scholarly journals Impaired trophoblast Toll-Like Receptor 3 signaling pathway involves in hepatitis B vaccine non- or hypo-response of infants born to HBsAg-positive mothers

2020 ◽  
Author(s):  
Lina Wu ◽  
Ruijun Zhang ◽  
Yongliang Feng ◽  
Tian Yao ◽  
Linzhu Yi ◽  
...  
Keyword(s):  
Hepatitis B ◽  
Signaling Pathway ◽  
Hepatitis B Surface Antigen ◽  
Quantitative Polymerase Chain Reaction ◽  
Hbv Dna ◽  
Enzyme Linked Immunosorbent Assay ◽  
Toll Like Receptor ◽  
Insufficient Response ◽  
Hb Vaccine ◽  
Tlr3 Signaling

Abstract Background: Babies born to hepatitis B surface antigen (HBsAg) positive mothers bear a high risk of being non- or hypo-responsive to hepatitis B (HB) vaccine with unilluminated mechanisms. Placental immunity is closely related to the development of baby immune system, however, the roles of the placental immunity in the insufficient response of these babies are unclear. This study was aimed to investigate the role of placental trophoblast Toll-Like Receptor 3（TLR3）signaling pathway in HB vaccine non- or hypo-response of these special babies. Methods: A total of 399 pairs of HBsAg-positive mothers and their neonates were recruited to perform a nested case-control study. The maternal and children’s HBV DNA and the HBV serological markers were detected by Fluorescence Quantitative Polymerase Chain Reaction (FQ-PCR) and Electrochemiluminescence Immunoassay (ECLIA). The trophoblast TLR3 signaling pathway proteins and infant cytokines IL-6, IL-12, TNF-α, IFN-α and IFN-γ were tested by immunohistochemistry (IHC) and Enzyme–Linked Immunosorbent Assay (ELISA). Results: The expression of TLR3 and NF-κB, a TLR3 downstream protein, were significantly decreased in the non- or hypo-responders ( Z= -3.00 and -2.46, P <0.01 and =0.01). Furthermore, the trophoblast TLR3 expression negatively correlated with maternal HBV DNA ( r = -0.29, P = 0.003), HBeAg ( r = -0.28, P = 0.01) and HBV DNA+HBeAg ( r = -0.24, P = 0.02). Besides, NF-κB positively correlated with infant IL-6 ( r = 0.24, P = 0.026). By comprehensive analysis of maternal, placental and infant information, a Bayesian network model showed that the trophoblast TLR3 signaling pathway contacted with the non- or hypo-responsiveness. onclusions: Maternal HBV infection affected the trophoblast TLR3 signaling pathway protein expression, and consequently the impaired TLR3 signaling pathway involved in the HB vaccine non- or hypo-responsiveness mainly by influencing infant IL-6.

scholarly journals Study on the Prevalence of Occult Hepatitis B Virus Infection in Patients Undergoing Hemodialysis

2020 ◽  
Author(s):  
Shahab Mahmoudvand ◽  
Somayeh Shokri ◽  
Habibollah Mirzaei ◽  
Manoochehr Makvandi ◽  
Ali Teimoori ◽  
...  
Keyword(s):  
Hepatitis B ◽  
Nested Pcr ◽  
Hepatitis B Surface Antigen ◽  
Hbv Dna ◽  
Enzyme Linked Immunosorbent Assay ◽  
Peripheral Blood Mononuclear ◽  
Cross Sectional ◽  
Occult Hepatitis ◽  
Occult Hepatitis B ◽  
Sera Samples

