scholarly journals Host genetic factors associated with hepatitis B virus infection and progression to chronic disease: A systematic review and Meta analysis

Author(s):  
Hussein Mukasa Kafeero ◽  
Dorothy Ndagire Ndagire ◽  
Hasifah Nanyingi Nanyingi ◽  
Hakim Sendagire Sendagire

Abstract Abstract Back ground Contradicting results from many laboratories on the role of genetic factors in the susceptibility/resistance to hepatitis B infection have been reported. In this review we examined 27 published full research articles and assessed the role of Th1/Th2 cytokine promoter and vitamin D receptor gene polymorphisms. We summarized the available data on the relationship between the gene polymorphisms and susceptibility/resistance to hepatitis B virus infection together with likely disease evolution to come up with candidate single nucleotide polymorphisms implicated in the disease state with the population. Method The study was done in tandem with the PRISMA standards and the Cochran’s Q test, I2 statistics for heterogeneity and the Odds ratio were calculated using a commercially available soft ware called MedCalcs (http://www.medcalc.org). A random effects model was used to pool the odds ratio for heterogeneities ≥50% or else a fixed effects model was used. All analyses were done at 95% Confidence Interval and a P<0.05 was considered statistically significant. Results We found that IL-10-592C/A genotype AA (P=0.017, OR=0.752, 95%CI=0.595 to 0.950) and TNF-α-238G/A genotype AA+ AG (P<0.001, OR=0.407, 95%CI=0.005 to 30.1) were significantly associated with reduced risk of hepatitis B infection by the random effects model. TNF-α-238G/A genotype GG had the risk of chronic infection (OR=3.587, 95% CI= 0.127 to 101.176) under the random effect model. Most of the other SNPs had borderline risk of HBV infection (OR 0.6 to 1.12) with a few cases of high risk, IL-10-1082A/G genotype AA (OR=1.608, 95%CI=0.861 to 3.003) and reduced risk, IL-10-1082A/G genotype AG (OR=0.485, 95% CI=0.232 to 1.014) Conclusion We found that IL-10-592C/A genotype AA and TNF-α-238G/A genotype AA+ AG were significantly associated with reduced risk of hepatitis B infection.

2004 ◽  
Vol 16 (8) ◽  
pp. 801-807 ◽  
Author(s):  
Harry LA Janssen ◽  
Monika van Zonneveld ◽  
Andeltje B van Nunen ◽  
Hubert GM Niesters ◽  
Solko W Schalm ◽  
...  

Addiction ◽  
2006 ◽  
Vol 101 (5) ◽  
pp. 726-730 ◽  
Author(s):  
Tara M. Vogt ◽  
Joseph F. Perz ◽  
Clayton K. Van Houten ◽  
Robert Harrington ◽  
Tia Hansuld ◽  
...  

2001 ◽  
Vol 75 (1) ◽  
pp. 215-225 ◽  
Author(s):  
Fei Su ◽  
Christian N. Theodosis ◽  
Robert J. Schneider

ABSTRACT Chronic infection with hepatitis B virus (HBV) promotes a high level of liver disease and cancer in humans. The HBV HBx gene encodes a small regulatory protein that is essential for viral replication and is suspected to play a role in viral pathogenesis. HBx stimulates cytoplasmic signal transduction pathways, moderately stimulates a number of transcription factors, including several nuclear factors, and in certain settings sensitizes cells to apoptosis by proapoptotic stimuli, including tumor necrosis factor alpha (TNF-α) and etopocide. Paradoxically, HBx activates members of the NF-κB transcription factor family, some of which are antiapoptotic in function. HBx induces expression of Myc protein family members in certain settings, and Myc can sensitize cells to killing by TNF-α. We therefore examined the roles of NF-κB, c-Myc, and TNF-α in apoptotic killing of cells by HBx. RelA/NF-κB is shown to be induced by HBx and to suppress HBx-mediated apoptosis. HBx also induces c-Rel/NF-κB, which can promote apoptotic cell death in some contexts or block it in others. Induction of c-Rel by HBx was found to inhibit its ability to directly mediate apoptotic killing of cells. Thus, HBx induction of NF-κB family members masks its ability to directly mediate apoptosis, whereas ablation of NF-κB reveals it. Investigation of the role of Myc protein demonstrates that overexpression of Myc is essential for acute sensitization of cells to killing by HBx plus TNF-α. This study therefore defines a specific set of parameters which must be met for HBx to possibly contribute to HBV pathogenesis.


1986 ◽  
Vol 16 (4) ◽  
pp. 543-548
Author(s):  
Emanuele Calabrese ◽  
Eleonora Gonnelli ◽  
Silvia Ambu ◽  
Valentino Patussi ◽  
Stefano Milani ◽  
...  

2020 ◽  
Vol 177 ◽  
pp. 104765 ◽  
Author(s):  
Tian Wu ◽  
Nan Wu ◽  
Yan-Xiu Ma ◽  
Jing Wu ◽  
Yan Gao ◽  
...  

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