- 现金
- 62111 元
- 精华
- 26
- 帖子
- 30437
- 注册时间
- 2009-10-5
- 最后登录
- 2022-12-28
|
Characterization of Hepatitis B Virus in Tenofovir-Treated and Untreated Chronically Infected Mothers and Their Immunoprophylaxis Failure Infants
Hong Yuan Hsu, Huey Ling Chen, Cheng Lun Chiang, Ming Wei Lai, Shu Chi Mu, Wan Hsin Wen, Shao Wen Cheng, Jen Jan Hu, Kai Chi Chang, Chien Nan Lee ... Show more
Clinical Infectious Diseases, ciac539, https://doi.org/10.1093/cid/ciac539
Published:
05 July 2022
Abstracts
Background
Maternal tenofovir disoproxil fumarate (TDF) therapy during late pregnancy can reduce mother-to-infant transmission of hepatitis B virus (HBV). We investigated HBV mutations associated with maternal TDF therapy and their role in infant immunonophylaxis failure (IPF).
Methods
Serum samples from untreated (n = 89) and TDF-treated (n = 68), highly-viremic, chronically infected mothers and their infants were analyzed for HBV DNA by nested-PCR and direct sequencing.
Results
At delivery, compared with untreated mothers, TDF-treated mothers had a lower HBV DNA titer and a higher frequency of basal core promoter (BCP) gene mutations, but they had similar frequencies in pre-S/S and pre-core/core mutations. The 14 mothers harboring surface “a” determinant mutants did not transmit the mutants to their immunized infants. Such mutants were found in 3 of 13 IPF infants; the 13 mothers had wild-type HBsAg. In univariable analysis, maternal HBV DNA titer (odds ratio [OR]: 1.54; 95% confidence intervals [CI]:1.02∼2.33; P = 0.039), genotype C (OR: 4.18; 95% CI: 1.28∼13.62; P = 0.018) and pre-S1 wild-type sequence (OR: 6.33; 95% CI: 1.85∼21.68; P = 0.003) at delivery were associated with infant IPF. Multivariable analyses showed that maternal genotype C (OR: 3.71; 95% CI: 1.11-12.36; P = 0.033) and pre-S1 wild-type (OR: 6.34; 95% CI: 1.79-22.44; P = 0.004) were associated with infant IPF independently of maternal viremia.
Conclusions
Conclusions
Along with high maternal HBV DNA titer at delivery, maternal genotype C and pre-S1 wild-type sequence were potential risk factors for infant IPF, while BCP mutations were not. The offspring of pregnant women harboring “a” determinant mutants as major strains seemed to be protected by immunoprophylaxis. |
|