Occult hepatitis B (OBI) is a major challenging clinical entity characterized by the absence of hepatitis B surface antigen (HBsAg). The persistence of OBI may progress to fibrosis, cirrhosis, and hepatocellular carcinoma. This study was aimed to investigate the prevalence of OBI among HD patients. In the present cross-sectional study, 89 sera samples of hemodialysis individuals were tested for HBsAg and HBcIgG by Enzyme-linked Immunosorbent Assay (ELISA). In addition, the HBV DNA has tested in sera and peripheral blood mononuclear cell (PBMC) samples by nested-PCR. Out of 89 patients, 51(57.3%) were males, and 38 (42.7%) females. The ages ranged from 24 to 90 years (with a mean of 57.5±1.37 years). All the sera samples had normal levels of Aspartate Aminotransferase (AST) and Alanine Transaminase (ALT) but had high levels of Creatinine (Cr) (6.9±2.17) and Blood Urea Nitrogen (BUN) (61.83±2.03). 2/89 (2.2%) sera samples were positive for both HBsAg and HBc-IgG test; in addition, HBV DNA was detected in both sera and their PBMC samples. The sera of 15/89 (16.85%) were only positive for the HBc-IgG test, including 10/51 (19.6%) males and 5/38 (13.2%) females (P=0.5). The high 16.85% prevalence OBI has been found among HD patients. To manage OBI infection, screening of HBV DNA should be implemented for HD patients by sensitive molecular means such as nested-PCR and real-time PCR.

Study of the relationship in pregnant women between hepatitis B markers and a placenta positive for hepatitis B surface antigen

2015 ◽  
Vol 43 (2) ◽  
Author(s):  
Junni Wei ◽  
Shulian Xue ◽  
Junfeng Zhang ◽  
Suping Wang ◽  
Bo Wang
Keyword(s):  
Hepatitis B ◽  
Synergistic Effect ◽  
Surface Antigen ◽  
Hepatitis B Surface Antigen ◽  
Significant Risk ◽  
Serum Markers ◽  
Hbv Dna ◽  
Enzyme Linked Immunosorbent Assay ◽  
Transplacental Transmission ◽  
Pass Through

AbstractA placenta with hepatitis B virus (HBV) is one of the main reasons for transplacental transmission during pregnancy. This study aims to explore the factors influencing the presence of hepatitis B surface antigen (HBsAg) in the placenta and the synergistic effect of these factors.A total of 155 placentae and blood specimens were collected from HBsAg-positive mothers and their newborns. HBsAg in placenta was detected using the immunohistochemistry method. HBV serum markers were detected using enzyme-linked immunosorbent assay (ELISA) and polymerase chain reaction (PCR) methods.The results showed that hepatitis B e antigen (HBeAg) positive, or HBV DNA positive status, is significantly associated with an HBsAg-positive placenta. A synergistic effect was present. The hazard ratio for a HBsAg-positive placenta in mothers with HBeAg and HBV DNA was 1.97 times higher than the sum of the independent relative risk of each separate effect (synergy index, S=1.97). There was a statistically significant association between HBsAg in newborns and HBsAg in placenta, and the risk of newborns with HBsAg was greater (odds ratio values 3.33 and 5.31, respectively) when placental cells close to the fetal side were HBsAg positive.Being positive for HBeAg and/or HBV DNA are significant risk factors for HBsAg in the placenta. HBsAg can pass through the placenta via cellular transfer, possibly contributing to transplacental transmission.

scholarly journals Prevalence of Hepatitis B Virus Genotypes Among Patients with Liver Disease in Eritrea

2020 ◽  
Author(s):  
Mohammed Elfatih A. Hamida ◽  
Saud Mohammed Raja ◽  
Yodahi Petros ◽  
Munir Wahab ◽  
Yemane Seyoum ◽  
...  
Keyword(s):  
Liver Disease ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Hepatitis B Surface Antigen ◽  
Hbv Dna ◽  
Enzyme Linked Immunosorbent Assay ◽  
African Countries ◽  
Hbv Genotype ◽  
Geographical Regions ◽  
B Virus

