ABSTRACT Controllable DNA condensation is important for nucleic‐acid packaging and non‐viral gene‐delivery systems. This study aimed to determine how the composition of mixed nonionic C 12 E 10 and cationic gemini C 12 C 6 C 12 Br 2 surfactants regulates DNA condensation, structure, thermodynamics, and cytotoxicity. Calf thymus DNA was mixed with surfactant formulations containing different mole fractions of C 12 C 6 C 12 Br 2 . DNA–surfactant interactions were evaluated by UV spectroscopy, dynamic light scattering, ζ‐potential measurements, atomic force microscopy, differential scanning calorimetry, isothermal titration calorimetry (ITC), and cell‐viability assays. Increasing the gemini‐surfactant fraction induced a transition from extended DNA chains to compact globular complexes. Maximum condensation occurred at = 0.5, producing complexes of approximately 100 nm with positive ζ‐potentials. ITC showed that complex formation was spontaneous and predominantly entropy‐driven, consistent with counterion release, water reorganization, and hydrophobic association. At higher gemini fractions, overcharging and aggregate reorganization occurred. Incorporation of C 12 E 10 reduced cytotoxicity relative to the cationic C 12 C 6 C 12 Br 2 alone. These results demonstrate that mixed gemini/nonionic surfactant composition provides a controllable strategy for tuning DNA condensation and biocompatibility.
The diagnosis of occult hepatitis B virus (HBV) infection (OBI) is influenced by factors such as the lower limit of detection (LOD) of the HBV DNA test. However, in clinical practice and scientific research, the lower limit of quantification (LOQ) is often misused as the LOD. This study aims to investigate the impact of misuse of the LOD of the HBV DNA test on the detection rate of OBI, as well as the risk factors for OBI. Four hundred twelve patients who were HBsAg-negative and had undergone high-sensitivity HBV DNA testing were included in this study. HBV DNA was detected using the Cobas 6800 System with an LOD of 2.4 IU/mL and an LOQ of 10 IU/mL. The effect of using the LOQ as the LOD on the detection rate of OBI was compared, and univariate and multivariate logistic regression analyses were used to explore the risk factors for OBI. (1) Of the 412 patients, 63.3% (n = 261) were male, with a median age of 47 (range 34-55) years. A total of 473 HBV DNA test results were obtained, with 366 individuals undergoing only one HBV DNA test and the remaining 46 patients undergoing 2 to 5 HBV DNA tests (resulting in a total of 107 test results). (2) Considering only the first HBV DNA test result, the detection rate of OBI was 4.1% (17/412). However, when the LOQ (10 IU/mL) was used as the LOD, the detection rate of OBI was only 1.5% (6/412) (p < 0.001). (3) Univariate analysis showed that there were statistically significant differences in age, anti-HBe positivity rate and anti-HBc positivity rate between OBI and non-OBI individuals (p < 0.05). Multivariate regression analysis showed that anti-HBe positivity was an independent risk factor for OBI in this study (odds ratio [OR] = 3.807, 95% confidence interval [CI]: 1.065-13.617, p = 0.040), while anti-HBs positivity was a protective factor against OBI (OR = 0.271, 95% CI: 0.093-0.787, p = 0.016). (4) Among the 46 patients who underwent repeated testing, a total of seven individuals were found to be HBV DNA-positive in the first test, and six individuals tested positive for HBV DNA one or more times in subsequent tests. When OBI was confirmed by ≥ 1 out of 1-5 tests with detectable HBV DNA, the detection rate of OBI in this study could increase from 4.1% to 5.6%. The detection rate of OBI among HBsAg-negative adult patients attending hepatology departments in this region is 4.1%. Misusing the LOQ as LOD can significantly decrease the detection rate of OBI. The presence of anti-HBe positivity and undergoing multiple HBV DNA tests can lead to a significant increase in the detection rate of OBI.
