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Neonatal Inflammatory Profiles Associated With Perinatally Acquired Hepatitis C Viral Infection
Stephanie A Fisher1, Grecio J Sandoval2, George R Saade3
1Department of Obstetrics and Gynecology, University of Alabama at Birmingham, Birmingham, Alabama.
The Pediatric Infectious Disease Journal
|May 5, 2026
Summary
Hepatitis C transmission from mother to infant was studied. Infants with perinatal hepatitis C infection showed higher levels of programmed death-ligand 1, a marker of T-cell exhaustion, at two months old.
Area of Science:
- Immunology
- Hepatology
- Pediatrics
Background:
- Hepatitis C virus (HCV) can be transmitted from mother to infant during pregnancy or delivery.
- Understanding the immunological consequences of perinatal HCV infection in infants is crucial for early diagnosis and management.
- Biomarkers indicating immune responses or dysfunction in infants exposed to HCV are needed.
Purpose of the Study:
- To investigate plasma cytokine and chemokine profiles in infants with in utero exposure to Hepatitis C virus.
- To identify potential biomarkers associated with perinatal Hepatitis C virus transmission and infection in early infancy.
Main Methods:
- A nested case-control study design was employed.
- Plasma samples were collected from infants at 2 months of age.
- Twenty-one plasma cytokines/chemokines were measured, comparing 11 infants with confirmed perinatal HCV transmission to 11 matched controls without HCV exposure.
Main Results:
- Six out of 21 assessed biomarkers were detectable in infant plasma.
- Infants with perinatal HCV infection exhibited significantly higher plasma levels of programmed death-ligand 1 (PD-L1).
- PD-L1 is a proposed marker associated with T-cell exhaustion.
Conclusions:
- Elevated PD-L1 in infants with perinatal Hepatitis C infection suggests a potential role in immune modulation or T-cell exhaustion.
- Further research is warranted to evaluate the significance of PD-L1 as a biomarker in infants with perinatal HCV infection.
- These findings may contribute to understanding the infant immune response to perinatal Hepatitis C virus exposure.
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