Abstract BackgroundHepatitis B virus (HBV) is a blood-borne hepatotrophic virus and a major causative agent of liver disease. The virus is highly endemic in African countries, and five genotypes (A–E) have been identified. This study aimed to establish the most prevalent genotypes of HBV among liver disease patients from different geographical regions of Eritrea, an East African multi-ethnic country.MethodsThis study included 293 Eritrean liver disease patients who were hepatitis B surface antigen (HBsAg)-positive. Enzyme-linked immunosorbent assay (ELISA)-based serological screening and multiplex-nested PCR using type-specific primer-based genotyping were performed to determine the prevalence of genotypes in the Eritrean population.ResultsThe mean (± standard deviation) age was 41.66 ± 13.84 years; 213 (72.7%) patients were males and 80 (27.3%) were females. The median (interquartile range) of HBV DNA and alanine aminotransferase levels were 3.47 (1.66) log IU/ml and 28 (15.3) IU/L, respectively. All patients’ sera were HBsAg- and anti-HBc-total positive; 20 (6.8%) were HBeAg-positive/anti-HBe-negative, 242 (82.6%) were HBeAg-negative/anti-HBe-positive, and 31 (10.6%) had neither HBeAg nor anti-HBe according to the ELISA screening test. Of the 293 patients, only 122 (41.6%) were positive for HBV DNA, 57.38% had a single genotype, and 42.62% had a mixed HBV genotype infection. Irrespective of mode of occurrence, HBV genotype D (n = 26; 21.3%) was the predominant circulating genotype, followed by genotypes C (n = 21; 17.2%), E (n = 19; 15.6%), C/D (n = 16; 13.1%), and C/E (n = 13; 10.7%). Genotypes C/D/E (n = 9; 7.4%), A/D (n = 6; 4.9%), D/E (n = 5; 4.1%), A (n = 3; 2.5%), and B, A/E, B/E, and A/D/C (each with n = 1; 0.8%) were also present.ConclusionHBV in Eritrea is comprised of a mixture of genotypes A, B, C, D, and E separately or in combinations. Our findings demonstrated that in Eritrea, the most prevalent HBV genotype in Eritrea is genotype D among theliver disease patients with higher HBeAg positivity. This is the first study of HBV genotyping based on PCR methods in Eritrea.

scholarly journals Prevalence of Anti-HBc Antibodies among HBsAg Negative Individuals and Its Association with Occult Hepatitis B

2021 ◽  
Author(s):  
Anitha Madhavan ◽  
Arun Sachu ◽  
Anu Kumar Balakrishnan ◽  
Sobha Balakrishnan ◽  
Jayalakshmi Vasudevapanicker
Keyword(s):  
Hepatitis B ◽  
Surface Antigen ◽  
Hepatitis B Surface Antigen ◽  
Hbv Dna ◽  
Hbv Infection ◽  
Enzyme Linked Immunosorbent Assay ◽  
Serum Samples ◽  
Occult Hbv Infection ◽  
Transmitted Infection ◽  
Occult Hbv

Abstract Introduction Hepatitis B virus (HBV) infection is an endemic in many Asian countries, and among the major routes of transmission, transfusion is the one that should be prevented. Occult HBV infection (OBI) is defined as the presence of HBV DNA in the absence of detectable HBsAg, with or without anti-HBV antibodies. The aim of this study was to detect the prevalence of anti-HBc total antibodies among the HB surface antigen (HBsAg) negative individuals by way of enzyme-linked immunosorbent assay (ELISA), and detect the presence of HBV DNA among the anti-HBc seropositives by polymerase chain reaction (PCR). Anti-HBs among the HBV DNA positives were also found out by enzyme-linked fluorescent assay (ELFA). Materials and Methods A total of 910 serum samples was subjected to initial screening for HBsAg by MERILISA HBsAg ELISA kits. The anti-HB core (HBc) total antibody titer was evaluated using MONOLISA ELISA (Biorad) kits. If found negative, the samples were discarded. If found positive, the samples underwent HBV DNA testing by nested PCR. Antibody to hepatitis B surface antigen (anti-HBs) was calculated among the DNA positives by ELFA. Results A total of 133 samples were positive for anti-HBC total antibody, resulting in an overall prevalence of 14.6%. Overall prevalence of HBV DNA among the anti-HBc seropositives was 2.2%. Conclusion Among the three HBV DNA positive patients, two belonged to the preoperative screening group, which is an alarming situation. Screening of blood for HBsAg has reduced the incidence of posttransfusion hepatitis, but HBV still remains the major source of transfusion transmitted infection in India.

