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HBV Transmission (hbv + transmission)
Selected AbstractsPrevalence, whole genome characterization and phylogenetic analysis of hepatitis B virus in captive orangutan and gibbonJOURNAL OF MEDICAL PRIMATOLOGY, Issue 6 2008Pattaratida Sa-nguanmoo Abstract Background, Hepatitis B virus (HBV) is a public health problem worldwide and apart from infecting humans, HBV has been found in non-human primates. Methods, We subjected 93 non-human primates comprising 12 species to ELISA screening for the serological markers HBsAg, antiHBs and antiHBc. Subsequently, we detected HBV DNA, sequenced the whole HBV genome and performed phylogenetic analysis. Results, HBV infection was detected in gibbon (4/15) and orangutan (7/53). HBV DNA isolates from two gibbons and seven orangutans were chosen for complete genome amplification. We aligned the Pre-S/S, Pre-C/C and entire genomes with HBV sequences and performed phylogenetic analysis. The gibbon and orangutan viruses clustered within their respective groups. Conclusions, Both geographic location and host species influence which HBV variants are found in gibbons and orangutans. Hence, HBV transmission between humans and non-human primates might be a distinct possibility and additional studies will be required to further investigate this potential risk. [source] Hepatitis B virus genotypes in children and adolescents in Japan: Before and after immunization for the prevention of mother to infant transmission of hepatitis B virusJOURNAL OF MEDICAL VIROLOGY, Issue 6 2007Ayano Inui Abstract The genotype distribution of hepatitis B virus (HBV) was investigated in 118 children in Japan. One hundred and sixteen children (98%) had chronic HBV infection, and the remainder had acute hepatitis. Genotyping of HBV was determined by PCR and sequencing analysis in the S gene. Genotype C (86%) was the most frequent, followed by genotype B (9%), D (2.5%), and A (1.0%). Transmission routes of HBV to children were from mothers in 91 patients (77%), fathers in 8 (6.5%), mother or father in 1 (1%), family members other than the parents in 5 (4%), and unknown in 13 (11.5%). The relationship between routes of HBV transmission and HBV genotypes was studied. Eighty-eight (97%) of 91 children of mother-to-infant transmission were genotype C, while 13 (49%) of 27 children of the routes other than the mother to infant transmission were genotype C. The number of children with genotype C who were infected from their mothers was significantly higher than those with genotype B, D, or A (P,<,0.01). In conclusion, HBV genotypes influence not only clinical characteristics but also the mechanisms of inter-personal HBV transmission. J. Med. Virol. 79: 670,675, 2007. © 2007 Wiley-Liss, Inc. [source] Perinatal and intrafamily transmission of hepatitis B virus in three generations of a low-prevalence populationJOURNAL OF MEDICAL VIROLOGY, Issue 2 2003Katalin Ördög Abstract Family members of 47 hepatitis B virus (HBV)-carrier pregnant women were tested for the presence of hepatitis B surface antigen (HBsAg), other markers of HBV infection, and hepatitis A virus (HAV) antibodies. Eleven members of six families were found to be HBV DNA positive. Five of the anti-HBe-positive persons were found to be HBV DNA carriers, too. The mean age of the HBV DNA carriers was found to be lower than that of Hbe carriers; therefore, it is suggested that seroconversion to HBe occurs before the resolution of HBV DNA carrier state. Superinfection with hepatitis A virus was not found to influence the elimination of HBV-carrier state, as there was no correlation found between the hepatitis A exposure and the hepatitis B virus markers in the families. The low HBV prevalence in the population (0.3%) was in contrast to the high prevalence of the families of the HBV-carrier mothers (27.1%) and family members with HBV markers (50.4%). Significant positive correlation was found in the proportion of HBV-positive children, and the HBV history of their parents. When fathers were shown to be seronegative, the probability of HBV transmission was reduced by a factor of 6 (12.5% instead of 75%) probably due to reduced viral load and possibly by other factors. Several results indicate, that the noncytocidal hepatitis B virus clearing mechanism suggested by Guidotti et al. [1996, 1999] was effective also in the HBV-carrier human population. J. Med. Virol. 