The CCR5-∆32 Mutation: Impact on Disease Outcome in Individuals with Hepatitis B Infection in the Southern Khorasan Population (East of Iran)
Background: Hepatitis B virus (HBV) is the main infectious agent that causes liver disease and may lead to an acute or chronic HBV infection. Evidence from many studies have determined that host genetic factors play a significant role in determining immunization, clinical course, and recovery from H...
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Veröffentlicht in: | Hepatitis monthly 2017-10, Vol.17 (10) |
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Sprache: | eng |
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Zusammenfassung: | Background: Hepatitis B virus (HBV) is the main infectious agent that causes liver disease and may lead to an acute or chronic HBV infection. Evidence from many studies have determined that host genetic factors play a significant role in determining immunization, clinical course, and recovery from HBV infection. A 32-bp deletion in the region of CCR5 gene (CCR5 ∆32) is one of the mutations that is known to provide genetic protection against chronic HBV infections. Objectives: In this study, the researchers aimed at assessing the protective effect of CCR5 ∆32 in subjects, who had recovered from HBV infection, as well as subjects that developed chronic HBV infection, in Birjand, Iran. Methods: The study consisted of 60 patients with chronic HBV infection (patient group) and 120 patients, who had previously recovered from HBV infection (control group). Genomic DNA was extracted from blood samples by the salting out method, and then samples were analyzed for the CCR5 ∆32 genotype utilizing the gap-polymerase chain reaction (Gap-PCR) technique. Variables were analyzed using the Chi-square test and P values less than 0.05 were considered as statistically significant. Results: The researchers found only one heterozygous CCR5 ∆32 mutation in the control group and absolutely no homozygous CCR5 Δ32 mutation in either the patient or control group. Conclusions: Because of no significant visible correlation between carrying the mutation and the possibility of recovery from HBV infection in the city of Birjand, it seems the protective effect of this mutation is absent in Birjand’s population. |
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ISSN: | 1735-143X 1735-3408 |
DOI: | 10.5812/hepatmon.55014 |