Presence of Host ICAM-1 in Laboratory and Clinical Strains of Human Immunodeficiency Virus Type 1 Increases Virus Infectivity and CD4<sup>+</sup>-T-Cell Depletion in Human Lymphoid Tissue, a Major Site of Replication In Vivo

Bounou, Salim; Leclerc, Jacinthe; Tremblay, Michel J.

doi:10.1128/jvi.76.3.1004-1014.2002

Cited by 185 publications

(177 citation statements)

References 65 publications

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“…The NL4-3 molecular construct was obtained through the National Institutes of Health AIDS Repository Reagent Program. The virus-containing supernatants were filtered through a 0.22-m cellulose acetate syringe filter and normalized for virion content using an inhouse, sensitive, double-Ab sandwich ELISA specific for the viral p24 gag protein (33). All virus preparations underwent only one freezethaw cycle before their use in subsequent experiments.…”

Section: Cell Lines Viruses and Bacteriamentioning

confidence: 99%

Leukotriene B4 Triggers the In Vitro and In Vivo Release of Potent Antimicrobial Agents

Flamand

Tremblay

Borgeat

2007

The Journal of Immunology

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Leukotriene B4 (LTB4) is a bioactive lipid derived from the metabolism of arachidonic acid. Mainly produced by polymorphonuclear leukocytes (PMN) and macrophages, LTB4 triggers several functional responses important in host defense, including the secretion of lysosomal enzymes, the activation of NADPH oxidase activity, NO formation, and phagocytosis. We report that LTB4, but not structural analogs thereof, stimulates primed human PMN to release molecules having potent antimicrobial activities. Exposure of bacteria (Escherichia coli and Staphylococcus aureus) or viruses (herpes simplex virus type 1 and HIV type 1) to supernatants of LTB4-activated PMN lead to ≥90% reduction in infectivity. ELISA and mass spectroscopy analysis of proteins released from LTB4-activated PMN have identified several antimicrobial proteins, including α-defensins, cathepsin G, elastase, lysozyme C, and LL-37, that are likely to participate in the killing of microorganisms. In addition to these in vitro observations, i.v. injections of LTB4 (50 μg/kg) to monkeys led to an increase in α-defensin plasmatic levels and enhanced ex vivo antimicrobial activities of plasma. These results demonstrate the ability of LTB4 to cause the release of potent antimicrobial agents from PMN in vitro as well as in vivo and add further support to the important role of LTB4 in host defense.

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Section: Cell Lines Viruses and Bacteriamentioning

confidence: 99%

Leukotriene B4 Triggers the In Vitro and In Vivo Release of Potent Antimicrobial Agents

Flamand

Tremblay

Borgeat

2007

The Journal of Immunology

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“…The virus-containing supernatants were filtered through a 0.22-m cellulose acetate syringe filter, ultracentrifuged, and normalized for virion content using an in-house sensitive double-antibody sandwich ELISA specific for the viral p24 protein. 18 Preparations of NL4-3 were produced also by acute infection of Raji-CD4 cells. …”

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confidence: 99%

DCIR-mediated enhancement of HIV-1 infection requires the ITIM-associated signal transduction pathway

Lambert

Barabé

Gilbert

et al. 2011

Blood

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Dendritic cell immunoreceptor (DCIR) is IntroductionIt is known that cell-free virions do not efficiently cross genital epithelial cells. Instead HIV-1 uses primarily dendritic cells (DCs) to penetrate the mucosal epithelium. 1,2 The virus is then transferred and disseminated from this entry site to T-cell zones in secondary lymphoid organs, where it can productively infect residing CD4 ϩ T cells. The infection process causes a marked depletion of CD4 ϩ T cells, 3 progressive impairment of the immune system, as well as chronic hyperactivation of both CD4 ϩ and CD8 ϩ T cells. 4 The initial attachment step of HIV-1 to DCs may occur through several complex interactions between the virus and the target cell surface (reviewed in Clapham and McKnight 5 and in Ugolini et al 6 ) such as the association between the oligosaccharides found on the external envelope glycoprotein gp120 and the mannose receptor (CD206), langerin (CD207), or 8 This will result in virus capture and transmission to CD4 ϩ T cells in an effective trans mode 9 (ie, transfer of virions bound onto DCs and/or localized in endosomes). Another lectin receptor, that is, the dendritic cell immunoreceptor (DCIR), can behave as an HIV-1 attachment factor for HIV-1 to participate actively in trans infection of CD4 ϩ T cells. 10 DCIR also contributes to cis-infection events, that is, infection of surrounding CD4 ϩ T cells by virions produced by DCs productively infected with HIV-1. 10 DCIR is a member of a recently described family of C-type lectin receptors (CLRs), which includes DCAR, dectin-2, BDCA-2, MCL, and MINCLE. These receptors carry a single carbohydrate recognition domain (CRD) at the COOH terminal and generally lack consensus signaling motifs in their cytoplasmic region. 11 Several members of the family, however, possess a positively charged residue in their transmembrane region, via which they associate with immunoreceptor tyrosine-based activation motif (ITAM)-containing adaptor molecules, such as the Fc receptor ␥ chains. Importantly, DCIR is the only family member harboring an immunoreceptor tyrosine-based inhibitory motif (ITIM), which is involved in modulation of cellular responses. 12 DCIR is expressed on the surface of most antigen-presenting cells (ie DCs, monocytes, macrophages, and B cells), as well as on granulocytes, and it is differentially expressed depending on the DC maturation status. 13 Lipopolysaccharide, IL-4, and TNF-␣ down-regulate DCIR expression on neutrophils. 14 The ITIM domain of DCIR contains the consensus sequence S/I/V/LxYxxI/V/L, including a tyrosine residue at position 7 (ie, ITYAEV). 13 Generally, when ITIM-containing receptors are engaged, they become tyrosine-phosphorylated and then transmit signals by binding and activating Src homology-2 domain (SH2)-containing tyrosine phosphatases (eg, SHP-1 and SHP-2) and/or the SH2-containing tyrosine inositol phosphate (SHIP). 15 In the case of DCIR, one study has demonstrated that, when phosphorylated, it recruits both SHP-1 and SHP-2. 16 Nevertheless, there is still no e...

