Characterization of HIV-1 RNA forms in the plasma of patients undergoing successful HAART

Lopez, Carlos A.; Vázquez, Manuel; Hill, Martin D.; Colón, María; Porrata-Doria, Tirtsa; Johnston, Ian; Lorenzo, Eric

doi:10.1007/s00705-010-0659-3

Cited by 16 publications

(16 citation statements)

References 53 publications

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“…Previous studies showed that the proportion of circulating CD16 + monocytes expands in a number of inflammatory conditions [79,80] and with HIV and SIV infection [45,46]. CD16 + monocytes in vivo and in vitro are more permissive for HIV infection when compared to CD16 − monocytes [81] and HIV is detected in CD14 + CD16 + monocytes from infected individuals undergoing successful cART [82]. In a recent study, CD14 low CD16 + and CD14 + CD16 + monocytes were shown to express distinct phenotypic and functional characteristics, including unique patterns of chemokine receptor expression and cytokine production in response to bacterial and viral pathogens [83].…”

Section: Discussionmentioning

confidence: 99%

“…We propose that there is a specific subpopulation of maturing monocytes in the circulation that will soon cross the vasculature, and that these cells are infectable by HIV. Several studies indicate that monocytes prone to HIV infection include a CD16 + subset(s) [81,82]. The subpopulation(s) of monocytes susceptible to HIV infection is so small it is difficult to study in freshly isolated monocytes.…”

Section: Discussionmentioning

confidence: 99%

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Characterization of monocyte maturation/differentiation that facilitates their transmigration across the blood–brain barrier and infection by HIV: Implications for NeuroAIDS

Buckner

Calderon

Willams

et al. 2011

Cellular Immunology

145

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The prevalence of human immunodeficiency virus 1 (HIV) associated neurocognitive disorders resulting from infection of the central nervous system (CNS) by HIV continues to increase despite the success of combination antiretroviral therapy. Although monocytes are known to transport HIV across the blood–brain barrier (BBB) into the CNS, there are few specific markers that identify monocyte subpopulations susceptible to HIV infection and/or capable of infiltrating the CNS. We cultured human peripheral blood monocytes and characterized the expression of the phenotypic markers CD14, CD16, CD11b, Mac387, CD163, CD44v6 and CD166 during monocyte/macrophage (Mo/Mac) maturation/differentiation. We determined that a CD14+CD16+CD11b+Mac387+ Mo/Mac subpopulation preferentially transmigrates across our in vitro BBB model in response to CCL2. Genes associated with Mo/Mac subpopulations that transmigrate across the BBB and/or are infected by HIV were identified by cDNA microarray analyses. Our findings contribute to the understanding of monocyte maturation, infection and transmigration into the brain during the pathogenesis of NeuroAIDS.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Characterization of monocyte maturation/differentiation that facilitates their transmigration across the blood–brain barrier and infection by HIV: Implications for NeuroAIDS

Buckner

Calderon

Willams

et al. 2011

Cellular Immunology

145

View full text Add to dashboard Cite

show abstract

“…A 525 bp fragment containing the HIV-1 env C2-V4 variable region was amplified by RT-PCR and nested PCR using primers against the conserved regions C2 and C4 (forward primer: 5′-CTGTTAAATGGCAGTCTAGC-3′; reverse primer: 5′-TGATGGGAGGGGTATACATT-3′ [43]. The PCR-amplified product was verified by agarose gel electrophoresis, gel-purified, and cloned into cloning vector pCR2.1 (Invitrogen).…”

Section: Methodsmentioning

confidence: 99%

Longitudinal Analysis of Cerebrospinal Fluid and Plasma HIV-1 Envelope Sequences Isolated From a Single Donor with HIV Asymptomatic Neurocognitive Impairment

