Dynamics of HIV-1 viral load rebound among patients with previous suppression of viral replication

AIDS ◽  
2000 ◽  
Vol 14 (11) ◽  
pp. 1481-1488 ◽  
Author(s):  
John P. A. Ioannidis ◽  
Diane V. Havlir ◽  
Pablo Tebas ◽  
Martin S. Hirsch ◽  
Ann C. Collier ◽  
...  
Keyword(s):  
Viral Load ◽  
Viral Replication ◽  
Viral Load Rebound ◽  
Hiv 1

scholarly journals Identification and Characterization of HIV-1 Latent Viral Reservoirs In Peripheral Blood

2014 ◽  
Vol 53 (1) ◽  
pp. 60-66 ◽  
Author(s):  
Amanda Chargin ◽  
Fangfang Yin ◽  
Min Song ◽  
Srividyabhuvaneswari Subramaniam ◽  
Grace Knutson ◽  
...  
Keyword(s):  
Viral Load ◽  
Viral Replication ◽  
Whole Blood ◽  
Peripheral Blood ◽  
Plasma Viral Load ◽  
Mononuclear Cells ◽  
Clinical Monitoring ◽  
Genotypic Resistance ◽  
Viral Loads ◽  
Hiv 1

Plasma viral load and CD4 counts are effective for clinical monitoring, but they do not give a full representation of HIV-1 quasispecies in cellular reservoirs, the major repository of replication-competent HIV-1 in infected individuals. We sought to develop a diagnostic system that might stimulate the replication-competent HIV-1 reservoirs for enhanced clinical monitoring, including selection of antiretroviral regimens. Whole-blood samples from 45 HIV-infected individuals were collected into 1 ViraStim HIV-1 activation tube and 1 EDTA tube. Samples were tested for viral load and cell type-specific HIV-1 replication. Further, 7 matched activated/nonactivated samples were sequenced using the Trugene HIV-1 genotyping kit. The percentage of patients with replication-competent virus in peripheral blood mononuclear cells (PBMCs) varied, depending on the baseline plasma viral load in the EDTA tubes. Six out of 24 patients with a starting plasma viral load of <20 copies/ml (cp/ml), 6 out of 8 patients with starting viral loads of >20 and <1,000 cp/ml, and 8 out of 13 patients with starting viral loads of >1,000 all showed increases in viral replication of >5-fold. These increases came from cellular reservoirs in blood as determined by simultaneous ultrasensitive subpopulation staining/hybridization in situ (SUSHI). When resistance genotypes in plasma from activation tubes were compared to those from EDTA tubes for 7 patients, all patients showed additional mutations in the activation tube, while 3 patients demonstrated additional genotypic resistance determinants. We show that HIV-1 viral replication can be stimulated directly from infected whole blood. The sequencing results showed that 3 of 7 cases demonstrated additional drug resistance following stimulation.

scholarly journals Receipt of opioid agonist treatment halves the risk of HIV-1 RNA viral load rebound through improved ART adherence for HIV-infected women who use illicit drugs

2020 ◽  
Vol 206 ◽  
pp. 107670
Author(s):  
Joëlla W. Adams ◽  
Brandon D.L. Marshall ◽  
Nur Afiqah Mohd Salleh ◽  
Rolando Barrios ◽  
Seonaid Nolan ◽  
...  
Keyword(s):  
Viral Load ◽  
Illicit Drugs ◽  
Art Adherence ◽  
Opioid Agonist ◽  
Opioid Agonist Treatment ◽  
Viral Load Rebound ◽  
Hiv 1

scholarly journals MAVS Genetic Variation Is Associated with Decreased HIV-1 Replication In Vitro and Reduced CD4+ T Cell Infection in HIV-1-Infected Individuals

Viruses ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 764
Author(s):  
Melissa Stunnenberg ◽  
Lisa van Pul ◽  
Joris K. Sprokholt ◽  
Karel A. van Dort ◽  
Sonja I. Gringhuis ◽  
...  
Keyword(s):  
Genetic Variation ◽  
Viral Load ◽  
T Cell ◽  
Viral Replication ◽  
Mononuclear Cells ◽  
Cd4 T Cell ◽  
Lower Percentage ◽  
Cell Counts ◽  
Hiv 1

The mitochondrial antiviral protein MAVS is a key player in the induction of antiviral responses; however, human immunodeficiency virus 1 (HIV-1) is able to suppress these responses. Two linked single nucleotide polymorphisms (SNPs) in the MAVS gene render MAVS insensitive to HIV-1-dependent suppression, and have been shown to be associated with a lower viral load at set point and delayed increase of viral load during disease progression. Here, we studied the underlying mechanisms involved in the control of viral replication in individuals homozygous for this MAVS genotype. We observed that individuals with the MAVS minor genotype had more stable total CD4+ T cell counts during a 7-year follow up and had lower cell-associated proviral DNA loads. Genetic variation in MAVS did not affect immune activation levels; however, a significantly lower percentage of naïve CD4+ but not CD8+ T cells was observed in the MAVS minor genotype. In vitro HIV-1 infection of peripheral blood mononuclear cells (PBMCs) from healthy donors with the MAVS minor genotype resulted in decreased viral replication. Although the precise underlying mechanism remains unclear, our data suggest that the protective effect of the MAVS minor genotype may be exerted by the initiation of local innate responses affecting viral replication and CD4+ T cell susceptibility.