70: 194,204, 2003. © 2003 Wiley-Liss, Inc. [source] Risk factors and mechanism of transplacental transmission of hepatitis B virus: A case-control studyJOURNAL OF MEDICAL VIROLOGY, Issue 1 2002De-Zhong Xu Abstract Intrauterine hepatitis B virus (HBV) infection has been suggested to be caused by transplacental transmission that cannot be blocked by hepatitis B vaccine. This would decrease the effectiveness of hepatitis B vaccine. This study examined the risk factors and mechanism of transplacental HBV transmission. A case-control study included 402 newborn infants from 402 HBsAg-positive pregnant women. Among these, 15 newborn infants infected with HBV by intrauterine transmission were selected as cases, and the rest as controls. A pathology study included 101 full-term placentas from the HBsAg-positive pregnant women above and 14 from HBsAg-negative pregnant women. Immunohistochemistry staining and HBV DNA in situ hybridization were used to estimate the association of intrauterine HBV infection and HBV infection in the placentas. HBeAg positivity in mothers' sera (OR,=,17.07, 95%CI 3.39,86.01) and threatened preterm labor (OR,=,5.44, 95%CI 1.15,25.67) were found to be associated with transplacental HBV transmission. The intrauterine infection rate increased linearly and significantly with maternal serum HBsAg titers (trend test P,=,0.0117) and HBV DNA concentration (trend test P,<,0.01). Results of the pathology study showed that HBV infection rates decreased gradually from the maternal side to the fetal side (trend test P,=,0.0009) in the placental cell layers. There was a significant association between intrauterine HBV transmission and HBV infection in villous capillary endothelial cells (VCEC) in the placenta (OR,=,18.46, P,=,0.0002). The main risk factors for intrauterine HBV infection are maternal serum HBeAg positivity, history of threatened preterm labor, and HBV in the placenta especially the villous capillary endothelial cells. Previous reports of transplacental leakage of maternal blood causing intrauterine infection are confirmed. In addition, there appears to be a "cellular transfer" of HBV from cell to cell in the placenta causing intrauterine infection. This latter hypothesis needs to be confirmed. J. Med. Virol. 67:20,26, 2002. © 2002 Wiley-Liss, Inc. [source] Transmission of hepatitis B infection from hepatitis B core antibody,positive liver allografts is prevented by lamivudine therapyLIVER TRANSPLANTATION, Issue 6 2001Andy S. Yu Donor shortage has led to the use of hepatitis B core antibody (anti-HBc)-positive (anti-HBc+) liver allografts for patients in need of relatively urgent orthotopic liver transplantation (OLT). Because anti-HBc+ allografts transmit hepatitis B virus (HBV) infection at a high rate, effective prophylaxis is required. We assessed the effectiveness of lamivudine in preventing HBV transmission by anti-HBc+ allografts. Between March 1996 and March 2000 at Cedars-Sinai Medical Center (Los Angeles, CA), 15 of 169 patients (8.9%) received liver allografts from anti-HBc+ donors. Six patients were hepatitis B surface antigen (HBsAg)+ (group 1), and 9 patients were HBsAg negative (HBsAg,; group 2) before OLT. All patients were administered lamivudine, 100 or 150 mg/d, orally after OLT. Patients who were HBsAg+ before OLT also were administered hepatitis B immunoglobulin (HBIG) prophylaxis. Hepatitis B serological tests were performed on all patients, and HBV DNA was determined in liver tissues in 10 patients. All 15 patients remained HBsAg, at their last follow-up 2 to 40 months (mean, 17 months) post-OLT. All patients in group 1 had antibody to HBsAg (anti-HBs) titers greater than 250 mIU/mL post-OLT (mean follow-up, 20 months; range, 7 to 40 months). Of the 2 patients in group 1 who underwent liver biopsy after OLT, 1 patient had detectable hepatic HBV DNA despite being anti-HBs+ and HBsAg,. Among the patients in group 2, none acquired anti-HBc or HBsAg. Hepatic HBV DNA was undetectable in the 7 patients in group 2 who underwent liver biopsy after OLT. Anti-HBc+ allografts can be safely used in patients who undergo OLT for chronic hepatitis B and susceptible transplant recipients if prophylaxis with combination HBIG and lamivudine or lamividine alone is administered after OLT, respectively. However, more data are needed to determine the efficacy of lamivudine monotherapy in preventing transmission of HBV infection from anti-HBc+ liver allografts to susceptible recipients. [source] | ||||||||||