scholarly journals Persistence of integrated HIV DNA in CXCR3 + CCR6 + memory CD4+ T cells in HIV-infected individuals on antiretroviral therapy

AIDS ◽  
2016 ◽  
Vol 30 (10) ◽  
pp. 1511-1520 ◽  
Author(s):  
Gabriela Khoury ◽  
Jenny L. Anderson ◽  
Rémi Fromentin ◽  
Wendy Hartogenesis ◽  
Miranda Z. Smith ◽  
...  
Keyword(s):  
T Cells ◽  
Antiretroviral Therapy ◽  
Cd4 T Cells ◽  
Hiv Dna ◽  
Memory Cd4 T Cells

scholarly journals HIV DNA Subspecies Persist in both Activated and Resting Memory CD4+ T Cells during Antiretroviral Therapy

2014 ◽  
Vol 88 (6) ◽  
pp. 3516-3526 ◽  
Author(s):  
J. M. Murray ◽  
J. J. Zaunders ◽  
K. L. McBride ◽  
Y. Xu ◽  
M. Bailey ◽  
...  
Keyword(s):  
T Cells ◽  
Antiretroviral Therapy ◽  
Cd4 T Cells ◽  
Hiv Dna ◽  
Memory Cd4 T Cells

scholarly journals Interleukin-7 promotes HIV persistence during antiretroviral therapy

Blood ◽  
2013 ◽  
Vol 121 (21) ◽  
pp. 4321-4329 ◽  
Author(s):  
Claire Vandergeeten ◽  
Rémi Fromentin ◽  
Sandrina DaFonseca ◽  
Mariam B. Lawani ◽  
Irini Sereti ◽  
...  
Keyword(s):  
T Cells ◽  
Antiretroviral Therapy ◽  
Cd4 T Cells ◽  
Viral Latency ◽  
Absolute Number ◽  
Hiv Persistence ◽  
Hiv Dna ◽  
Interleukin 7 ◽  
Key Points ◽  
Latently Infected

Key Points IL-7 does not disrupt viral latency in highly pure resting latently infected CD4+ T cells from HIV-infected subjects receiving ART. IL-7 therapy leads to a 70% increase in the absolute number of circulating CD4+ T cells harboring integrated HIV DNA 4 weeks posttherapy.

scholarly journals Most HIV DNA in PBMC is present in non-gut homing, resting memory CD4+ T cells with a ß7-CD38-CD127 high phenotype

2010 ◽  
Vol 13 (Suppl 3) ◽  
pp. O2 ◽  
Author(s):  
KK Koelsch ◽  
Y Xu ◽  
M Bailey ◽  
K McBride ◽  
N Seddiki ◽  
...  
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
Hiv Dna ◽  
Memory Cd4 T Cells

Metabolic Features of Activated Memory CD4+ T-Cells Derived from HIV-Infected Immunological Non-responders to Highly Active Antiretroviral Therapy

2021 ◽  
Vol 501 (1) ◽  
pp. 206-209
Author(s):  
V. V. Vlasova ◽  
E. V. Saidakova ◽  
L. B. Korolevskaya ◽  
N. G. Shmagel ◽  
V. A. Chereshnev ◽  
...  
Keyword(s):  
T Cells ◽  
Antiretroviral Therapy ◽  
Highly Active Antiretroviral Therapy ◽  
Cd4 T Cells ◽  
Highly Active ◽  
Memory Cd4 T Cells

scholarly journals Blind Uneven Proliferation of CD4+ T cells During Primary Infection Generates the Majority of the HIV Reservoir

2020 ◽  
Author(s):  
Florencia A. T. Boshier ◽  
Daniel B. Reeves ◽  
Elizabeth R. Duke ◽  
David A. Swan ◽  
Martin Prlic ◽  
...  
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
Cellular Proliferation ◽  
Chromosomal Dna ◽  
Hiv Replication ◽  
Hiv Reservoir ◽  
Viral Spread ◽  
Hiv Dna ◽  
Latently Infected ◽  
Memory Cd4 T Cells