scholarly journals Thyroid dysfunction is associated with the loss of hepatitis B surface antigen in patients with chronic hepatitis B undergoing treatment with α-interferon

2021 ◽  
Vol 49 (6) ◽  
pp. 030006052110251
Author(s):  
Wenfan Luo ◽  
Shuai Wu ◽  
Hongjie Chen ◽  
Yin Wu ◽  
Jie Peng
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis B ◽  
Thyroid Function ◽  
Thyroid Dysfunction ◽  
Hepatitis B Surface Antigen ◽  
Hbv Dna ◽  
Interferon Treatment ◽  
Normal Thyroid ◽  
Normal Thyroid Function ◽  
Hbsag Loss

Objective To investigate the influence of thyroid dysfunction on the antiviral efficacy of α-interferon in adult patients with chronic hepatitis B (CHB). Methods We performed a retrospective study of 342 patients with CHB who underwent interferon treatment for >12 weeks. Patients with thyroid dysfunction before or during treatment were defined as the thyroid dysfunction group (n = 141) and those with normal thyroid function were defined as the normal thyroid function group (n = 201). The prevalences of hepatitis B virus (HBV) DNA undetectability, low hepatitis B surface antigen (HBsAg) titre (<250 IU/mL), HBsAg loss, and hepatitis B envelope antigen loss were compared. Results During interferon treatment, 69 of 270 (25.6%) participants with normal thyroid function at baseline developed thyroid dysfunction, whereas 11 of 72 (15.3%) with thyroid dysfunction at baseline regained normal thyroid function. The thyroid dysfunction group had significantly higher prevalences of low HBsAg titre (29.8% vs. 18.9%) and HBV DNA undetectability (66.0% vs. 40.3%). Multivariate logistic regression analysis showed that thyroid dysfunction was associated with HBsAg loss (odds ratio 4.945, 95% confidence interval 1.325–18.462). Conclusions These results suggest that thyroid dysfunction is not an absolute contraindication, but is associated with HBsAg loss, in patients with CHB undergoing α-interferon treatment.

scholarly journals Interleukin-6 via Toll-Like Receptor 3 Signaling Attenuates the Expression of Proinflammatory Chemokines in Human Podocytes

2021 ◽  
Vol 46 (2) ◽  
pp. 207-218
Author(s):  
Hidenori Umetsu ◽  
Shojiro Watanabe ◽  
Tadaatsu Imaizumi ◽  
Tomomi Aizawa ◽  
Koji Tsugawa ◽  
...  
Keyword(s):  
Rna Interference ◽  
Molecular Mechanisms ◽  
Kidney Diseases ◽  
Enzyme Linked Immunosorbent Assay ◽  
Toll Like Receptor ◽  
Induced Expression ◽  
Inflammatory Reactions ◽  
Monocyte Chemoattractant Protein 1 ◽  
Polycytidylic Acid ◽  
Tlr3 Signaling