Vázquez-Santiago

García

Rivera-Román

et al. 2015

J Virol Antivir Res

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Objective Combined antiretroviral treatment (cART) has changed the clinical presentation of HIV-associated neurocognitive disorders (HAND) to that of the milder forms of the disease. Asymptomatic neurocognitive impairment (ANI) is now more prevalent and is associated with increased morbidity and mortality risk in HIV-1–infected people. HIV-1 envelope (env) genetic heterogeneity has been detected within the central nervous system (CNS) of individuals with ANI. Changes within env determine co-receptor use, cellular tropism, and neuropathogenesis. We hypothesize that compartmental changes are associated with HIV-1 env C2V4 during ANI and sought to analyze paired HIV-1 env sequences from plasma and cerebrospinal fluid (CSF) of a female subject undergoing long-term cART. Methods Paired plasma and CSF samples were collected at 12-month intervals and HIV-1 env C2V4 was cloned and sequenced. Results Phylogenetic analysis of paired samples consistently showed genetic variants unique to the CSF. Phenotypic prediction showed CCR5 (R5) variants for all CSF-derived sequences and showed minor X4 variants (or dual-tropic) in the plasma at later time points. Viral compartmentalization was evident throughout the study, suggesting that the occurrence of distinctive env strains may contribute to the neuropathogenesis of HAND. Conclusions Our study provides new insights about the genetic characteristics within the C2V4 of HIV-1 env that persist after long-term cART and during the course of persistent ANI.

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“…Viral reservoirs represent a continuous burden because of their ability to replenish the viral pool as a means of inducing persistent infection. For example, in some patients, C2V3 plasma variants have been recovered despite those patients having undergone successful therapy (76). Reactivation of HIV-1 strains occurs because of therapy failure or after antiretroviral treatment interruption (77).…”

Section: Hiv-1 Cns Viral Reservoirs and Combined Antiretroviral Theramentioning

confidence: 99%

Envelope Gene Evolution and HIV-1 Neuropathogenesis

Vázquez-Santiago

Rivera‐Amill

2015

J Neuroinfect Dis

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In the era of combined antiretroviral therapy (cART), HIV-associated neurocognitive disorders (HAND) account for 40 to 56% of all HIV+ cases. During the acute stage of HIV-1 infection (<6 months), the virus invades and replicates within the central nervous system (CNS). Compared to peripheral tissues, the local CNS cell population expresses distinct levels of chemokine receptors, which levels exert selective pressure on the invading virus. HIV-1 envelope (env) sequences recovered from the brains and cerebrospinal fluid (CSF) of neurocognitively impaired HIV+ subjects often display higher nucleotide variability as compared to non-impaired HIV+ subjects. Specifically, env evolution provides HIV-1 with the strategies to evade host immune response, to reduce chemokine receptor dependence, to increase co-receptor binding efficiency, and to potentiate neurotoxicity. The evolution of env within the CNS leads to changes that may result in the emergence of novel isolates with neurotoxic and neurovirulent features. However, whether specific factors of HIV-1 evolution lead to the emergence of neurovirulent and neurotropic isolates remains ill-defined. HIV-1 env evolution is an ongoing phenomenon that occurs independently of neurological and neurocognitive disease severity; thus HIV env evolution may play a pivotal and reciprocal role in the etiology of HAND. Despite the use of cART, the reactivation of latent viral reservoirs represents a clinical challenge because of the replenishment of the viral pool that may subsequently lead to persistent infection. Therefore, gaining a more complete understanding of how HIV-1 env evolves over the course of the disease should be considered for the development of future therapies aimed at controlling CNS burden, diminishing persistent viremia, and eradicating viral reservoirs. Here we review the current literature on the role of HIV-1 env evolution in the setting of HAND disease progression and on the impact of cART on the dynamics of viral evolution.

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Characterization of HIV-1 RNA forms in the plasma of patients undergoing successful HAART

Cited by 16 publications

References 53 publications

Characterization of monocyte maturation/differentiation that facilitates their transmigration across the blood–brain barrier and infection by HIV: Implications for NeuroAIDS

Characterization of monocyte maturation/differentiation that facilitates their transmigration across the blood–brain barrier and infection by HIV: Implications for NeuroAIDS

Longitudinal Analysis of Cerebrospinal Fluid and Plasma HIV-1 Envelope Sequences Isolated From a Single Donor with HIV Asymptomatic Neurocognitive Impairment

Envelope Gene Evolution and HIV-1 Neuropathogenesis

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