Genetic Protection against Hepatitis B Virus Conferred by<i>CCR5Δ32</i>: Evidence that CCR5 Contributes to Viral Persistence

Thio, Chloe L.; Astemborski, Jacquie; Bashirova, Arman; Mosbruger, Timothy; Greer, Spencer; Witt, Mallory D.; Goedert, James J.; Hilgartner, Margaret W.; Majeske, Audrey J.; O’Brien, Stephen J.; Thomas, David L.; Carrington, Mary

doi:10.1128/jvi.01897-06

Cited by 76 publications

(71 citation statements)

References 40 publications

(38 reference statements)

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“…A number of host genes contain polymorphisms that associate with outcome to HBV infection, including CCR5, RANTES, and, most notably, HLA (24)(25)(26)(27). A recent GWAS confirmed the primary involvement of HLA class II with chronic HBV infection, but surprisingly, the most significant genetic marker correlating with HBV outcome resided in the HLA-DP region (8) rather than in the commonly investigated HLA-DR and -DQ genes.…”

Section: Discussionmentioning

confidence: 99%

A Novel Variant Marking HLA-DP Expression Levels Predicts Recovery from Hepatitis B Virus Infection

Thomas

Thio

Apps

et al. 2012

J Virol

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144

186

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:01), whereas 550A/G does not. 496A/G has a stronger effect than any individual HLA-DPB1 or DPA1 allele and any other HLA alleles that showed an association with HBV recovery in our European-American cohort. The 496GG genotype, which confers recessive susceptibility to HBV persistence, also associates in a recessive manner with significantly higher levels of HLA-DP surface protein and transcript level expression in healthy donors, suggesting that differences in expression of HLA-DP may increase the risk of persistent HBV infection.

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Section: Discussionmentioning

confidence: 99%

A Novel Variant Marking HLA-DP Expression Levels Predicts Recovery from Hepatitis B Virus Infection

Thomas

Thio

Apps

et al. 2012

J Virol

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144

186

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“…This has led to suggestions that interspecific interactions are of little importance in shaping pathogen communities under natural conditions [6][7][8][9][10][11][12][13][14][15][16]. This debate continues despite the fact that the importance of pathogen interactions is becoming increasingly obvious in clinical settings [17][18][19][20][21]. One possible explanation for the apparent lack of interactions between pathogen species in wild host systems is that the pathogens may be temporally asynchronous within their hosts, resulting in a form of niche segregation and reducing the likelihood of direct interaction [12,22].…”

Section: Introductionmentioning

confidence: 97%

Pathogen Interactions, Population Cycles, and Phase Shifts

Lello¹,

Norman²,

Boag³

et al. 2008

The American Naturalist

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Interspecific pathogen interactions can profoundly affect pathogen population dynamics and the efficacy of control strategies. However, many pathogens exhibit cyclic abundance patterns (e.g. seasonality) and temporal asynchrony between interacting pathogens has the potential to reduce the impact of those interactions. Here we use an extension of our previously published model to investigate the effects of cyclic abundance patterns on pathogen interaction. We demonstrate that for interactions mediated through host immunity, immune memory can maintain the impact of an interaction even when the effector pathogen abundance is low or the pathogen is absent. Paradoxically, immune memory can result in pathogens interacting more strongly when temporally out of phase.We find that interactions between species can not only alter pathogen abundance but can also result in changes to the temporal pattern of the affected species. We further demonstrate that this phenomenon may be observed in a natural host / pathogen data set.Given that there is both a continuing debate as to the relevance of pathogen interactions in natural systems and increasing concern regarding treatment of coinfections of veterinary and medical importance, both the discovery of this measurable shift in cycle in the empirical data and the mechanism by which we identified the shift are important. Finally, as the model structure used here is analogous to simple predator-prey system models we also consider the consequences of these findings in the context of that system.

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“…Most individuals who acquire HBV infection as adults sponta- neously clear it. 5,6 In those who progress to chronic HBV infection, the initial phase is typically immune active; the liver is injured by inflammation (necroinflammation) and develops scarring that can progress to cirrhosis. Hepatitis B e antigen (HBeAg) status has been used to classify the natural history of infection.…”

Section: Natural History Of Chronic Hbv Infectionmentioning

confidence: 99%

The Dawn of a New Era: Transforming Our Domestic Response to Hepatitis B & C

El–Serag

Lok²,

Thomas

2010

Gastroenterology

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Genetic Protection against Hepatitis B Virus Conferred byCCR5Δ32: Evidence that CCR5 Contributes to Viral Persistence

Abstract: Recovery from acute hepatitis B virus (HBV) infection requires a broad, vigorous T-cell response, which is

Cited by 76 publications

References 40 publications

A Novel Variant Marking HLA-DP Expression Levels Predicts Recovery from Hepatitis B Virus Infection

A Novel Variant Marking HLA-DP Expression Levels Predicts Recovery from Hepatitis B Virus Infection

Pathogen Interactions, Population Cycles, and Phase Shifts

The Dawn of a New Era: Transforming Our Domestic Response to Hepatitis B & C

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