scholarly journals Roles of Toll-like Receptor 3 in Intrauterine Transmission of Hepatitis B Virus in Mothers with High Viral Load

2021 ◽  
Vol 1 (1) ◽  
pp. 6-13
Author(s):  
Hong Gao ◽  
◽  
Ling Xu ◽  
Xiangying Zhang ◽  
Zhihao Fan ◽  
...  
Keyword(s):  
Viral Load ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Protein Expression ◽  
Pregnant Women ◽  
High Viral Load ◽  
Toll Like Receptor ◽  
Viral Loads ◽  
B Virus ◽  
Mrna And Protein Expression

Backgrounds: Despite passive and active immunization, perinatal mother-to-infant transmission (MTIT) of hepatitis B virus (HBV) still occurs in women with high levels of viremia. Thus, understanding the mechanisms of MTIT is essential to prevent MTIT. The aims of this study were to clarify the roles of toll-like receptor 3 (TLR3) in the prevention of hepatitis B transmission in mothers with a high viral load. Methods: Placental samples were collected from 87 HBV-positive pregnant women and 25 normal pregnant women. Choriocarcinoma JEG-3 cell lines were exposed to different HBV viral loads to mimic the trophoblast barrier affected by HBV in the placenta. The mRNA and protein expression levels of TLR3 were analyzed by qRT-PCR and western blotting assays in placenta and JEG-3 cells, respectively. Results: In terms of mRNA and protein expression, the expression of TLR3 in the placenta among the control, low viral load, medium viral load and high viral load groups were significantly different, showing significant upregulation in the medium load and high load groups compared with the control; TLR3 expression in the placenta of the HBeAg-positive group was higher than that in the HBeAg-negative group, and TLR3 expression in the placenta of the infant-infected group was lower than that of the infant-noninfected group. Expression of TLR3 was gradually increased in JEG-3 cells exposed to low HBV viral loads or with shortterm HBV exposure and was decreased in JEG-3 cells exposed to high HBV viral loads or with longterm HBV exposure. Conclusions: TLR3 contribute to HBV intrauterine infection in mothers with a high viral load and, importantly, prevents mother-to-infant transmission.

scholarly journals Transmission of Hepatitis B Virus From an Orthopedic Surgeon With a High Viral Load

2012 ◽  
Vol 56 (2) ◽  
pp. 218-224 ◽  
Author(s):  
Kyle B. Enfield ◽  
Umid Sharapov ◽  
Keri K. Hall ◽  
John Leiner ◽  
Carl L. Berg ◽  
...  
Keyword(s):  
Viral Load ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
High Viral Load ◽  
Orthopedic Surgeon ◽  
B Virus

scholarly journals Mother-to-Child Transmission of Hepatitis B Virus in Ethiopia

Vaccines ◽  
2021 ◽  
Vol 9 (5) ◽  
pp. 430
Author(s):  
Asgeir Johannessen ◽  
Bitsatab Mekasha ◽  
Hailemichael Desalegn ◽  
Hanna Aberra ◽  
Kathrine Stene-Johansen ◽  
...  
Keyword(s):  
Risk Factors ◽  
Chronic Hepatitis ◽  
Viral Load ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
High Viral Load ◽  
Hbv Infection ◽  
Child Transmission ◽  
B Virus ◽  
Mother To Child

High viral load and positive hepatitis B e-antigen (HBeAg) results are risk factors for mother-to-child transmission (MTCT) of hepatitis B virus (HBV). In sub-Saharan Africa, little is known about the distribution of these risk factors, as well as early childhood HBV transmission. In this study, Ethiopian women aged 18–45 years with chronic hepatitis B were assessed for the presence of HBeAg and high viral load. Their children below 4 years of age were invited for assessment of viral markers, defining active HBV infection as a positive hepatitis B s-antigen (HBsAg) and/or detectable HBV DNA. In total, 61 of 428 HBV-infected women (14.3%) had a positive HBeAg result and/or a high viral load. Of note, 26 of 49 women (53.1%) with viral load above 200,000 IU/mL were HBeAg negative. Among 89 children born of HBV-infected mothers (median age 20 months), 9 (10.1%) had evidence of active HBV infection. In conclusion, one in seven women with chronic hepatitis B had risk factors for MTCT, and HBeAg was a poor predictor of high viral load. One in ten children born of HBV-infected women acquired HBV-infection despite completing their scheduled HBV vaccination at 6, 10 and 14 weeks of age.

scholarly journals Downregulation of MicroRNA-145 Caused by Hepatitis B Virus X Protein Promotes Expression of CUL5 and Contributes to Pathogenesis of Hepatitis B Virus-Associated Hepatocellular Carcinoma

2015 ◽  
Vol 37 (4) ◽  
pp. 1547-1559 ◽  
Author(s):  
Feng Gao ◽  
Xiaoyu Sun ◽  
Likun Wang ◽  
Shunxiong Tang ◽  
Changqing Yan
Keyword(s):  
Hepatocellular Carcinoma ◽  
Hepatitis B Virus ◽  
Cell Growth ◽  
Hepatitis B ◽  
Protein Expression ◽  
Host Cells ◽  
Luciferase Reporter ◽  
X Protein ◽  
B Virus ◽  
Mrna And Protein Expression

Background: Hepatitis B viral infection-induced hepatocellular carcinoma (HCC) is a major threat to human health in China. Hepatitis B virus X protein (HBX), an HBV protein, has been reported to be involved in regulating the cellular activities of the host cells and is responsible for HCC oncogenesis. Methods and Results: In this study, we performed real-time PCR in tumor tissue samples collected from 53 HCC patients (25 HBV-positive cases and 28 HBV-negative cases) to screen the candidate miRNAs that have previously been reported to be aberrantly expressed in HBV-associated HCC and found that miR-145 was significantly downregulated. The following computational analysis identified CUL5 and RAB5C as virtual targets of miR-145, whereas only CUL5 was verified as a validated target gene of miR-145 in liver cells via luciferase reporter assay. In line with this result, we found that both the mRNA and protein expression levels of CUL5 were significantly higher in HBV-positive than in HBV-negative HCC. An in vitro experiment demonstrated a significant decrease in the expression of miRNA-145, a substantial increase in the mRNA and protein expression of CUL5, and an enhanced proliferation of HBX over-expressing HepG2 cells compared with the control. In HepG2.2.15, we found significant decreases in both the expression of CUL5 and the cell growth rate of H cells transfected with 60 nM miR-145 mimics compared with the scramble controls. Conclusion: HBV infection promotes cell growth, at least partially, through the HBX-induced downregulation of miRNA-145 expression, which is responsible for the oncogenesis of HBV-associated HCC.

Sign in / Sign up

Export Citation Format

Share Document