PreS/S gene mutations could impact virus secretion, infection and immune evasion. However, the relationship between PreS/S mutations and intrauterine transmission has not yet been clarified. Thus, we aimed to explore the associations between PreS/S gene mutations of HBV isolated from mothers and intrauterine transmission. We analyzed the mutations of PreS/S regions of the HBV genome in mothers with HBV DNA levels ≥ 106 IU/mL whose neonates experienced HBV intrauterine transmission (transmission group, GT) and those whose neonates did not experience intrauterine transmission (control group, GC) analyzed using clone-based sequencing. In total, 206 sequences were successfully amplified, including 98 sequences (from 21 mothers) from GT and 108 sequences (from 20 mothers) from GC of genotype C for mutational analysis. Among the 1203 nucleotides of PreS/S regions, there were 219 (18.20%) base substitutions, of which 103 (47.03%) base mutations caused amino acid changes. F80S, A90V and I68T were mutation hotspots. Mothers in GT had a higher mutation rate of A90V in the PreS1 gene than mothers in GC. The A90V mutation increased the risk of HBV intrauterine transmission after adjusting the maternal age and the mode of delivery (OR = 6.23, 95% CI: 1.18-32.97). Moreover, the area under the ROC curve (AUC) for intrauterine transmission due to A90V and a combination of A90V with the mode of delivery were 0.723 (95% CI: 0.575 to 0.891, P = 0.011) and 0.848 (95% CI: 0.723 to 0.972, P < 0.001), respectively. Mothers with the A90V mutation in the PreS1 gene may be a potential risk factor for HBV intrauterine transmission.
Background Although hepatitis B vaccination has a significant impact on the reduction hepatitis B virus (HBV) infection, babies born to hepatitis B surface antigen (HBsAg) positive mothers bear a high risk of being poor responsive to the vaccine with unilluminated mechanism. Toll-like receptor 3 (TLR3) plays a vital role in placental immunity, which affects the immune response of these babies. This study investigated the role of placental TLR3 in the immune responses of babies born to HBsAg-positive mothers to the HBV vaccine. Methods One hundred pairs of HBsAg-positive mothers and their newborns were recruited. Maternal blood samples were collected before delivery, and placental tissues were collected after delivery. Newborns were administered standard passive and active immunoprophylaxis and followed up until the age of 1. Infant blood samples were collected at 1 year of age. Mothers and infants were tested for HBV serological markers and HBV DNA by electrochemiluminescence immunoassay and fluorescence quantitative polymerase chain reaction. respectively. Placental TLR3 was detected by immunohistochemistry and score in a semi-quantitative fashion, circulating cytokines in infants were detected by enzyme-linked immunosorbent assay. Infants with anti-HBs ≥100 and <100 mIU/mL were classified into the high-responsiveness group and the non- or hypo-responsiveness group. Results The TLR3 protein was expressed in all placentas. Compared with the high-responsiveness group, the expression of TLR3 in the non- or hypo-responsiveness group was significantly decreased (χ2=10.39, P=0.001). A non-conditional logistic regression model showed that the increased expression of placental TLR3 protein decreased the odds of HBV vaccine non- or hypo-responsiveness in the babies of HBsAg-positive mothers [OR =0.25 (95% CI: 0.11–0.58)], and this association remained significant after accounting for maternal factors, such as HBeAg and HBV DNA, as well as infant cytokines, including IL-6, IL-12, TNF-α, IFN-α, and IFN-γ [OR =0.15 (95% CI: 0.05–0.44)]. Conclusions Decreased placental TLR3 expression is associated with impaired responsiveness to HBV vaccination in babies born to HBsAg-positive mothers.
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 ≥ 10 6 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.
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.
