Cellular adherence enhances HIV replication in monocytic cells

Shattock, Robin J.; Griffin, George E.

doi:10.1016/s0923-2516(07)80015-x

Cited by 12 publications

(6 citation statements)

References 30 publications

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“…Similar results were obtained for activation of HIV-1 LTR in cultures of peripheral blood lymphocytes and human colonic carcinoma cells (HT29), or HT29 cells only (Faure et al, 1994). Other studies have shown that adherence to tissue-culture plastic or to confluent endothelial cells is essential for enhanced expression of a HIV-LTR reporter construct in lipopolysaccharidestimulated cells and that infected macrophages that adhere to endothelial cells may produce large amounts of HIV-1 (Shattock and Griffin, 1994). These data strongly suggest that NF-KB activation by cellular adhesion and cell-to-cell contact could play an important role in the activation of latent provirus in HIVinfected cells.…”

supporting

confidence: 75%

Cell‐to‐Cell Contact Activates the Long Terminal Repeat of Human Immunodeficiency Virus 1 Through its κB Motif

Faure

Lécine

Lipcey

et al. 1997

European Journal of Biochemistry

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Cell-to-cell contact between peripheral blood lymphocytes and transfected human colonic carcinoma cell line HT29 activates transcription of the long terminal repeats (LTR) of human immunodeficiency virus. HIV-1 LTR transcription is controlled by a complex array of virus-encoded and cellular proteins.Using various constructs expressing a 2acZ reporter gene under the control of the intact or three deleted forms of HIV-1 LTR, we obtained evidence that the KB regulatory elements located in the U3 region are involved in cell-to-cell activation of HIV-1 LTR. Cell-to-cell contact activates in vitro binding of the nuclear factor KB (NF-KB) p50/p65 heterodimer to an HIV-1 KB oligonucleotide. Cell-to-cell contact activation of NF-kB was only partially inhibited by 100 pM pyrrolidine dithiocarbamate and was not correlated with a significant decrease of cellular inhibitor KBa. NF-KB nuclear activation was not detectable before I h after cell contact and was dependent on protein synthesis.

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supporting

confidence: 75%

Cell‐to‐Cell Contact Activates the Long Terminal Repeat of Human Immunodeficiency Virus 1 Through its κB Motif

Faure

Lécine

Lipcey

et al. 1997

European Journal of Biochemistry

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“…It has been reported that interaction of infected macrophages with endothelial cells induces up-regulation of human immunodeficiency virus [24][25][26] and cytomegalovirus [27] replication in macrophages and results in transmission of cytomegalovirus infection to vascular cells [27]. However, enhancement of microbial growth in nonphagocytic vascular cells by monocytes/ macrophages via cell-to-cell contact or soluble mediators has not been reported.…”

Section: Discussionmentioning

confidence: 99%

Monocyte–Endothelial Cell Coculture Enhances Infection of Endothelial Cells withChlamydia pneumoniae

et al. 2000

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To determine the mechanism(s) by which Chlamydia pneumoniae homes to and establishes persistent infection in atheromatous lesions, the effect of the interaction of monocytes/macrophages (U937 cells) with human umbilical vein endothelial cells (HUVECs) and transformed human arterial endothelial cells (HMEC-1s) on the susceptibility of endothelial cells to infection with C. pneumoniae was investigated. Infection was enhanced 4.7-fold (HUVECs) and 4.4-fold (HMEC-1s) after coculture at monocyte-to-endothelial cell ratios of 5 and 2.5, respectively. U937 cells also directly transmitted infection to the endothelial cells, and addition of U937 cell-conditioned media dose-dependently enhanced the infectivity 2.0- to 2.5-fold. The stimulation of infectivity was specific to endothelial cells, because coculturing of monocytes with epithelial cells did not enhance the susceptibility of epithelial cells to infection. The susceptibility of endothelial cells to infection with C. trachomatis and C. psittaci was not enhanced by the monocyte-derived factor(s).

