Presence of HIV-1 in human parenchymal and non-parenchymal liver cells in vivo

Housset, Chantal; Lamas, Eugenia; Courgnaud, Valérie; Boucher, O.; Girard, Pierre‐Marie; Marche, C; Bréchot, Christian

doi:10.1016/s0168-8278(05)80579-3

Cited by 78 publications

(50 citation statements)

References 31 publications

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“…This process of general fusion between two membranes (in this case, between the exosomal and target cell membranes) is thought to occur in most cell types as a method of information exchange between cells that does not require direct intercellular contact. It has been shown that HIV is able to infect a broad spectrum of cell types, including cells that lack viral receptors such as fibroblasts (48,49), hepatocytes (50), and epithelial cells (51,52). These observations strongly support the Trojan exosome model, which predicts that many cell types will be infected at low efficiency by the uptake of HIV through the existing pathway for exosomal exchange.…”

Section: Half-maximal Signal Titers In Exosomes For Five Proteins Of mentioning

confidence: 75%

Evidence That HIV Budding in Primary Macrophages Occurs through the Exosome Release Pathway

Nguyen

Booth

Gould

et al. 2003

Journal of Biological Chemistry

297

270

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Section: Half-maximal Signal Titers In Exosomes For Five Proteins Of mentioning

confidence: 75%

Evidence That HIV Budding in Primary Macrophages Occurs through the Exosome Release Pathway

Nguyen

Booth

Gould

et al. 2003

Journal of Biological Chemistry

297

270

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“…Nevertheless, two groups have clearly identified the presence of HIV-1 in hepatocytes in vivo (i.e. RNA, proviral DNA or viral proteins) (Cao et al, 1992;Housset et al, 1993).…”

Section: Introductionmentioning

confidence: 99%

Inefficient fusion due to a lack of attachment receptor/co-receptor restricts productive human immunodeficiency virus type 1 infection in human hepatoma Huh7.5 cells

Fromentin¹,

Tardif²,

Tremblay³

2010

Journal of General Virology

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“…It has been established that HIV-1 infects hepatocytes, Kupffer cells, and endothelial cells in the liver (8,23); cholangiocyte infection has never been documented. During active replication, HIV-1 can also affect uninfected cells via release of HIV-derived soluble peptides from directly infected cells (27,45,46).…”

mentioning

confidence: 99%

The Human Immunodeficiency Virus Type 1 Tat Protein EnhancesCryptosporidium parvum-Induced Apoptosis in Cholangiocytes via a Fas Ligand-Dependent Mechanism

et al. 2007

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While Cryptosporidium parvum infection of the intestine has been reported in both immunocompetent and immunocompromised individuals, biliary infection is seen primarily in adult AIDS patients and is associated with development of AIDS cholangiopathy. However, the mechanisms of pathogen-induced AIDS cholangiopathy remain unclear. Since we previously demonstrated that the Fas/Fas ligand (FasL) system is involved in paracrine-mediated C. parvum cytopathicity in cholangiocytes, we also tested the potential synergistic effects of human immunodeficiency virus type 1 (HIV-1) transactivator of transcription (Tat)-mediated FasL regulation on C. parvum-induced apoptosis in cholangiocytes by semiquantitative reverse transcription-PCR, immunoblotting, immunofluorescence analysis, and immunogold electron microscopy. H69 cells do not express CXCR4 and CCR5, which are receptors required for direct HIV-1 viral infection. However, recombinant biologically active HIV-1-associated Tat protein increased FasL expression in the cytoplasm of cholangiocytes without a significant increase in apoptosis. We found that C. parvum-induced apoptosis was associated with translocation of intracellular FasL to the cell membrane surface and release of full-length FasL from infected H69 cells. Tat significantly (P < 0.05) increased C. parvum-induced apoptosis in bystander cells in a dose-dependent manner. Moreover, Tat enhanced both C. parvum-induced FasL membrane translocation and release of full-length FasL. In addition, the FasL neutralizing antibody NOK-1 and the caspase-8 inhibitor Z-IETD-fmk both blocked C. parvum-induced apoptosis in cholangiocytes. The data demonstrated that HIV-1 Tat enhances C. parvum-induced cholangiocyte apoptosis via a paracrine-mediated, FasL-dependent mechanism. Our results suggest that concurrent active HIV replication, with associated production of Tat protein, and C. parvum infection synergistically increase cholangiocyte apoptosis and thus jointly contribute to AIDS-related cholangiopathies.

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Presence of HIV-1 in human parenchymal and non-parenchymal liver cells in vivo

Cited by 78 publications

References 31 publications

Evidence That HIV Budding in Primary Macrophages Occurs through the Exosome Release Pathway

Evidence That HIV Budding in Primary Macrophages Occurs through the Exosome Release Pathway

Inefficient fusion due to a lack of attachment receptor/co-receptor restricts productive human immunodeficiency virus type 1 infection in human hepatoma Huh7.5 cells

The Human Immunodeficiency Virus Type 1 Tat Protein EnhancesCryptosporidium parvum-Induced Apoptosis in Cholangiocytes via a Fas Ligand-Dependent Mechanism

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