目的 探讨乙型肝炎病毒表面抗原(hepatitis B surface antigen,HBsAg)阳性母亲外周血单个核细胞(peripheral blood monouclear cell,PBMC)中乙型肝炎病毒(hepatitis B virus,HBV) 共价闭合环状DNA (covalently closed circular DNA,cccDNA)对新生儿辅助性T细胞1(T help cell 1,Th1)、辅助性T细胞2(T help cell 2,Th2)型细胞因子及Th1/Th2比值的影响.方法 以2011年6月-2013年7月在太原市第三人民医院妇产科分娩的HBsAg阳性母亲及其新生儿作为研究对象.采用电化学发光法(e1ectrochemiluminescence immunoassay,ECLIA)检测HBV血清学标志物,real-time PCR-TaqMan探针法检测母亲PBMC HBV cccDNA,ProcartaPlex多因子分析技术检测新生儿外周血Th1型细胞因子白介素-2(interleukin 2,IL-2),干扰素-γ(interferon-γ,IFN-γ)和肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)以及Th2型细胞因子白介素-4(interleukin 4,IL-4),白介素-6(interleukin 6,IL-6)和白介素-10(interleukin 10,IL-10)水平.结果 单因素分析显示:与阴性组相比,母亲PBMC HBV cccDNA阳性组IL-2、IL-6和IL-10水平升高,Th1/Th2比值降低(P=0.034;P=0.007;P =0.048;P=0.029);经阴道分娩新生儿IL-6和IL-10明显高于剖宫产新生儿,Th1/Th2比值低于剖宫产组(均有P<0.001);新生儿HBsAg阳性组IL-10水平明显高于阴性组,TNF-α水平以及Th1/Th2比值明显低于阴性组(P=0.011;P<0.001;P=0.027).以Th1/Th2比值反映新生儿Th2优势应答程度,分析母亲PBMC HBV复制对新生儿Th2优势应答的影响,调整相关因素后,logistic回归分析结果显示母亲PBMC HBV cccDNA阳性新生儿发生Th2强优势应答的风险是母亲PBMC HBV cccDNA阴性新生儿的2.42倍(OR =2.42,95% CI:1.16~5.04,P=0.018),经阴道分娩新生儿发生Th2强优势应答的风险是剖宫产新生儿的5.06倍(OR=5.06,95% CI:2.95-8.67,P<0.001).结论 HBsAg阳性母亲PBMC HBV复制和阴道产可能加重新生儿Th2优势应答程度,提示需注重母亲PBMC HBV复制和分娩方式对新生儿Th1/Th2型细胞因子的影响.
Objective To investigate the relationship between maternal peripheral blood mononuclear cells (PBMC) hepatitis B virus (HBV) covalenty closed circular deoxyribonucleic acid (cccDNA) and other HBV serological markers and its effects on HBV intrauterine transmission. Methods We enrolled 290 newborns and their hepatitis B surface antigen (HBsAg) positive mothers. HBV cccDNA in PBMC and HBV DNA in serum were detected by a real-time PCR-TaqMan probe while HBV serological markers were detected with an electrochemiluminescence immunoassay. Results There was a positive correlation between the levels of PBMC HBV cccDNA and serum HBV DNA and HBeAg (r = 0.436 and 0.403, P < 0.001). The detection rate of pattern A ['HBsAg (+), HBeAg (+), and anti-HBc (+)'] was significantly higher in the PBMC HBV cccDNA positive group than in the control group (chi(2) = 48.48, P < 0.001). There was a significant association between HBV intrauterine transmission and PBMC HBV cccDNA (chi(2) = 9.28, P = 0.002). In the presence of serum HBV DNA, HBeAg, and PBMC HBV cccDNA, the risk of HBV intrauterine transmission was three times higher (OR = 3.69, 95% CI: 1.30-10.42) than that observed in their absence. The risk of HBV intrauterine transmission was the greatest (OR = 5.89, 95% CI: 2.35-14.72) when both PBMC HBV cccDNA and pattern A were present. A Bayesian network model showed that maternal PBMC HBV cccDNA was directly related to HBV intrauterine transmission. Conclusion PBMC HBV cccDNA may be a direct risk factor for HBV intrauterine transmission. Our study suggests that serological markers could be combined with PBMC-related markers in prenatal testing.