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“…Receptor expression by formerly uninfected cells renders them susceptible to HIV infection. In addition, upregulation of adhesion molecules on inflammatory cells and high local concentrations of HIV support the spread of the virus between cells [12][13][14]. The "damage" caused by the immune response to HIV or other exogenous agents, is dependent on the localization and the degree of "combat": Systemic immune activation appears to accelerate disease progression and significantly decrease survival of patients [5,15,16], but also local immune activation in the genital tract seems to increase the risk of sexual and mother-to child transmission of HIV [17].…”

Section: Human Immunodeficiency Virus Infection and Immune Activationmentioning

confidence: 99%

Indoleamine-2, 3-Dioxygenase and Other Interferon-γ-Mediated Pathways in Patients with Human Immunodeficiency Virus Infection

Schroecksnadel

Zangerle

Bellmann‐Weiler

et al. 2007

CDM

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Human immunodeficiency virus type 1 (HIV) infection is characterized by progressive immunodeficiency despite of an overwhelming cellular immune activation. Patients show highly elevated serum/plasma concentrations of the proinflammatory cytokine interferon-(IFN-), which induces human monocytes to form neopterin, to produce reactive oxygen species (ROS) and in parallel, to degrade tryptophan. Enhanced tryptophan degradation by the enzyme indoleamine-2, 3-dioxygenase (IDO) contributes importantly to disease progression and "complications" of HIV infection: By a subsequent impairment of protein metabolism and serotonin formation, the development of neuropsychiatric disorders and weight loss in HIV infected patients can be enforced. Furthermore, increased IDO-activation efficiently suppresses the growth and proliferation of pathogens as well as host T-cells. IDO and other IFN--mediated pathways are strongly induced in patients with HIV infection and are also linked with disease progression: Neopterin formation by GTPcyclohydrolase I sensitively reflects the stage of the disease, and determination of the pteridine in body fluids is useful to monitor the efficacy of antiretroviral therapy. Neopterin is an independent prognostic factor for the outcome of disease, and well suited to estimate the degree of immune activation in vivo and the responsiveness of immunocompetent cells to stimulation in vitro. ROS formation may contribute to the development of oxidative stress in HIV infection, resulting in depletion of antioxidants. The cause-effective role of an overwhelming Th1-type immune response together with the activation of IDO and other IFN--mediated biochemical pathways for the course of HIV infection, the development of immunodeficiency, anemia and weight loss in HIV patients is discussed.

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Cellular adherence enhances HIV replication in monocytic cells

Cited by 12 publications

References 30 publications

Cell‐to‐Cell Contact Activates the Long Terminal Repeat of Human Immunodeficiency Virus 1 Through its κB Motif

Cell‐to‐Cell Contact Activates the Long Terminal Repeat of Human Immunodeficiency Virus 1 Through its κB Motif

Monocyte–Endothelial Cell Coculture Enhances Infection of Endothelial Cells withChlamydia pneumoniae

Indoleamine-2, 3-Dioxygenase and Other Interferon-γ-Mediated Pathways in Patients with Human Immunodeficiency Virus Infection

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Cellular adherence enhances HIV replication in monocytic cells

Cited by 12 publications

References 30 publications

Cell‐to‐Cell Contact Activates the Long Terminal Repeat of Human Immunodeficiency Virus 1 Through its κB Motif

Cell‐to‐Cell Contact Activates the Long Terminal Repeat of Human Immunodeficiency Virus 1 Through its κB Motif

Monocyte–Endothelial Cell Coculture Enhances Infection of Endothelial Cells withChlamydia pneumoniae

Indoleamine-2, 3-Dioxygenase and Other Interferon-&#947;-Mediated Pathways in Patients with Human Immunodeficiency Virus Infection

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Product

Resources

About

Indoleamine-2, 3-Dioxygenase and Other Interferon-γ-Mediated Pathways in Patients with Human Immunodeficiency Virus Infection