 in the majority of individuals (4,27,34). It is not known if these represent infections that are truly latent at the molecular level; we have been able to detect viral RNA in some individuals with less than 100 copies/ml by a qualitative RT-PCR (S. Popper, unpublished data), suggesting that virus may be produced at very low levels and that the proviruses present in these individuals are not defective.…”

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confidence: 99%

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Low Plasma Human Immunodeficiency Virus Type 2 Viral Load Is Independent of Proviral Load: Low Virus Production In Vivo

Popper¹,

Sarr²,

Guèye-Ndiaye

et al. 2000

J Virol

128

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Levels of virus in the plasma are closely related to the pathogenicity of human immunodeficiency virus type 1 (HIV-1). HIV-2 is much less pathogenic than HIV-1, and infection with HIV-2 leads to significantly lower plasma viral load. To identify the source of this difference, we measured both viral RNA and proviral DNA in matched samples from 34 HIV-2-infected individuals. Nearly half had undetectable viral RNA loads (<100 copies/ml), but levels of proviral DNA were relatively high and confirmed that quantities of provirus in HIV-1 and HIV-2 infection were similar. Overall, HIV-2 proviral DNA load did not correlate with viral RNA load, and higher viral RNA load was associated with increased production of plasma virus from the proviral template. These results suggest that low viral load in HIV-2 infection is due to decreased rates of viral production, rather than differences in target cell infectivity.

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confidence: 79%

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confidence: 99%

mentioning

confidence: 99%

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Low Plasma Human Immunodeficiency Virus Type 2 Viral Load Is Independent of Proviral Load: Low Virus Production In Vivo

Popper¹,

Sarr²,

Guèye-Ndiaye

et al. 2000

J Virol

128

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“…However, those effects that are operative in vivo to impair CD4 ϩ T lymphocyte homeostasis are unclear. Whereas the magnitude of viral replication, as measured by plasma viral load, is predictive of the rate of disease progression, asymptomatic infection is reflected by low to undetectable levels of viral replication and CD4 ϩ T lymphocyte homeostasis (10,11). This non-progressive infection is the result of host genetic factors such as coreceptor polymorphisms (12), which may limit the permissiveness of the host to viral replication, as well as viral factors such as accessory gene defects, which may impact viral replication capacity (13)(14)(15).…”

mentioning

confidence: 99%

Evidence for a cytopathogenicity determinant in HIV-1 Vpr

Somasundaran

Sharkey

Břicháček

et al. 2002

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

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HIV-1 is cytopathic for CD4 ؉ T lymphocytes in vitro and this property of HIV-1 is generally considered to account for some of its in vivo cytopathogenicity. Thus, the extent of lymphocyte depletion correlates with the level of viremia whereas low levels of viral replication are typically associated with stable lymphocyte levels and asymptomatic infection such as is observed in non-progressors. Here, we describe a non-progressor who did not fit this general pattern in that CD4 ؉ T lymphocyte homeostasis was maintained in the face of high-level viral replication. Biological viral isolates from this patient replicated in primary lymphocytes without inducing cytopathicity. Because this phenotype is reminiscent of Vpr-deleted viruses, we examined the contribution of the Vpr gene to the viral phenotype. Vpr alleles derived from this patient contained both premature stop codons and an unusual Q3R polymorphism. Insertion of patientderived Vpr alleles or a Q3R substitution into a cytopathic HIV-1 clone resulted in a marked impairment of cytopathicity without affecting viral replication efficiency. The effect of Vpr on cytopathicity was unrelated to reported activities of Vpr including virion association, interaction with uracil DNA glycosylase, G 2 arrest, or enhancement of macrophage infection but correlated with the ability of Vpr to induce host cell apoptosis. This study suggests the presence of a determinant of in vivo cytopathogenicity within HIV-1 Vpr and further indicates that viral replication can be uncoupled from cytopathicity in vitro and in vivo.

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“…Antiretroviral therapy (ART) blocks viral replication, reverses CD4 T cell depletion (2), and reconstitutes immunity to most opportunistic pathogens. Replication of HIV within CD4 T cells significantly contributes to plasma viral load and thus to HIV disease progression (3). It is well established that intracellular HIV DNA loads in vivo are influenced by CD4 T cell differentiation (4)(5)(6), functional properties of CD4 T cells (7), and pathogen specificity (8)(9)(10) and that T cell activation and proliferation contribute to productive HIV infection of memory CD4 T cells (11)(12)(13)(14)(15).…”

mentioning

confidence: 99%

CD25⁺FoxP3⁺Memory CD4 T Cells Are Frequent Targets of HIV InfectionIn Vivo

Chachage¹,

Pollakis

Kuffour

et al. 2016

J Virol

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Interleukin 2 (IL-2) signaling through the IL-2 receptor alpha chain (CD25) facilitates HIV replication in vitro AIDS is caused by human immunodeficiency virus (HIV) infection and is characterized by the failure of the immune system to control diverse opportunistic infections facilitated by the progressive loss of CD4 T cells. The rate of CD4 T cell depletion correlates with set point levels of HIV-1 viral load in plasma (1) and is critically dependent on ongoing viral replication. Antiretroviral therapy (ART) blocks viral replication, reverses CD4 T cell depletion (2), and reconstitutes immunity to most opportunistic pathogens. Replication of HIV within CD4 T cells significantly contributes to plasma viral load and thus to HIV disease progression (3). It is well established that intracellular HIV DNA loads in vivo are influenced by CD4 T cell differentiation (4-6), functional properties of CD4 T cells (7), and pathogen specificity (8-10) and that T cell activation and proliferation contribute to productive HIV infection of memory CD4 T cells (11)(12)(13)(14)(15). Together these results imply that, depending on their biological properties, different CD4 T cell subsets might differ in their susceptibilities to HIV infection and their contributions to virion production in vivo. Perhaps the best characterized CD4 T cell subset in this re-

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Evaluation of proviral copy number and plasma RNA level as early indicators of progression in HIV-1 infection

Cited by 76 publications

References 0 publications

Low Plasma Human Immunodeficiency Virus Type 2 Viral Load Is Independent of Proviral Load: Low Virus Production In Vivo

Low Plasma Human Immunodeficiency Virus Type 2 Viral Load Is Independent of Proviral Load: Low Virus Production In Vivo

Evidence for a cytopathogenicity determinant in HIV-1 Vpr

CD25⁺FoxP3⁺Memory CD4 T Cells Are Frequent Targets of HIV InfectionIn Vivo

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Evaluation of proviral copy number and plasma RNA level as early indicators of progression in HIV-1 infection

Cited by 76 publications

References 0 publications

Low Plasma Human Immunodeficiency Virus Type 2 Viral Load Is Independent of Proviral Load: Low Virus Production In Vivo

Low Plasma Human Immunodeficiency Virus Type 2 Viral Load Is Independent of Proviral Load: Low Virus Production In Vivo

Evidence for a cytopathogenicity determinant in HIV-1 Vpr

CD25+FoxP3+Memory CD4 T Cells Are Frequent Targets of HIV InfectionIn Vivo

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CD25⁺FoxP3⁺Memory CD4 T Cells Are Frequent Targets of HIV InfectionIn Vivo