scholarly journals HIV-1 Vpr Accelerates Viral Replication during Acute Infection by Exploitation of Proliferating CD4+ T Cells In Vivo

2013 ◽  
Vol 9 (12) ◽  
pp. e1003812 ◽  
Author(s):  
Kei Sato ◽  
Naoko Misawa ◽  
Shingo Iwami ◽  
Yorifumi Satou ◽  
Masao Matsuoka ◽  
...  
Keyword(s):  
T Cells ◽  
Viral Replication ◽  
Cd4 T Cells ◽  
Acute Infection ◽  
Hiv 1

scholarly journals Preferential infection and depletion of Mycobacterium tuberculosis–specific CD4 T cells after HIV-1 infection

2010 ◽  
Vol 207 (13) ◽  
pp. 2869-2881 ◽  
Author(s):  
Christof Geldmacher ◽  
Njabulo Ngwenyama ◽  
Alexandra Schuetz ◽  
Constantinos Petrovas ◽  
Klaus Reither ◽  
...  
Keyword(s):  
T Cells ◽  
Mycobacterium Tuberculosis ◽  
Hiv Infection ◽  
Cd4 T Cells ◽  
Staphylococcal Enterotoxin B ◽  
Opportunistic Pathogens ◽  
Rapid Loss ◽  
Hiv 1

HIV-1 infection results in the progressive loss of CD4 T cells. In this study, we address how different pathogen-specific CD4 T cells are affected by HIV infection and the cellular parameters involved. We found striking differences in the depletion rates between CD4 T cells to two common opportunistic pathogens, cytomegalovirus (CMV) and Mycobacterium tuberculosis (MTB). CMV-specific CD4 T cells persisted after HIV infection, whereas MTB-specific CD4 T cells were depleted rapidly. CMV-specific CD4 T cells expressed a mature phenotype and produced very little IL-2, but large amounts of MIP-1β. In contrast, MTB-specific CD4 T cells were less mature, and most produced IL-2 but not MIP-1β. Staphylococcal enterotoxin B–stimulated IL-2–producing cells were more susceptible to HIV infection in vitro than MIP-1β–producing cells. Moreover, IL-2 production was associated with expression of CD25, and neutralization of IL-2 completely abrogated productive HIV infection in vitro. HIV DNA was found to be most abundant in IL-2–producing cells, and least abundant in MIP-1β–producing MTB-specific CD4 T cells from HIV-infected subjects with active tuberculosis. These data support the hypothesis that differences in function affect the susceptibility of pathogen-specific CD4 T cells to HIV infection and depletion in vivo, providing a potential mechanism to explain the rapid loss of MTB-specific CD4 T cells after HIV infection.

scholarly journals Loss of HIV-1–specific CD8+ T Cell Proliferation after Acute HIV-1 Infection and Restoration by Vaccine-induced HIV-1–specific CD4+ T Cells

2004 ◽  
Vol 200 (6) ◽  
pp. 701-712 ◽  
Author(s):  
Mathias Lichterfeld ◽  
Daniel E. Kaufmann ◽  
Xu G. Yu ◽  
Stanley K. Mui ◽  
Marylyn M. Addo ◽  
...  
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
Chronic Infection ◽  
Cell Function ◽  
Acute Infection ◽  
T Helper Cell ◽  
T Helper ◽  
Functional Defect ◽  
Hiv 1

Virus-specific CD8+ T cells are associated with declining viremia in acute human immunodeficiency virus (HIV)1 infection, but do not correlate with control of viremia in chronic infection, suggesting a progressive functional defect not measured by interferon γ assays presently used. Here, we demonstrate that HIV-1–specific CD8+ T cells proliferate rapidly upon encounter with cognate antigen in acute infection, but lose this capacity with ongoing viral replication. This functional defect can be induced in vitro by depletion of CD4+ T cells or addition of interleukin 2–neutralizing antibodies, and can be corrected in chronic infection in vitro by addition of autologous CD4+ T cells isolated during acute infection and in vivo by vaccine-mediated induction of HIV-1–specific CD4+ T helper cell responses. These data demonstrate a loss of HIV-1–specific CD8+ T cell function that not only correlates with progressive infection, but also can be restored in chronic infection by augmentation of HIV-1–specific T helper cell function. This identification of a reversible defect in cell-mediated immunity in chronic HIV-1 infection has important implications for immunotherapeutic interventions.

