PMID- 33038386 OWN - NLM STAT- MEDLINE DCOM- 20211118 LR - 20211118 IS - 1879-0542 (Electronic) IS - 0165-2478 (Linking) VI - 228 DP - 2020 Dec TI - IL-18 variant increases risk of enhanced HBV DNA replication in chronic hepatitis. PG - 70-75 LID - S0165-2478(20)30398-9 [pii] LID - 10.1016/j.imlet.2020.10.002 [doi] AB - BACKGROUND: The outcome ofhepatitis B (HBV) infection is influenced by immune responses and host genetics. Interleukin-18 (IL-18) is a determinant factor in controlling the balance of Th1/Th2 during antiviral response.Weexamine therole of two functional polymorphisms -607A/C and-137A/C inIL-18 gene with risk of chronic HBV infection. METHODS AND RESULTS: Genomic DNA isolates were obtained from 200 seropositive cases stratified according to their HBV DNA loads, and 200 blood donorsas a control population. Genotypes of the two polymorphisms were identified by ARMS-PCR method. The -607A allele, the-607AA and -607AC genotypes were associated with increased risk to develop chronic HBV infection (1.98, 5.11 and 3.5-fold risks, respectively). By contrast, the -137C minor allele and CG genotype had protected effects against chronic HBV infection. We found that -607A allele, -607AA and -607AC genotypes were significantly more frequent in patient's group with high HBV DNA levels compared to patient group with low HBV DNA level. Additionally, they were associated with increased 1.72, 6.04 and 3.28-fold risk of high HBV DNA replication. Patients carrying "-607A/-137 C" or "-607A/-137 G" haplotypes presented a high risk to develop chronic HBV infection (OR = 3.27; OR = 4.32, respectively). CONCLUSIONS: Taken together, our data suggest that theIL-18 -607A/C functional polymorphism was associated with susceptibility to enhanced replicative form of HBV DNA in chronic infection. CI - Copyright (c) 2020. Published by Elsevier B.V. FAU - Ben Selma, Walid AU - Ben Selma W AD - Laboratory of Microbiology, UR12SP34, University Hospital Farhat Hached, Sousse, Tunisia; Laboratory of Biological and Genetic Markers Studying for Early Diagnosis and Follow-Up of Neurological Diseases, LR18ES47, Faculty of Medicine, Sousse, Tunisia; Higher Institute of Applied Sciences and Technology, Mahdia, Tunisia. Electronic address: walid.bensalma@issatmh.u-monastir.tn. FAU - Alibi, Sana AU - Alibi S AD - Laboratory of Biological and Genetic Markers Studying for Early Diagnosis and Follow-Up of Neurological Diseases, LR18ES47, Faculty of Medicine, Sousse, Tunisia. FAU - Smach, Mohamed Ali AU - Smach MA AD - Laboratory of Biological and Genetic Markers Studying for Early Diagnosis and Follow-Up of Neurological Diseases, LR18ES47, Faculty of Medicine, Sousse, Tunisia. FAU - Saad, Afef AU - Saad A AD - Department of Microbiology, Faculty of Medicine, Sousse, Tunisia. FAU - Boukadida, Jalel AU - Boukadida J AD - Laboratory of Microbiology, UR12SP34, University Hospital Farhat Hached, Sousse, Tunisia; Laboratory of Biological and Genetic Markers Studying for Early Diagnosis and Follow-Up of Neurological Diseases, LR18ES47, Faculty of Medicine, Sousse, Tunisia; Department of Microbiology, Faculty of Medicine, Sousse, Tunisia. LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20201007 PL - Netherlands TA - Immunol Lett JT - Immunology letters JID - 7910006 RN - 0 (DNA, Viral) RN - 0 (IL18 protein, human) RN - 0 (Interleukin-18) SB - IM MH - Adult MH - Aged MH - *DNA Replication MH - DNA, Viral/*biosynthesis/genetics MH - Female MH - Genetic Predisposition to Disease MH - Haplotypes MH - Hepatitis B virus/genetics/*growth & development/immunology MH - Hepatitis B, Chronic/diagnosis/*genetics/immunology/virology MH - Humans MH - Interleukin-18/*genetics MH - Male MH - Middle Aged MH - *Polymorphism, Single Nucleotide MH - Protective Factors MH - Retrospective Studies MH - Risk Assessment MH - Risk Factors MH - Tunisia MH - *Virus Replication MH - Young Adult OTO - NOTNLM OT - Chronic HBV infection OT - DNA replication OT - Interleukin-18 OT - Polymorphism OT - Susceptibility EDAT- 2020/10/11 06:00 MHDA- 2021/11/19 06:00 CRDT- 2020/10/10 20:09 PHST- 2020/07/15 00:00 [received] PHST- 2020/09/24 00:00 [revised] PHST- 2020/10/01 00:00 [accepted] PHST- 2020/10/11 06:00 [pubmed] PHST- 2021/11/19 06:00 [medline] PHST- 2020/10/10 20:09 [entrez] AID - S0165-2478(20)30398-9 [pii] AID - 10.1016/j.imlet.2020.10.002 [doi] PST - ppublish SO - Immunol Lett. 2020 Dec;228:70-75. doi: 10.1016/j.imlet.2020.10.002. Epub 2020 Oct 7.