scholarly journals GAS5 rs2067079 and miR-137 rs1625579 functional SNPs and risk of chronic hepatitis B virus infection among Egyptian patients

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Rania H. Mahmoud ◽  
Enas Mamdouh Hefzy ◽  
Olfat G. Shaker ◽  
Tarek I. Ahmed ◽  
Noha K. Abdelghaffar ◽  
...  

AbstractHepatitis B virus (HBV) infection is a significant health issue worldwide.. We attempted to fulfill the molecular mechanisms of epigenetic and genetic factors associated with chronic HBV (CHBV). Expression levels of the lncRNA growth arrest-specific 5 (GAS5) and miR-137 and their corresponding SNPs, rs2067079 (C/T) and rs1625579 (G/T) were analyzed in 117 CHBV patients and 120 controls to investigate the probable association between these biomarkers and CHBV pathogenesis in the Egyptian population. Serum expression levels of GAS5 and miR-137 were significantly down-regulated in cases vs controls. Regarding GAS5 (rs2067079), the mutant TT genotype showed an increased risk of CHBV (p < 0.001), while the dominant CC was a protective factor (p = 0.004). Regarding miR-137 rs1625579, the mutant genotype TT was reported as a risk factor for CHBV (p < 0.001) and the normal GG genotype was a protective factor, p < 0.001. The serum GAS5 was significantly higher in the mutant TT genotype of GAS5 SNP as compared to the other genotypes (p = 0.007). Concerning miR-137 rs1625579, the mutant TT genotype was significantly associated with a lower serum expression level of miR-137 (p = 0.018). We revealed the dysregulated expression levels of GAS5 and miR-137 linked to their functioning SNPs were associated with CHBV risk and might act as potential therapeutic targets.

2015 ◽  
Vol 88 (5) ◽  
pp. 837-842 ◽  
Author(s):  
Rabab Fouad ◽  
Mahmoud Abdo ◽  
Hadeel Gamal Eldeen ◽  
Dina Sabry ◽  
Mira Atef ◽  
...  

2021 ◽  
Vol 4 (9) ◽  
pp. e202101036
Author(s):  
Frank Jühling ◽  
Antonio Saviano ◽  
Clara Ponsolles ◽  
Laura Heydmann ◽  
Emilie Crouchet ◽  
...  

Chronic hepatitis B virus (HBV) infection is a major cause of hepatocellular carcinoma (HCC) world-wide. The molecular mechanisms of viral hepatocarcinogenesis are still partially understood. Here, we applied two complementary single-cell RNA-sequencing protocols to investigate HBV–HCC host cell interactions at the single cell level of patient-derived HCC. Computational analyses revealed a marked HCC heterogeneity with a robust and significant correlation between HBV reads and cancer cell differentiation. Viral reads significantly correlated with the expression of HBV-dependency factors such as HLF in different tumor compartments. Analyses of virus-induced host responses identified previously undiscovered pathways mediating viral carcinogenesis, such as E2F- and MYC targets as well as adipogenesis. Mapping of fused HBV–host cell transcripts allowed the characterization of integration sites in individual cancer cells. Collectively, single-cell RNA-Seq unravels heterogeneity and compartmentalization of both, virus and cancer identifying new candidate pathways for viral hepatocarcinogenesis. The perturbation of pro-carcinogenic gene expression even at low HBV levels highlights the need of HBV cure to eliminate HCC risk.


2020 ◽  
Vol 23 ◽  
pp. S168-S169
Author(s):  
M.H.M. Solayman ◽  
N.E.S. Nassar ◽  
S.A. Abdel-kader ◽  
S. Afify ◽  
H. Soltan ◽  
...  

2020 ◽  
Vol 22 (1) ◽  
pp. 213
Author(s):  
Hye Won Lee ◽  
Jae Seung Lee ◽  
Sang Hoon Ahn

Chronic hepatitis B virus (HBV) infection is a major global health problem. It can cause progressive liver fibrosis leading to cirrhosis with end-stage liver disease, and a markedly increased risk of hepatocellular carcinoma. In the last two decades, substantial progress has been made in the treatment of chronic hepatitis, B. However, HBV is often reactivated after stopping nucloes(t)ide analogues because antivirals alone do not directly target covalently closed circular DNA, which is the template for all viral RNAs. Therefore, although currently available antiviral therapies achieve suppression of HBV replication in the majority of patients, hepatitis B surface antigen (HBsAg) loss and seroconversion is rarely achieved despite long-term antiviral treatment (HBsAg loss of less than 10% in 5 years). Various clinical trials of agents that interrupt the HBV life cycle in hepatocytes have been conducted. Potential treatment strategies and new agents are emerging as HBV cure. A combination of current and new anti-HBV agents may increase the rate of HBsAg seroclearance; thus, optimized regimens must be validated. Here, we review the newly investigated therapeutic compounds and the results of preclinical and/or clinical trials.