scholarly journals Productive Infection of Plasmacytoid Dendritic Cells with Human Immunodeficiency Virus Type 1 Is Triggered by CD40 Ligation

2002 ◽  
Vol 76 (21) ◽  
pp. 11033-11041 ◽  
Author(s):  
Lawrence Fong ◽  
Manuela Mengozzi ◽  
Nancy W. Abbey ◽  
Brian G. Herndier ◽  
Edgar G. Engleman
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cells ◽  
Dendritic Cells ◽  
Viral Replication ◽  
Cd4 T Cells ◽  
Cd40 Ligand ◽  
Immunodeficiency Virus ◽  
Hiv 1

ABSTRACT Immature plasmacytoid dendritic cells are the principal alpha interferon-producing cells (IPC), responsible for primary antiviral immunity. IPC express surface molecules CD4, CCR5, and CXCR4, which are known coreceptors required for human immunodeficiency virus (HIV) infection. Here we show that IPC are susceptible to and replicate HIV type 1 (HIV-1). Importantly, viral replication is triggered upon activation of IPC with CD40 ligand, a signal physiologically delivered by CD4 T cells. Immunohistochemical staining of tonsil from HIV-infected individuals reveals HIV p24+ IPC, consistent with in vivo infection of these cells. IPC exposed in vitro to HIV produce alpha interferon, which partially inhibits viral replication. Nevertheless, IPC efficiently transmit HIV-1 to CD4 T-cells, and such transmission is also augmented by CD40 ligand activation. IPC produce RANTES/CCL5 and MIP-1α/CCL3 when exposed to HIV in vitro. IPC also induce naïve CD4 T cells to proliferate and would therefore preferentially infect these cells. These results indicate that IPC may play an important role in the dissemination of HIV.

scholarly journals Regulatory T Cells Contribute to HIV-1 Reservoir Persistence in CD4+ T Cells Through Cyclic Adenosine Monophosphate–Dependent Mechanisms in Humanized Mice In Vivo

2017 ◽  
Vol 216 (12) ◽  
pp. 1579-1591 ◽  
Author(s):  
Guangming Li ◽  
Jun-ichi Nunoya ◽  
Liang Cheng ◽  
Natalia Reszka-Blanco ◽  
Li-Chung Tsao ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Cd4 T Cells ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Humanized Mice ◽  
Hiv 1

scholarly journals Preferential Infection of α4β7+ Memory CD4+ T Cells During Early Acute Human Immunodeficiency Virus Type 1 Infection

2020 ◽  
Vol 71 (11) ◽  
pp. e735-e743 ◽  
Author(s):  
Andrey Tokarev ◽  
Lyle R McKinnon ◽  
Amélie Pagliuzza ◽  
Aida Sivro ◽  
Tosin E Omole ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cells ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Cd4 T Cells ◽  
Acute Infection ◽  
Immunodeficiency Virus ◽  
Memory Cd4 T Cells ◽  
Hiv 1