AbstractThe HIV reservoir is a population of 1-10 million anatomically dispersed, latently infected memory CD4+ T cells in which an HIV DNA molecule is quiescently integrated into human chromosomal DNA. When antiretroviral therapy (ART) is stopped and HIV replication initiates in one of these cells, systemic viral spread resumes, rekindling progression to AIDS. Therefore, HIV latency prevents cure. The HIV reservoir contains clones: identical HIV sequences that are integrated within identical human chromosomal DNA locations. The presence of these clones demonstrates that proliferation of CD4+ T cells sustains infection despite ART. The reservoir has a precise structure consisting of a small number of large clones and a large number of small clones. However, the mechanisms leading to this structure have not been identified. We developed a mathematical model that recapitulates the profound depletion and brisk recovery of CD4+ T cells, reservoir creation, and viral load trajectory during primary HIV infection. We extended the model to simulate stochastically individual HIV reservoir clones and identified that uneven proliferation among clones during recovery from CD4+ lymphopaenia is sufficient to explain the observed clonal reservoir distribution. We project that within one month of infection 75-95% of reservoir cells are generated from cellular proliferation rather than denovo viral infection. Recent detection of HIV infected clones during the first 5 weeks of infection support our model’s predictions.

scholarly journals Memory CD4 + T-Cells Expressing HLA-DR Contribute to HIV Persistence During Prolonged Antiretroviral Therapy

2019 ◽  
Vol 10 ◽  
Author(s):  
Eunok Lee ◽  
Peter Bacchetti ◽  
Jeffery Milush ◽  
Wei Shao ◽  
Eli Boritz ◽  
...  
Keyword(s):  
T Cells ◽  
Antiretroviral Therapy ◽  
Cd4 T Cells ◽  
Hiv Persistence ◽  
Hla Dr ◽  
Memory Cd4 T Cells

scholarly journals Human Immunodeficiency Virus (HIV)–Infected CCR6+ Rectal CD4+ T Cells and HIV Persistence On Antiretroviral Therapy

2019 ◽  
Vol 221 (5) ◽  
pp. 744-755 ◽  
Author(s):  
Jenny L Anderson ◽  
Gabriela Khoury ◽  
Rémi Fromentin ◽  
Ajantha Solomon ◽  
Nicolas Chomont ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cells ◽  
Antiretroviral Therapy ◽  
Cd4 T Cells ◽  
People Living With Hiv ◽  
Hiv Persistence ◽  
Hiv Dna ◽  
Immunodeficiency Virus ◽  
Infected Cells ◽  
Living With Hiv

Abstract Background Identifying where human immunodeficiency virus (HIV) persists in people living with HIV and receiving antiretroviral therapy is critical to develop cure strategies. We assessed the relationship of HIV persistence to expression of chemokine receptors and their chemokines in blood (n = 48) and in rectal (n = 20) and lymph node (LN; n = 8) tissue collected from people living with HIV who were receiving suppressive antiretroviral therapy. Methods Cell-associated integrated HIV DNA, unspliced HIV RNA, and chemokine messenger RNA were quantified by quantitative polymerase chain reaction. Chemokine receptor expression on CD4+ T cells was determined using flow cytometry. Results Integrated HIV DNA levels in CD4+ T cells, CCR6+CXCR3+ memory CD4+ T-cell frequency, and CCL20 expression (ligand for CCR6) were highest in rectal tissue, where HIV-infected CCR6+ T cells accounted for nearly all infected cells (median, 89.7%). Conversely in LN tissue, CCR6+ T cells were infrequent, and there was a statistically significant association of cell-associated HIV DNA and RNA with CCL19, CCL21, and CXCL13 chemokines. Conclusions HIV-infected CCR6+ CD4+ T cells accounted for the majority of infected cells in rectal tissue. The different relationships between HIV persistence and T-cell subsets and chemokines in rectal and LN tissue suggest that different tissue-specific strategies may be required to eliminate HIV persistence and that assessment of biomarkers for HIV persistence may not be generalizable between blood and other tissues.

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