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“…Virions were then frozen at Ϫ85°C until assayed. Virus preparations were quantified using an in-house sensitive double Ab sandwich enzymatic specific for the major core viral p24 protein (33).…”

Section: Production Of Virus Stocksmentioning

confidence: 99%

HIV Type 1 Can Act as an APC upon Acquisition from the Host Cell of Peptide-Loaded HLA-DR and CD86 Molecules

Roy

Martin

Giguère

et al. 2005

The Journal of Immunology

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It is well documented that a wide range of host-derived cell surface constituents is inserted within HIV type 1 (HIV-1) and located on the exterior of the virion. Although no virus-associated protein of host origin has been shown to be absolutely required for virus replication, studies have revealed that many of these proteins are functional and can affect several steps of the virus life cycle. In this study, we found that HIV-1 acquires peptide-loaded class II MHC (MHC-II) and the costimulatory CD86 molecules from the host cell. Moreover, we present evidence that virions bearing such peptide-loaded MHC-II and CD86 proteins can lead to activation of the transcription factors NF-κB and NF-AT in an Ag-specific human T cell line. A linear correlation was found between activation of NF-κB and the amount of peptide-loaded MHC-II molecules inserted within HIV-1. Finally, transcription of unintegrated and integrated HIV-1 DNA was promoted upon exposure of peptide-specific human T cells to viruses bearing both peptide-loaded MHC-II and CD86 proteins. These data suggest that HIV-1 can operate as an APC depending on the nature of virus-anchored host cell membrane components. It can be proposed that HIV-1 can manipulate one of its primary targets through the process of incorporation of host-derived proteins.

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Presence of Host ICAM-1 in Laboratory and Clinical Strains of Human Immunodeficiency Virus Type 1 Increases Virus Infectivity and CD4⁺-T-Cell Depletion in Human Lymphoid Tissue, a Major Site of Replication In Vivo

Cited by 185 publications

References 65 publications

Leukotriene B4 Triggers the In Vitro and In Vivo Release of Potent Antimicrobial Agents

Leukotriene B4 Triggers the In Vitro and In Vivo Release of Potent Antimicrobial Agents

DCIR-mediated enhancement of HIV-1 infection requires the ITIM-associated signal transduction pathway

HIV Type 1 Can Act as an APC upon Acquisition from the Host Cell of Peptide-Loaded HLA-DR and CD86 Molecules

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Presence of Host ICAM-1 in Laboratory and Clinical Strains of Human Immunodeficiency Virus Type 1 Increases Virus Infectivity and CD4+-T-Cell Depletion in Human Lymphoid Tissue, a Major Site of Replication In Vivo

Cited by 185 publications

References 65 publications

Leukotriene B4 Triggers the In Vitro and In Vivo Release of Potent Antimicrobial Agents

Leukotriene B4 Triggers the In Vitro and In Vivo Release of Potent Antimicrobial Agents

DCIR-mediated enhancement of HIV-1 infection requires the ITIM-associated signal transduction pathway

HIV Type 1 Can Act as an APC upon Acquisition from the Host Cell of Peptide-Loaded HLA-DR and CD86 Molecules

Contact Info

Product

Resources

About

Presence of Host ICAM-1 in Laboratory and Clinical Strains of Human Immunodeficiency Virus Type 1 Increases Virus Infectivity and CD4⁺-T-Cell Depletion in Human Lymphoid Tissue, a Major Site of Replication In Vivo