Background: Although many studies have measured HBV cccDNA molecules in Peripheral Blood Mononuclear Cells (PBMC) from patients with active chronic hepatitis B, the current pilot study found PBMC HBV cccDNA in PBMC among HBsAg-positive mothers and their neonates. However, the risk factor of HBV cccDNA in PBMC among HBsAg-positive pregnant female's neonates remains unclear. Objectives: The aim of this studywas to explore influential factors of HBVcccDNA in PBMC among HBsAg-positive pregnant female's neonates. Methods: Peripheral blood samples and clinical data were collected from 151 pregnant females, who were positive for hepatitis B surface antigen (HBsAg) in the Third People Hospital of Taiyuan City. Blood samples from 152 neonates were collected before immune prophylaxes administration and tested for HBV markers, HBV DNA in serum, and HBV DNA in PBMC. Bayesian logistic regression with Cauchy prior were used to measure the association between maternal characteristics, neonatal characteristics, and HBV cccDNA in PBMC of neonates. Results: Among neonates of HBsAg-positive mothers, the positive rate of cccDNA in PBMC was 4.61% (7/152). Maternal PBMC HBV cccDNA positivity (OR = 18.411, 9 5%a 3.025 - 6 6.022 ) and neonates PBMC rcDNA positivity (OR =13.529, 95% CI: 1.948 - 93.690) were associated with HBV cccDNA in neonatal PBMC, respectively. Conclusions: The study suggested that HBV cccDNA can be detected in PBMC of HBsAg-positive mother's neonates. Maternal PBMC HBV cccDNA positivity and neonatal PBMC rcDNA positivity are risk factors of HBV cccDNA in PBMC of neonates.
目的 通过检测HBsAg阳性母亲分娩的新生儿外周血中T/B淋巴细胞亚群水平,分析HBV宫内传播对新生儿免疫功能的影响.方法 选择2011年1月至2014年12月太原市第三人民医院妇产科HBsAg阳性母亲分娩新生儿220例作为研究对象.采用酶联免疫吸附试验(ELISA)方法检测HBsAg阳性母亲及新生儿外周血HBV血清学标志物,实时荧光定量PCR检测HBsAg阳性母亲及新生儿外周血HBVDNA含量,流式细胞术(FCM)检测新生儿外周血T/B淋巴细胞亚群水平.新生儿出生24 h内静脉血HBsAg阳性或/和HBVDNA值>103 copies/ml者判定为发生HBV宫内传播.结果 HBsAg阳性母亲分娩新生儿HBV宫内传播发生率为11.36%.宫内传播新生儿组(n=25)与非宫内传播新生儿组(n=195)外周血T淋巴细胞亚群(CD3+、CD4+、CD8+)相对计数[(60.71±13.64)% vs (60.04±15.06)%,(43.37±12.69)%vs(43.77±13.39)%,(15.03±6.32)%vs(15.14±6.14)%],CD4+/CD8+[(3.42±1.66)% vs(3.33±1.71)%]及B淋巴细胞中CD19+相对计数[(6.64±3.63)%vs(6.39 ±3.99)%]差异均无统计学意义(P均>0.05).依据HBsAg阳性母亲分娩新生儿外周血HBVDNA不同载量,分为高载量组(HBVDNA≥107copies/ml)、低载量组(HBVDNA< 107 copies/ml)、阴性组(HBVDNA< 103 copies/ml).随着HBsAg阳性母亲分娩新生儿外周血HBVDNA载量增加,新生儿外周血CD3+、CD4+、CD8+相对计数及CD4 +/CD8+值逐渐增高,CD19+相对计数比例逐渐减低.高载量组新生儿CD3+、CD4+相对计数高于低载量组和阴性组,差异有统计学意义(P均<0.05);3组新生儿CD8+、CD19+相对计数及CD4+/CD8+比较差异均无统计学意义(P均>0.05).结论 随着HBVDNA载量的增加,HBsAg阳性母亲分娩的新生儿外周血中T淋巴细胞亚群(CD3+、CD4+)比例上升,新生儿细胞免疫功能处于活跃状态,易出现自身免疫反应,应采取相应措施防止自身免疫性疾病的发生.
