Could FIV zoonosis responsible of the breakdown of the pathocenosis which has reduced the European CCR5-Delta32 allele frequencies

Faure, Éric

doi:10.1186/1743-422x-5-119

Cited by 2 publications

(2 citation statements)

References 163 publications

(254 reference statements)

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“…Subsequently, a deletion polymorphism in CCR5, known as CCR5delta32, was recognized and found to lead to near complete resistance to HIV‐1 infection in the homozygous state, and slower progression to AIDS in heterozygotes (Dean et al ., 1996; Huang et al ., 1996; Liu et al ., 1996; Samson et al ., 1996b; Zimmerman et al ., 1997). The age of this polymorphism is still in dispute (Stephens et al ., 1998; Hummel et al ., 2005), as are the selection pressures that lead to the maintenance of this polymorphism (Novembre et al ., 2005; Cohn and Weaver, 2006; Hedrick and Verrelli, 2006; Faure, 2008; Faure and Royer‐Carenzi, 2008). This 32 base pair deletion causes a shift in the reading frame, the creation of an early stop codon and the production of a truncated protein that is retained in the endoplasmic reticulum.…”

Section: Ccr5 Is a Co‐receptor For Hiv Infectionmentioning

confidence: 99%

Chemokine receptor CCR5: from AIDS to atherosclerosis

Jones

Maguire

Davenport

2011

British J Pharmacology

153

123

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There is increasing recognition of an important contribution of chemokines and their receptors in the pathology of atherosclerosis and related cardiovascular disease. The chemokine receptor CCR5 was initially known for its role as a co-receptor for HIV infection of macrophages and is the target of the recently approved CCR5 antagonist maraviroc. However, evidence is now emerging supporting a role for CCR5 and its ligands CCL3 (MIP-1α), CCL4 (MIP-1β) and CCL5 (RANTES) in the initiation and progression of atherosclerosis. Specifically, the CCR5 deletion polymorphism CCR5delta32, which confers resistance to HIV infection, has been associated with a reduced risk of cardiovascular disease and both CCR5 antagonism and gene deletion reduce atherosclerosis in mouse models of the disease. Antagonism of CCL5 has also been shown to reduce atherosclerotic burden in these animal models. Crucially, CCR5 and its ligands CCL3, CCL4 and CCL5 have been identified in human and mouse vasculature and have been detected in human atherosclerotic plaque. Not unexpectedly, CC chemokines have also been linked to saphenous vein graft disease, which shares similarity to native vessel atherosclerosis. Distinct roles for chemokine-receptor systems in atherogenesis have been proposed, with CCR5 likely to be critical in recruitment of monocytes to developing plaques. With an increased burden of cardiovascular disease observed in HIV-infected individuals, the potential cardiovascular-protective effects of drugs that target the CCR5 receptor warrant greater attention. The availability of clinically validated antagonists such as maraviroc currently provides an advantage for targeting of CCR5 over other chemokine receptors.

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Section: Ccr5 Is a Co‐receptor For Hiv Infectionmentioning

confidence: 99%

Chemokine receptor CCR5: from AIDS to atherosclerosis

Jones

Maguire

Davenport

2011

British J Pharmacology

153

123

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“…The first virus, feline immunodeficiency virus (FIV), uses Felis catus (domestic cat) as its primary host and CD4 as its receptor. According to the literature [ 22 , 23 ], FIV infection of humans is rare but has been reported. Our method categorized this case as near-infection (G = 3).…”

Section: Resultsmentioning

confidence: 99%

Classification of viral zoonosis through receptor pattern analysis

Bae

Son

2011

BMC Bioinformatics

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BackgroundViral zoonosis, the transmission of a virus from its primary vertebrate reservoir species to humans, requires ubiquitous cellular proteins known as receptor proteins. Zoonosis can occur not only through direct transmission from vertebrates to humans, but also through intermediate reservoirs or other environmental factors. Viruses can be categorized according to genotype (ssDNA, dsDNA, ssRNA and dsRNA viruses). Among them, the RNA viruses exhibit particularly high mutation rates and are especially problematic for this reason. Most zoonotic viruses are RNA viruses that change their envelope proteins to facilitate binding to various receptors of host species. In this study, we sought to predict zoonotic propensity through the analysis of receptor characteristics. We hypothesized that the major barrier to interspecies virus transmission is that receptor sequences vary among species--in other words, that the specific amino acid sequence of the receptor determines the ability of the viral envelope protein to attach to the cell.ResultsWe analysed host-cell receptor sequences for their hydrophobicity/hydrophilicity characteristics. We then analysed these properties for similarities among receptors of different species and used a statistical discriminant analysis to predict the likelihood of transmission among species.ConclusionsThis study is an attempt to predict zoonosis through simple computational analysis of receptor sequence differences. Our method may be useful in predicting the zoonotic potential of newly discovered viral strains.

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Could FIV zoonosis responsible of the breakdown of the pathocenosis which has reduced the European CCR5-Delta32 allele frequencies

Cited by 2 publications

References 163 publications

Chemokine receptor CCR5: from AIDS to atherosclerosis

Chemokine receptor CCR5: from AIDS to atherosclerosis

Classification of viral zoonosis through receptor pattern analysis

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