Abstract Background Establishment of persistent human immunodeficiency virus type 1 (HIV-1) reservoirs occurs early in infection, and biomarkers of infected CD4+ T cells during acute infection are poorly defined. CD4+ T cells expressing the gut homing integrin complex α4β7 are associated with HIV-1 acquisition, and are rapidly depleted from the periphery and gastrointestinal mucosa during acute HIV-1 infection. Methods Integrated HIV-1 DNA was quantified in peripheral blood mononuclear cells obtained from acutely (Fiebig I–III) and chronically infected individuals by sorting memory CD4+ T-cell subsets lacking or expressing high levels of integrin β7 (β7negative and β7high, respectively). HIV-1 DNA was also assessed after 8 months of combination antiretroviral therapy (cART) initiated in Fiebig II/III individuals. Activation marker and chemokine receptor expression was determined for β7-defined subsets at acute infection and in uninfected controls. Results In Fiebig I, memory CD4+ T cells harboring integrated HIV-1 DNA were rare in both β7high and β7negative subsets, with no significant difference in HIV-1 DNA copies. In Fiebig stages II/III and in chronically infected individuals, β7high cells were enriched in integrated and total HIV-1 DNA compared to β7negative cells. During suppressive cART, integrated HIV-1 DNA copies decreased in both β7negative and β7high subsets, which did not differ in DNA copies. In Fiebig II/III, integrated HIV-1 DNA in β7high cells was correlated with their activation. Conclusions β7high memory CD4+ T cells are preferential targets during early HIV-1 infection, which may be due to the increased activation of these cells.

HIV-1-infected CD8+CD4+ T cells decay in vivo at a similar rate to infected CD4 T cells during HAART

AIDS ◽  
2008 ◽  
Vol 22 (1) ◽  
pp. 57-65 ◽  
Author(s):  
Gareth J Hughes ◽  
Alexandra Cochrane ◽  
Clifford Leen ◽  
Sheila Morris ◽  
Jeanne E Bell ◽  
...  
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
Similar Rate ◽  
Hiv 1

scholarly journals Slow Turnover of HIV-1 Receptors on Quiescent CD4+ T Cells Causes Prolonged Surface Retention of gp120 Immune Complexes In Vivo

PLoS ONE ◽  
2014 ◽  
Vol 9 (2) ◽  
pp. e86479 ◽  
Author(s):  
Yasuhiro Suzuki ◽  
Hiroyuki Gatanaga ◽  
Natsuo Tachikawa ◽  
Shinichi Oka
Keyword(s):  
T Cells ◽  
Immune Complexes ◽  
Cd4 T Cells ◽  
Hiv 1 ◽  
Slow Turnover

scholarly journals Type I Interferon Is a Powerful Inhibitor of in Vivo HIV-1 Infection and Preserves Human CD4+ T Cells from Virus-Induced Depletion in SCID Mice Transplanted with Human Cells

Virology ◽  
1999 ◽  
Vol 263 (1) ◽  
pp. 78-88 ◽  
Author(s):  
Caterina Lapenta ◽  
Stefano M. Santini ◽  
Enrico Proietti ◽  
Paola Rizza ◽  
Mariantonia Logozzi ◽  
...  
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
Type I Interferon ◽  
Human Cells ◽  
Scid Mice ◽  
Type I ◽  
Hiv 1

scholarly journals In vivo HIV-1 infection of CD45RA+CD4+ T cells is established primarily by syncytium-inducing variants and correlates with the rate of CD4+ T cell decline

2000 ◽  
Vol 97 (3) ◽  
pp. 1269-1274 ◽  
Author(s):  
H. Blaak ◽  
A. B. van't Wout ◽  
M. Brouwer ◽  
B. Hooibrink ◽  
E. Hovenkamp ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cd4 T Cells ◽  
Cd4 T Cell ◽  
Cell Decline ◽  
Hiv 1

scholarly journals Helios + Regulatory T cell frequencies are correlated with control of viral replication and recovery of absolute CD4 T cells counts in early HIV-1 infection

2017 ◽  
Vol 18 (1) ◽  
Author(s):  
Raquel Matavele Chissumba ◽  
Eduardo Namalango ◽  
Vânia Maphossa ◽  
Ivalda Macicame ◽  
Nilesh Bhatt ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Viral Replication ◽  
Regulatory T Cell ◽  
Cd4 T Cells ◽  
Hiv 1
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