This study determined the effect of hepatitis B virus (HBV) replication in peripheral blood mononuclear cell (PBMC) from HBsAg-positive mothers on HBV intrauterine transmission. A total of 150 HBsAg-positive mothers and their neonates were recruited in this study. Within 24 h after birth, HBV serological markers, serum HBV DNA, PBMC HBV relaxed circular DNA (rcDNA), and covalently closed circular DNA (cccDNA) were measured in the HBsAg-positive mothers and their neonates before passive-active immune prophylaxis. The relationship between HBV replication in PBMC and HBV intrauterine transmission was examined through Chi-square test and logistic regression. The rate of HBV intrauterine transmission was 8.00% (12/150) in the 150 neonates born to HBsAg-positive mothers. The positivities of PBMC HBV rcDNA and cccDNA in the HBsAg-positive mothers were 36.67% (55/150) and 10% (15/150), respectively. Maternal PBMC HBV cccDNA was a risk factor of HBV intrauterine transmission (OR= 6.003, 95% CI: 1.249–28.855). Maternal serum HBeAg was a risk factor of PBMC HBV rcDNA (OR= 3.896, 95% CI: 1.929–7.876) and PBMC HBV cccDNA (OR= 3.74, 95% CI: 1.186–11.793) in the HBsAg-positive mothers. Administration of hepatitis B immune globulin was a protective factor of PBMC HBV cccDNA (OR= 0.312, 95% CI: 0.102–0.954) during pregnancy. The positivity of PBMC HBV rcDNA was related to that of cccDNA in the HBsAg-positive mothers (c2=5.087, P= 0.024). This study suggests that PBMC is a reservoir of HBV and an extrahepatic site for virus replication and plays a critical role in HBV intrauterine transmission.
Maternal-infant transmission of hepatitis B virus(HBV) occurs even after passive-active immunization. Some scholars speculate that in-utero infection may be the main cause of immunoprophylaxis failure. However, there is a lack of evidence about the possible occurrence periods of perinatal transmission.
Background: An outbreak of a novel human avian influenza (H7N9) [h-H7N9 AI] took place in China from February 2013 to April 2015, with 628 reported cases. However, there were no exact answers on epidemiological patterns and its origin. Purpose: To examine the epidemiological patterns and its origin compared with other influenza outbreaks by combined analysis of risk factor surveillance and epidemiological characteristics, and to explore new surveillance methods for tracking infectious disease outbreaks.
Background: Novel Human Avian Influenza (H7N9) (h-H7N9 AI) occurred in China in February, 2013 and continued today. Although there were many reports on epidemiology, the reservoir and origin have not been confirmed. Methods: Until April 2015, 628 cases collected from WHO. Descriptive epidemiology was used to compare differences between h-H7N9 AI and other h-AI with statistical analysis. Results: Compared with only 18 cases of h-H5N1 AI located just in Hong Kong during 7 months, 571 cases with 212 died (37%) occurred up to February, 2015 and only limited in the mainland. It is suggested h-H7N9 AI were fully different from other h-AI, and may belong to very new type of “Natural Focus Disease (Zoonosis)”. H7N9 AIV was not detected in farms and wild birds in China before and during the early phase, and quite different from h-H5N1 AI occurred in geese of Guangdong in 1996 and in farms in 1997. So, h-H7N9 AI should have occurred in countries with it in birds and poultry for long time, rather than in China. The mean age was 62 years old in the beginning, then decreased to 59.0, 58.0 and 2 years later to 54.8, with correlation of the epidemic-lasting days (r=-0.953P=0.047). It indicated that the senior had no specific immunity and H7N9 AIV was absolutely new virus and never existed in China. Interpretation: We have creatively identified that h-H7N9 AI is with unique pattern based on abnormities in incidence and distributions and should has occurred in another country with it for long time.
Aims: A 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. Methods: 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. Results: 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. Conclusions: 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.
Hepatitis B virus (HBV) infection is of high prevalence in China. Mother-to-infant transmission is the major route for HBV transmission and subsequent chronicity. This study aimed to investigate current HBsAg-positive rate among pregnant women and immunoprophylaxis outcome in China. Multicenter prospective study was conducted in 10 centers. From 2008 to 2012, 67,720 pregnant women were screened and 1,150 HBsAg-carrier mothers and their infants aged 8–12 months were studied in four out of all centers, among whom HBV markers (HBsAg, HBsAb, HBeAg, HBeAb, and HBcAb) and HBV DNA (in three centers) were measured. The results showed that HBsAg-positive rate of pregnant women was 6.7 % (4,533/67,720) and infants’ immunoprophylaxis failure rate was 3.4 % (39/1,150). Immunoprophylaxis failure infants were all born to mothers of HBeAg-positive and HBV DNA ≥6 log10 copies/ml. Among infants of HBeAg-positive mothers, multivariable analyses showed the following: mother’s age <28 years vs ≥28 years, RR = 0.157, 95 % confidence interval (CI) [0.067, 0.369], p = 0.000; Neonates receiving vaccine vs vaccine plus hepatitis B immune globulin (HBIG), RR = 0.371, 95 % CI [0.167, 0.825], p = 0.015. Pregnant women receiving HBIG in the third trimester, vaginal delivery and breastfeeding had no significant effects on HBV mother-to-infant transmission. Conclusions: Pregnant women are still of high HBsAg prevalence in China. HBV mother-to-infant transmission still occurs after passive-active immunization. Pregnant women of high HBV replication levels are the major risk population of HBV mother-to-infant transmission. Passive-active immunization is necessary for neonates of HBeAg-positive mothers. Mother’s age <28 years and neonate receiving vaccine only were the risk factors for HBV mother-to-infant transmission. Breastfeeding did not put children at risk of mother-to-infant transmission.
