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Review
. 2024 Jun 16;13(6):508.
doi: 10.3390/pathogens13060508.

Direct-Acting Antiviral Agents in Prevention of Maternal-Fetal Transmission of Hepatitis C Virus in Pregnancy

Affiliations
Review

Direct-Acting Antiviral Agents in Prevention of Maternal-Fetal Transmission of Hepatitis C Virus in Pregnancy

Christopher Hartley et al. Pathogens. .

Abstract

Prior to the Food and Drug Administration approval of ledipaspavir/sofosbuvir (Harvoni®) in 2014, the treatment of hepatitis C was interferon plus or minus ribavirin. This treatment had low cure rates for hepatitis C virus and was teratogenic and therefore avoided in pregnant patients. Vertical transmission is the most common transmission of hepatitis C in pediatric patients, whereas medical equipment that was not properly cleaned and sterilized, blood products which were not checked (historically), sharing and reusing syringes and needles, and dialysis are the most common forms of hepatitis C transmission in adults. The treatment of pregnant women with direct-acting antivirals is important because the treatment of pediatric patients cannot begin until three years of age and does not always occur prior to the symptom development of hepatitis C. This review article will include glecaprevir/pibrentasvir (Mayvret®), sofosbuvir/velpatasvir (Epclusa®), and sofosbuvir/velpatasvir plus voxilaprevir (Vosevi®). We aim to review the teratogenic risk of direct-acting antivirals as well as currently published clinical trials and ongoing research on direct-acting antiviral hepatitis C treatment in pregnancy in this publication.

Keywords: direct-acting-antiviral agents; hepatitis C; pregnancy.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
(Reprint of figure from Le Campion and colleagues [22]). Three potential modes of HCV fetal transmission: transcytosis, receptor binding, and lesion. The trophoblast, the epithelial layer of the placenta, consists of syncytiotrophoblast and cytotrophoblast. Cytotrophoblast serves as the inner layer of the trophoblast and eventually matures into the syncytiotrophoblast, which serves as the trophoblast’s outer layer. HCV from the mother can directly infect the fetus through cytotrophoblast transcytosis, binding to trophoblast’s HCV receptors, or injuries that affect the placental junction’s integrity [22].

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