PEDIATRICS ◽  
1983 ◽  
Vol 71 (2) ◽  
pp. 289-292
Author(s):  
JAMES CHIN

Transmission of hepatitis B virus (HBV) from mothers who either have an acute HBV infection or who are chronic hepatitis B surface antigen (HBsAg) carriers to their infants has been well documented.1-3 In countries where HBV is hyperendemic, transmission from carrier mothers to their infants has been estimated to be the cause of 20% to 40% of all chronic HBV carriers in the population. Such transmission might account for as many as 50 million chronic HBV carriers throughout the world. Most HBV infections in infants are asymptomatic. Infected infants who develop antibody to HBsAg (anti-HBs) are presumably immune for life and are not believed to be at any increased risk of subsequent liver disease.


2020 ◽  
Vol 222 (8) ◽  
pp. 1345-1352 ◽  
Author(s):  
Wei-Yuan Chang ◽  
Yen-Cheng Chiu ◽  
Fang-Wei Chiu ◽  
Yao-Chun Hsu ◽  
Tai-Chung Tseng ◽  
...  

Abstract Background Prophylaxis with nucleos(t)ide analogue (NA) is recommended to prevent hepatitis B virus (HBV) reactivation in hepatitis B surface antigen (HBsAg)–positive patients receiving rituximab-based B-cell depletion therapy. However, little is known about the risk of clinical relapse after withdrawal of NA. Methods We retrospectively analyzed 77 noncirrhotic HBsAg carriers with hematological cancer who received rituximab-containing chemotherapy. All of them received either prophylactic entecavir or tenofovir therapy. The risk of clinical relapse and hepatic decompensation after cessation of NA was explored. Results Clinical relapse and hepatic decompensation developed in 25 (32.5 %) and 11 (14.3 %) of the patients, respectively, and 2 patients died of hepatic decompensation. Most of the hepatic events occurred within 1 year (20 of 25; 80.0%) after stopping NA. A higher pretreatment viral load (≥2000 vs &lt;2000 IU/mL) was associated with increased risks of clinical relapse (hazard ratio, 3.47; 95% confidence interval, 1.56–7.73) and hepatic decompensation (9.91; 2.14–45.92). Of 51 patients with pretreatment viral load &lt;2000 IU/mL, clinical relapse occurred in 10 (19.6 %) and hepatic decompensation in 2 (3.9%). Conclusions Pretreatment HBV DNA ≥2000 IU/mL is associated with increased risk of liver-related disease after cessation of prophylactic NA therapy in patients who received rituximab-containing chemotherapy.


2017 ◽  
Vol 4 (suppl_1) ◽  
pp. S41-S41
Author(s):  
Ruth Link-Gelles ◽  
Alaya Koneru ◽  
Julie Lazaroff ◽  
Patrick Fineis ◽  
Noele Nelson ◽  
...  

Abstract Background Individuals with chronic hepatitis B virus (HBV) infection are at increased risk for cirrhosis and hepatocellular carcinoma. Chronic HBV infection develops in 90% of persons infected at birth. Although postexposure prophylaxis (PEP), consisting of hepatitis B vaccine and immune globulin at birth, and completion of the three-dose vaccine series prevents up to 95% of perinatal HBV infections; however, breakthrough infections can occur, especially among infants born to women with high viral loads (VLs). Maternal antiviral treatment during pregnancy can reduce perinatal HBV transmission by 70% above the effect of infant PEP alone. We assessed factors associated with maternal antiviral treatment in a cohort of HBV-infected pregnant women with high VL. Methods During 2013–2015, the CDC-funded Supplemental Perinatal Hepatitis B Prevention Program collected information from interviews and medical charts of HBV-infected pregnant women in two sites. We assessed the association of demographic and clinical factors with maternal treatment in women with high VL (&gt;200,000 IU/mL), considering statistical significance at P &lt; 0.05. Results Among 1,521 women with maternal treatment and VL data, 151 (10%) had high VL. Among these 151 women, 66 (44%) received antiviral treatment (Table), all of whom were of Asian/Pacific Island race. None of the seven women of other races were treated (P = 0.02). Fifty-nine women (48%) receiving Medicaid were treated compared with six women (24%) who had private insurance (P = 0.04). Conclusion Mother’s race, country of birth, and insurance status were significantly associated with treatment in women with high VL. Because most women with high VL did not receive antiviral treatment during pregnancy, opportunities to reduce perinatal HBV transmission exist. Disclosures All authors: No reported disclosures.


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