Works (4)

Updated: July 5th, 2023 15:58

2005 journal article

Different thresholds of T cell activation regulate FIV infection of CD4(+)CD25(+) and CD4(+)CD25(-) cells

VIROLOGY, 335(2), 212–221.

By: A. Joshi n, H. Garg n, M. Tompkins n & W. Tompkins n

author keywords: treg cells; latency; activation; reservoirs; HIV; FIV; IL-2
MeSH headings : Animals; Apoptosis; CD4-Positive T-Lymphocytes / drug effects; CD4-Positive T-Lymphocytes / immunology; CD4-Positive T-Lymphocytes / metabolism; CD4-Positive T-Lymphocytes / virology; Cats; Cell Proliferation / drug effects; Cells, Cultured; Concanavalin A / pharmacology; Dose-Response Relationship, Drug; Immunodeficiency Virus, Feline / drug effects; Immunodeficiency Virus, Feline / immunology; Immunodeficiency Virus, Feline / physiology; Interleukin-2 / pharmacology; Lymphocyte Activation / drug effects; Lymphocyte Activation / immunology; Mitogens / pharmacology; Receptors, Interleukin-2 / genetics; Receptors, Interleukin-2 / immunology; Receptors, Interleukin-2 / metabolism; Up-Regulation / drug effects; Virus Latency / drug effects; Virus Replication / drug effects
TL;DR: The results suggest that CD4(+)CD25(+) and CD4 (+)CD 25(+) T cells have different activation requirements which can be modulated by both viral and cytokine stimuli to reach threshold activation levels in order to harbor a productive FIV infection. (via Semantic Scholar)
Source: Web Of Science
Added: August 6, 2018

2005 journal article

Preferential feline immunodeficiency virus (FIV) infection of CD4(+) CD25(+) T-regulatory cells correlates both with surface expression of CXCR4 and activation of FIV long terminal repeat binding cellular transcriptional factors

JOURNAL OF VIROLOGY, 79(8), 4965–4976.

By: A. Joshi n, H. Garg n, M. Tompkins n & W. Tompkins n

MeSH headings : Animals; Benzylamines; CD4-Positive T-Lymphocytes / immunology; CD4-Positive T-Lymphocytes / virology; Cats; Cells, Cultured; Cyclams; Feline Acquired Immunodeficiency Syndrome / immunology; Heterocyclic Compounds / pharmacology; Immunodeficiency Virus, Feline / immunology; Immunodeficiency Virus, Feline / physiology; Lymph Nodes / immunology; Lymph Nodes / virology; Receptors, CXCR4 / antagonists & inhibitors; Receptors, CXCR4 / genetics; Receptors, Interleukin-2 / immunology; T-Lymphocytes / immunology; T-Lymphocytes / virology; Virus Replication
TL;DR: This is the first report elucidating the mechanisms that allow for productive lentiviral infection of CD4+ CD25+ Treg cells and constitutive and IL-2-responsive transactivation of activating transcription factor, CAAT enhancer binding protein, and activating protein 1 transcription factors that are important for FIV replication. (via Semantic Scholar)
Source: Web Of Science
Added: August 6, 2018

2004 journal article

Feline immunodeficiency virus envelope glycoprotein mediates apoptosis in activated PBMC by a mechanism dependent on gp41 function

VIROLOGY, 330(2), 424–436.

By: H. Garg n, A. Joshi n & W. Tompkins n

author keywords: FIV; envelope; apoptosis; fusion; syncytia; CD134; CXCR4
MeSH headings : Animals; Anti-HIV Agents / pharmacology; Apoptosis; Benzylamines; Cats; Cell Fusion; Cell Survival; Cells, Cultured; Cyclams; Glycoproteins / genetics; Glycoproteins / physiology; Heterocyclic Compounds / pharmacology; Immunodeficiency Virus, Feline / pathogenicity; Leukocytes, Mononuclear / cytology; Leukocytes, Mononuclear / virology; Membrane Fusion; Mutation / genetics; Mutation / physiology; Receptors, CXCR4 / antagonists & inhibitors; Receptors, OX40; Receptors, Tumor Necrosis Factor; Viral Envelope Proteins / genetics; Viral Envelope Proteins / physiology; Viral Fusion Proteins / genetics; Viral Fusion Proteins / physiology
TL;DR: It is demonstrated that membrane-expressed FIV Env induces apoptosis in activated feline peripheral blood mononuclear cells (PBMC) by a mechanism that requires CX CR4 binding, as the process was inhibited by CXCR4 antagonist AMD3100 in a dose-dependent manner. (via Semantic Scholar)
Source: Web Of Science
Added: August 6, 2018

2004 journal article

Preferential replication of FIV in activated CD4(+)CD25(+)T cells independent of cellular proliferation

VIROLOGY, 321(2), 307–322.

By: A. Joshi n, T. Vahlenkamp n, H. Garg n, W. Tompkins n & M. Tompkins n

author keywords: FIV; HIV; AIDS; latency; stimulation; anergy; apoptosis; reservoir
MeSH headings : Animals; Apoptosis; CD4-Positive T-Lymphocytes / immunology; CD4-Positive T-Lymphocytes / virology; Cats; Cell Division / immunology; Disease Models, Animal; Feline Acquired Immunodeficiency Syndrome / immunology; Feline Acquired Immunodeficiency Syndrome / virology; Immunodeficiency Virus, Feline / physiology; Lymphocyte Activation; Receptors, Interleukin-2 / analysis; Virus Latency; Virus Replication
TL;DR: The ability of CD4(+)CD25(+) cells to replicate FIV efficiently in the presence of IL-2 but remain anergic and unresponsive to apoptotic signaling suggests that these cells may provide a reservoir of productive FIV infection. (via Semantic Scholar)
Source: Web Of Science
Added: August 6, 2018

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