Objective: This study was designed to explore if hepatitis B virus (HBV) may be transmitted via breast milk through mother-to-child transmission (MTCT), and assay the immunoprophylaxis efficacy after passive-active immunization.Method: From year 2008 to 2012, 67 720 pregnant women were screened and 1186 HBsAg-carrier mothers and their infants aged 8-12 months were followed in multi-centers of China, among whom HBV markers (HBsAg, HBsAb, HBeAg, HBeAb and HBcAb) and HBV-DNA were measured.Results: HBsAg positive rate of pregnant women was 6.7% (4533/67 720) and infants' immunoprophylaxis failure rate was 3.3% (39/1186). Immunoprophylaxis failure infants were all born to mothers of HBeAg positive and HBV-DNA >6 log(10) copies/ml. Among infants of HBeAg positive mothers, HBV infection rate was 9.0% and HBsAg positive rate was 8.3% in breast-feeding group versus 9.2% in formula-feeding group, P = 0.761. Occurrence of perinatal HBV infection was indicated in uterus or during delivery. Different feeding patterns had no effects on HBsAb conversion of infants with the implementation of immunization.Conclusions: HBsAg prevelance rate of pregnant women enrolled was 6.7% and immunoprophylaxis failure rate of infants was 3.3%, while the infection rate reached 9.0% in infants of HBeAg positive mothers. Breast feeding did not increase the occurrence of HBV MTCT.
OBJECTIVE:To explore the interrelated influence factors of HBV intrauterine infection in newborns of pregnant women with HBsAg. METHODS:HBsAg positive pregant women,who were prenatal diagnosis and partal, and their newborns were as subjects. Data of general situation of pregnant women and HBIG Jection history before delivery and HBV infection history in family and HBVM and HBVM in newborns at birth within 24h were collected. By if newborns occurred HBV intrauterine infection, 379 cases HBsAg-positive pregnant women are divided into two groups: 36 cases of HBV intrauterine infection, 343 cases of no HBV intrauterine infection. Then the relationship between the general situation of pregnant women, HBV infection history in family, the state of HBV replication, HBIG injection history, HBVM positive modes and HBV intrauterine infection in newborns were analyzed. RESULTS:Single factors analysis show: The difference of age, the state of HBV replication, HBVM positive modes of HBsAg positive pregant women between HBV intrauterine infection group and no HBV intrauterine infection group is significant (p < 0.05). But cultural levels,HBV infection history in family and HBIG injection history of HBsAg positive pregant women between the two groups isn't significant (p > 0.05). Multiariate Logistic regression analysis display: the age (OR = 0.398, 0.159-0.996) and both postitivity of HBeAg and HBV DNA (OR = 2.539,1.233- 5.227) go into regression equation. Meanwhile, the analysis of relation of HBV DNA load grade of HBsAg positive pregnant women and HBV intrauterine infection show: the different is significant (chi2 = 10.983, P = 0.004 < 0.05); and the analysis of trend chi-quare test show: when HBV DNA copy number is more than 10(6), the rate of HBV intrauterine infection obviously rise. CONCLUSIONS:The age (> 30 years) are the protected factors of HBV intrauterine infection in HBsAg positive pregant women. But when HBsAg positive pregant women is both postitivity of HBeAg and HBV DNA, the possibility is bigger to occur HBV intrauterine infection.