Works (5)

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

Mechanism of feline immunodeficiency virus envelope glycoprotein-mediated fusion

VIROLOGY, 321(2), 274–286.

By: H. Garg n, F. Fuller n & W. Tompkins n

author keywords: feline immunodeficiency virus; glycoprotein-mediated fusion; lentiviruses
MeSH headings : Amino Acid Sequence; Animals; Benzylamines; CD4-Positive T-Lymphocytes / metabolism; CD4-Positive T-Lymphocytes / virology; Cats; Cell Line; Cyclams; Giant Cells; Heterocyclic Compounds / pharmacology; Immunodeficiency Virus, Feline / isolation & purification; Immunodeficiency Virus, Feline / physiology; Molecular Sequence Data; Peptides / chemical synthesis; Peptides / pharmacology; Protein Conformation; Protein Structure, Tertiary; Receptors, CXCR4 / antagonists & inhibitors; Receptors, CXCR4 / physiology; Sequence Alignment; Tryptophan; Viral Fusion Proteins / genetics; Viral Fusion Proteins / metabolism; Viral Fusion Proteins / physiology
TL;DR: It is shown that a conserved tryptophan-rich region in the membrane proximal ectodomain of gp41 is critical for fusion, possibly at steps post hairpin structure formation, and that the mechanism and kinetics are similar to HIV env. (via Semantic Scholar)
Sources: Web Of Science, NC State University Libraries
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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