Is HIV infection a TNF receptor signalling-driven disease?

Herbein, Georges; Khan, Kashif Aziz

doi:10.1016/j.it.2007.10.008

Cited by 93 publications

(96 citation statements)

References 63 publications

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“…TNFα significantly contributes to the elimination of infectious factors (Keefe et al 1997), and it can also promote the progression of disease (Herbein and Khan 2008). Viruses can modulate or deregulate the TNF/TNFR pathway to evade the immune response and facilitate viral dissemination (Herbein and O'Brien 2000).…”

Section: Discussionmentioning

confidence: 99%

“…Viruses can modulate or deregulate the TNF/TNFR pathway to evade the immune response and facilitate viral dissemination (Herbein and O'Brien 2000). Many viruses, including cowpox, poxvirus, EBV and HIV, encode proteins that can bind with TNFα and/or the TNFR component to inhibit TNFα functions or modulate the TNF signaling pathway (Rahman andMcFadden 2006, Herbein andKhan 2008). Some viruses, such as HIV (subfamily Lentiviridae), use the complement system to penetrate the cell, maximize replication and spread through the host's body (Stoiber et al 1997, Bouhlal et al 2007.…”

Section: Discussionmentioning

confidence: 99%

“…Similarly to humans, mTNFα could also be used by viral protein/proteins in cattle to modulate the TNF/TNFR signaling pathway and control BLV replication in CD11b+TNFα+p24+ cells. In early stages of infection, viral proteins (mainly Nef, Vpr and Tat) modulate the TNF/TNFR signaling pathway, thus enhancing HIV replication and virion production in infected CD4+ T-cells and macrophages (Herbein and Khan 2008).…”

Section: Discussionmentioning

confidence: 99%

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Tumor necrosis factor-alpha (TNFα) gene polymorphism and expression of membrane-bound TNFα protein on CD11b+ and IgM+ cells in cows naturally infected with bovine leukemia virus

Bojarojć-Nosowicz¹,

Kaczmarczyk²,

Stachura³

et al. 2015

Polish Journal of Veterinary Sciences

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The aim of this study was to determine whether SNP at position -824 (promoter region) of the TNFα gene significantly differentiates the size of IgM+, CD5+ and CD11b+ cell subpopulations and affects the expression of membrane-bound TNFα protein (mTNFα) on these cells and their susceptibility to BLV infections.In this study, significant differences were determined for the first time between TNFα genotypes and the percentage of cells with the CD11b+TNFα+p24+ immunophenotype. Furthermore, greater expansion of lymphocytes with the IgM+TNFα+p24+ immunophenotype was reported in cows with the G/G genotype than in A/A homozygotes. Cells with the above immunophenotype were more frequently observed in cows with persistent leukocytosis than in aleukemic cattle.Our results suggest that polymorphism of the TNFα -824 A>G gene and mTNFα protein expression play an important role in the pathogenesis of enzootic bovine leukosis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Tumor necrosis factor-alpha (TNFα) gene polymorphism and expression of membrane-bound TNFα protein on CD11b+ and IgM+ cells in cows naturally infected with bovine leukemia virus

Bojarojć-Nosowicz¹,

Kaczmarczyk²,

Stachura³

et al. 2015

Polish Journal of Veterinary Sciences

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“…+ T-cell depletion due to chronic immune activation Prolonged exposure of CD4 + T-cells to HIV-derived proteins such as Vpr and Tat, as well as to the family of common γ-chain cytokines (interleukin (IL)-2, -4, -7, -9, -15 and -21), represent generalised mechanisms of apoptosis mediated by various pathways [29][30][31][32]. These include Fas/Fas ligand, tumour necrosis factor (TNF)/TNF receptor-1/-2, TNF-related apoptosis-inducing ligand/death receptors 4/5 and others, programmed death receptor (PD)-1 and its ligand (PD-L1) and apoptotic microparticles released from apoptotic cells [29][30][31][32].…”

Section: Cd4mentioning

confidence: 99%

Impact of HIV infection and smoking on lung immunity and related disorders

2015

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HIV-infected persons not only have higher rates of smoking than the general population, but are also unusually vulnerable to the associated adverse health effects, both infective and noninfective in origin. Indeed, in the setting of well-organised care and availability of highly active antiretroviral therapy, HIV-infected smokers lose more life-years to smoking than to HIV infection per se, presenting a major challenge to healthcare providers. Not surprisingly, the respiratory system is particularly susceptible to the damaging interactive chronic inflammatory and immunosuppressive effects of HIV and smoking, intensifying the risk of the development of opportunistic infections, as well as lung cancer and obstructive lung disorders. The impact of smoking on the immunopathogenesis and frequencies of these respiratory conditions in the setting of HIV infection, as well as on the efficacy of antiretroviral therapy, represent the primary focus of this review. @ERSpublications Smoking exacerbates the immunosuppressive/pro-inflammatory effects of HIV, increasing the risk of pulmonary disease

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“…The mechanism inducing apoptosis resistance of persistently infected cells is not well understood yet. It has been proposed that the modulation of TNFR signaling by viral proteins such as Tat, Nef, and Vpr could explain the formation of viral reservoirs during HIV-1 infection [107]. Recently, a microarray approach has been used to investigate the gene expression signature in the circulating monocytes from HIV-1-infected patients [105].…”

Section: Establishment Of Hiv-1 Latencymentioning

confidence: 99%