<b><i>Background:</i></b> Although toll-like receptor 3 (TLR3) signaling is involved in the development of certain chronic kidney diseases, the specific molecular mechanisms underlying inflammatory reactions via activation of TLR3 signaling in human podocytes remain unclear. Interleukin (IL)-6 is a pleiotropic cytokine associated with innate and adaptive immune responses; however, little is known about the implication of IL-6 via the activation of regional TLR3 signaling in the inflammatory reactions in human podocytes. <b><i>Methods:</i></b> We treated immortalized human podocytes with polyinosinic-polycytidylic acid (poly IC), an authentic viral double-stranded RNA, and assessed the expression of IL-6, monocyte chemoattractant protein-1 (MCP-1), and C-C motif chemokine ligand 5 (CCL5) using quantitative real-time reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay. To further elucidate the poly IC-induced signaling pathway, we subjected the cells to RNA interference against IFN-β and IL-6. <b><i>Results:</i></b> We found that the activation of TLR3 induced expression of IL-6, MCP-1, CCL5, and IFN-β in human podocytes. RNA interference experiments revealed that IFN-β was involved in the poly IC-induced expression of IL-6, MCP-1, and CCL5. Interestingly, IL-6 knockdown markedly increased the poly IC-induced expression of MCP-1 and CCL5. Further, treatment of cells with IL-6 attenuated the expression of CCL5 and MCP-1 mRNA and proteins. <b><i>Conclusion:</i></b> IL-6 induced by TLR3 signaling negatively regulates the expression of representative TLR3 signaling-dependent proinflammatory chemokines in human podocytes.

scholarly journals The Absence of TLR4 Prevents Fetal Brain Injury in the Setting of Intrauterine Inflammation

2018 ◽  
Vol 26 (8) ◽  
pp. 1082-1093 ◽  
Author(s):  
Natalia M. Tulina ◽  
Amy G. Brown ◽  
Guillermo O. Barila ◽  
Michal A. Elovitz
Keyword(s):  
Brain Injury ◽  
Notch Signaling ◽  
Signaling Pathway ◽  
Quantitative Polymerase Chain Reaction ◽  
Fetal Brain ◽  
Notch Signaling Pathway ◽  
Mouse Strains ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tlr4 Signaling ◽  
Tlr4 Signaling Pathway

Background: Exposure to intrauterine inflammation during pregnancy is linked to brain injury and neurobehavioral disorders in affected children. Innate immunity, specifically Toll-like receptor (TLR) signaling pathways are present throughout the reproductive tract as well as in the placenta, fetal membranes, and fetus. The TLR pathways are mechanistically involved in host responses to foreign pathogens and may lead to brain injury associated with prenatal inflammation. Objective: We aimed to determine whether the activation of the TLR4 signaling pathway, in the mother and fetus, is critical to fetal brain injury in the setting of intrauterine inflammation. Methods: A mini-laparotomy was performed on time pregnant C57B6 mice and 2 knockout mouse strains lacking the function of the Tlr4 and Myd88 genes on embryonic day 15. Intrauterine injections of Escherichia coli lipopolysaccharide or saline were administered as described previously. Dams were killed 6 hours postsurgery, and placental, amniotic fluid, and fetal brain tissue were collected. To assess brain injury, quantitative polymerase chain reaction (qPCR) analysis was performed on multiple components of the NOTCH signaling pathway, including Hes genes. Interleukin (IL) IL6, IL1β, and CCL5 expression was assessed using qPCR and enzyme-linked immunosorbent assay. Results: Using an established mouse model of intrauterine inflammation, we demonstrate that the abrogation of TLR4 signaling eliminates the cytokine response in mother and fetus and prevents brain injury associated with increased expression of transcriptional effectors of the NOTCH signaling pathway, Hes1 and Hes5. Conclusions: These data show that the activation of the TLR4 signaling pathway is necessary for the development of fetal brain injury in response to intrauterine inflammation.

scholarly journals Hepatitis B Reactivation in the Treatment of Non-Hodgkin Lymphoma

