HIV infection and the brain

Gulevich, Steven; Wiley, Clayton A.

doi:10.1097/00002030-199101001-00007

Cited by 3 publications

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“…IFN-y also stimulates macrophages and microglial cells to release TNF-ot (9). TNF-o and TNF-, stimulate astrocytes to proliferate (46) and may contribute to the reactive gliosis, which is one of the characteristic histopathologic alterations in encephalopathic brains of HIV-1-infected individuals (6,13,38,43). In addition, TNF-a has been implicated in demyelination in the central nervous system (47).…”

Section: Ctlmentioning

confidence: 99%

Human immunodeficiency virus type 1-specific cytotoxic T lymphocytes release gamma interferon, tumor necrosis factor alpha (TNF-alpha), and TNF-beta when they encounter their target antigens

Jassoy

Harrer

Rosenthal

et al. 1993

J Virol

112

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Human immunodeficiency virus type 1 (HIV-1) infection is associated with elevated levels of inflammatory cytokines in the serum and cerebrospinal fluid of infected persons, but the sources of these proteins as well as the specific stimuli which trigger their production and release have not been fully defined. In this study, we evaluated the ability of HIV-1-specific cytotoxic T-lymphocyte (CTL) clones derived from seropositive persons to release gamma interferon (IFN-y), tumor necrosis factor alpha (TNF-a), and TNF-13 upon contact with target cells presenting viral antigen. Peripheral blood-and cerebrospinal fluid-derived HIV-1-specific CD3+ CD4-CD8+ CTL clones as well as freshly isolated peripheral blood mononuclear cells from infected persons were tested in parallel for HIV-1-specific cytotoxicity and cytokine release. Target cells consisted of autologous and allogeneic B-lymphoblastoid cell lines sensitized with synthetic HIV-1 peptides containing the epitopes recognized by these CTL. Cytokine production was measured by specific enzyme-linked immunosorbent assay of culture supernatant fluid. HIV-1-specific CTL clones directed at envelope, Gag, reverse transcriptase, and

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Section: Ctlmentioning

confidence: 99%

Human immunodeficiency virus type 1-specific cytotoxic T lymphocytes release gamma interferon, tumor necrosis factor alpha (TNF-alpha), and TNF-beta when they encounter their target antigens

Jassoy

Harrer

Rosenthal

et al. 1993

J Virol

112

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The role of the envelope glycoprotein in the depletion of T helper cells in human immunodeficiency virus infection

Jassoy

Heinkelein

Sopper

1997

Pathol. Oncol. Res.

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Infection with the human immunodeficiency virus (HIV) causes gradual depletion of CD4+ T helper lymphocytes and destruction of the lymphoid tissue, which ultimately leads to a fatal defect of the cellular immune system. Paramount to the understanding of the pathogenesis of HIV infection is to elucidate the mechanism which underlies the loss of T helper cells. Various ideas have been proposed in order to explain this issue. Several hypotheses have focused on the role of the envelope glycoprotein in this process. This review summarizes the data obtained and concepts proposed regarding the involvement of the HIV glycoprotein in the pathology of CD4+ T cell depletion.

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Syncytium Formation in Cultured Human Lymphoid Tissue: Fusion of Implanted HIV Glycoprotein 120/41-Expressing Cells with Native CD4⁺Cells

Margolis¹,

Glushakova²,

Baibakov³

et al. 1995

AIDS Research and Human Retroviruses

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While glycoprotein gp120/41 clearly causes HIV-infected cells to form syncytia in monolayers and in suspension, there is unfortunately scant knowledge on syncytium formation in tissues. We implanted gp120/41-expressing cells labeled with fluorescent particles inside blocks of human lymphoid tissue kept in long-term histoculture. Observed by confocal microscopy, together with immunohistochemical and morphological analysis of implanted cells, more than one-third of these gp120/41-expressing cells fused with native CD4+ cells of the host tissue, yielding small (three to five nuclei) syncytia. Such widespread fusion of gp120/41-expressing cells in tissue in vitro, together with the finding of increased virulence of syncytium-inducing isolates of HIV, support the hypothesis that syncytium formation within lymph tissue of HIV-infected individuals contributes to AIDS pathogenesis. This system and the methods developed may provide a way to study HIV-infected cells inside the very tissue whose destruction may prevent immune system repopulation.

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HIV infection and the brain

Cited by 3 publications

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Human immunodeficiency virus type 1-specific cytotoxic T lymphocytes release gamma interferon, tumor necrosis factor alpha (TNF-alpha), and TNF-beta when they encounter their target antigens

Human immunodeficiency virus type 1-specific cytotoxic T lymphocytes release gamma interferon, tumor necrosis factor alpha (TNF-alpha), and TNF-beta when they encounter their target antigens

The role of the envelope glycoprotein in the depletion of T helper cells in human immunodeficiency virus infection

Syncytium Formation in Cultured Human Lymphoid Tissue: Fusion of Implanted HIV Glycoprotein 120/41-Expressing Cells with Native CD4⁺Cells

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HIV infection and the brain

Cited by 3 publications

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Human immunodeficiency virus type 1-specific cytotoxic T lymphocytes release gamma interferon, tumor necrosis factor alpha (TNF-alpha), and TNF-beta when they encounter their target antigens

Human immunodeficiency virus type 1-specific cytotoxic T lymphocytes release gamma interferon, tumor necrosis factor alpha (TNF-alpha), and TNF-beta when they encounter their target antigens

The role of the envelope glycoprotein in the depletion of T helper cells in human immunodeficiency virus infection

Syncytium Formation in Cultured Human Lymphoid Tissue: Fusion of Implanted HIV Glycoprotein 120/41-Expressing Cells with Native CD4+Cells

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Syncytium Formation in Cultured Human Lymphoid Tissue: Fusion of Implanted HIV Glycoprotein 120/41-Expressing Cells with Native CD4⁺Cells