scholarly journals No Significant Changes to Residual Viremia After Switch to Dolutegravir and Lamivudine in a Randomized Trial

2019 ◽  
Vol 6 (3) ◽  
Author(s):  
Jonathan Z Li ◽  
Paul E Sax ◽  
Vincent C Marconi ◽  
Jesse Fajnzylber ◽  
Baiba Berzins ◽  
...  
Keyword(s):  
Viral Load ◽  
Antiretroviral Therapy ◽  
Viral Replication ◽  
Randomized Trial ◽  
Viral Suppression ◽  
Group Differences ◽  
Residual Viremia ◽  
Ultrasensitive Assay ◽  
Hiv 1

Abstract In the ASPIRE trial, antiretroviral therapy (ART) switch to dolutegravir plus lamivudine (DTG+3TC) was comparable to 3-drug ART in maintaining viral suppression by standard viral load assays. We used an ultrasensitive assay to assess whether this switch led to increased residual viremia. At entry, levels of residual viremia did not differ significantly between arms (DTG+3TC vs 3-drug ART: mean, 5.0 vs 4.2 HIV-1 RNA copies/mL; P = .64). After randomization, no significant between-group differences were found at either week 24 or 48. These results show no evidence for increased viral replication on DTG+3TC and support its further investigation as a dual ART strategy.

scholarly journals Stage-Dependent Inhibition of HIV-1 Replication by Antiretroviral Drugs in Cell Culture

2009 ◽  
Vol 54 (3) ◽  
pp. 1047-1054 ◽  
Author(s):  
Daniel A. Donahue ◽  
Richard D. Sloan ◽  
Björn D. Kuhl ◽  
Tamara Bar-Magen ◽  
Susan M. Schader ◽  
...  
Keyword(s):  
Viral Load ◽  
Viral Replication ◽  
Reverse Transcription ◽  
Antiretroviral Drugs ◽  
Proteolytic Processing ◽  
Viral Inhibition ◽  
Dependent Inhibition ◽  
Infected Cells ◽  
Hiv 1

ABSTRACT Recent clinical trials have shown that the use of the HIV-1 integrase (IN) inhibitor raltegravir (RAL) results in drops in the viral load that are more rapid than those achieved by use of the reverse transcriptase (RT) inhibitor efavirenz. Previously, mathematical modeling of viral load decay that takes into account the stage of viral replication targeted by a drug has yielded data that closely approximate the clinical trial results. This model predicts greater inhibition of viral replication by drugs that act later in the viral replication cycle. In the present study, we have added drugs that target entry, reverse transcription, integration, or proteolytic processing to acutely infected cells and have shown modest viral inhibition by entry inhibitors, intermediate levels of inhibition by RT and IN inhibitors, and high levels of inhibition by protease inhibitors relative to the levels of growth for the no-drug controls. When dual or triple combinations of these drugs were added to acutely infected cells, we found that the levels of inhibition achieved by any given combination were comparable to those achieved by the latest-acting drug in the combination. In single-round infections in which the kinetics of reverse transcription and integration had been determined by quantitative PCR, addition of IN inhibitors at various times postinfection resulted in levels of inhibition equal to or greater than those achieved by addition of RT inhibitors. Collectively, our data provide in vitro evidence of the stage-dependent inhibition of HIV-1 by clinically relevant drugs. We discuss how stage-dependent inhibition helps to explain the unique viral load decay dynamics observed clinically with RAL.

scholarly journals Substance use patterns and HIV-1 RNA viral load rebound among HIV-positive illicit drug users in a Canadian setting

2018 ◽  
Vol 24 (1) ◽  
pp. 19-25 ◽  
Author(s):  
Farah Ladak ◽  
Eugenia Socias ◽  
Seonaid Nolan ◽  
Huiru Dong ◽  
Thomas Kerr ◽  
...  
Keyword(s):  
Substance Use ◽  
Viral Load ◽  
Drug Users ◽  
Illicit Drug ◽  
Hiv Positive ◽  
Illicit Drug Users ◽  
Use Patterns ◽  
Canadian Setting ◽  
Viral Load Rebound ◽  
Hiv 1

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

2011 ◽  
Vol 53 (4) ◽  
pp. 193-196 ◽  
Author(s):  
Paulo Pereira Christo ◽  
Dirceu Bartolomeu Greco ◽  
Agdemir Waleria Aleixo ◽  
Jose António Livramento
Keyword(s):  
Cerebrospinal Fluid ◽  
Viral Load ◽  
Viral Replication ◽  
Highly Active Antiretroviral Therapy ◽  
Plasma Viral Load ◽  
Highly Active ◽  
Csf Proteins ◽  
The Central Nervous System ◽  
Hiv 1 ◽  
Rna Levels

The 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/mm³, 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/mm³ 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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