2018 ◽  
Vol 25 (1) ◽  
pp. 107327481876787
Author(s):  
Matthew Kelling ◽  
Lubomir Sokol ◽  
Samir Dalia
Keyword(s):  
Cancer Therapy ◽  
Hepatitis B ◽  
Hodgkin Lymphoma ◽  
Hepatitis B Surface Antigen ◽  
Liver Function Tests ◽  
Hbv Dna ◽  
Hbv Reactivation ◽  
Hepatitis B Infection ◽  
Serological Testing ◽  
Non Hodgkin Lymphoma

Chronic active hepatitis B infection (HBV) has been implicated in lymphomagenesis of non-Hodgkin lymphoma (NHL). Treatment of cancer including NHL with chemotherapy or immunotherapy can lead to HBV reactivation in previously infected patients. Serological testing of HBV prior to initiation of this therapy is recommended by several national and international medical agencies and expert panels. Patients with positive hepatitis B surface antigen (HBsAg) and anti-hepatitis B core antibody (anti-HBc ab) need to start antiviral therapy with entecavir or tenofovir prior to initiation of chemotherapy or immunotherapy and continue this treatment for 6 to 12 months after completion of cancer therapy to avoid late HBV reactivation. Monitoring of HBV DNA viral load and liver function tests should be done during cancer therapy in infected patients. Hepatitis B infection vaccination resulted in decreases prevalence of HBV virus carriers and decreased incidence of virus-induced malignancies.

The possible role of S gene mutations of hepatitis B virus in intrauterine transmission

2020 ◽  
Author(s):  
Jiaxin Wu ◽  
Yongliang Feng ◽  
Zhiqing Yang ◽  
Ruijun Zhang ◽  
Dandan Wang ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Hepatitis B Surface Antigen ◽  
Gene Mutations ◽  
Hbv Dna ◽  
Mutation Rates ◽  
Control Group ◽  
Intrauterine Transmission ◽  
S Gene ◽  
B Virus

Abstract Background: Many hepatitis B virus (HBV) substances could inevitably enter fetuses and occurred neonatal intrauterine transmission. HBV often occurs mutation, especially S gene, and may lead to different outcomes on intrauterine transmission. We explored the associations between HBV S gene mutations of hepatitis B surface antigen positive (HBsAg-positive) mothers and intrauterine transmission. Methods: A total of 399 HBsAg-positive mothers and neonates were recruited and their general demographic information was collected between June 2011 and July 2013. The mothers with HBV DNA levels ≥ 106 IU/ml were selected, 22 mothers whose neonates occurred HBV intrauterine transmission were in the HBV intrauterine transmission group (GT) and 22 mothers were randomly selected from the remaining controls were in the control group (GC). Maternal whole-genome HBV DNA was extracted, amplified, cloned, and sequenced. Obtained sequences were adjusted, genotyped, and analyzed for mutation rates. A case-control study was designed to analyze the relationship between mutations in the S gene of HBV and intrauterine transmission. Results: Fifty-five neonates were found to have experienced intrauterine transmission (13.78%). Genotype B (4.55%), genotype C (88.64%) and inter-genotype B/C (6.81%) were found in the 44 HBsAg-positive mothers. The mutation rates of the S gene, in both genotypes B (0.58% vs 1.41%, P = 0.040) and C (7.56% vs 14.71%, P＜0.001), were lower in group T than in group C. Missense substitutions such as L84I, P47S, K10Q, A41P, M133L, A60V, and I42T only existed in group C. The mutation rates of G73S, I126T, and I126S in group C were higher (P < 0.001, P < 0.001, P = 0.010). Deletions occurred in the S gene. The occurrence of intrauterine transmission with maternal mutation A90V was higher (P < 0.001). This may have increased the risk of neonatal HBsAg expression (P = 0.022). Conclusions: The HBV S gene mutations of HBsAg-positive mothers may reduce the occurrence of HBV intrauterine transmission. It is possible for HBsAg-positive mothers infected with A90V to develop HBV chronic infection and transmit it to the fetus during pregnancy, resulting in neonatal HBV infection.

Sign in / Sign up

Export Citation Format

Share Document