Fulminant hepatitis B virus (HBV) infection in an infant following mother-to-child transmission of an e-minus HBV mutant: Time to relook at HBV prophylaxis in South African infants

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Abstract

The prevalence of hepatitis B virus (HBV) infection in pregnant women is high in South Africa (SA), yet prophylaxis to prevent mother-to-child transmission (MTCT) falls short of international recommendations. We describe a 10-week-old infant who developed fulminant hepatic failure following MTCT. The mother was hepatitis e-antibody positive and had a viral load of only 760 IU/mL. Genetic analysis of virus from mother and infant showed that both had the G1896A mutation in the preC/C gene, which truncates hepatitis e antigen (HBeAg) during translation, causing an HBeAg-negative phenotype. HBeAg attenuates antiviral immune responses, and its absence was probably responsible for the infant's fulminant hepatitis, due to an uncontrolled immune attack on infected liver cells. Pregnant women are not tested for HBV infection in SA and MTCT rates are unknown. Addition of a birth dose of vaccine, HBV screening of pregnant women and antiviral prophylaxis to positive mothers should be prioritised.

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Vaccine-induced escape mutant of hepatitis B virus.

Rudolph E. Tanzi, Valerie J. Waters, Glenn Carman … (1990)

In southern Italy, 44 contacts of hepatitis B virus carriers, including infants of carrier mothers, became HBsAg positive despite passive and active immunisation according to standard protocols. In 32 of these vaccinees infection was confirmed by the presence of additional markers of viral replication. In 1 infant, serious disease occurred. The virus from this patient is an escape mutant with a different sequence from that of the isolate from the mother. A point mutation from guanosine to adenosine at nucleotide position 587 resulted in an aminoacid substitution from glycine to arginine in the highly antigenic a determinant of HBsAg. This mutation is stable: it is present in an isolate from the child 5 years later. In some of these patients, including this child, the a determinant, to which a large part of the vaccine-induced immunity is directed, has been partly lost. Binding to HBsAg of a monoclonal antibody, previously mapped to the region of the mutation, was reduced in the child relative to that of the mother.

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Effects of maternal screening and universal immunization to prevent mother-to-infant transmission of HBV.

Ling Chen, Wen-Hsiang Lin, Yueng-Hsiang Chu … (2012)

Mother-to-infant transmission is the major cause of hepatitis B virus (HBV) infection among immunized children. There has been much debate about screening pregnant women and administering hepatitis B immunoglobulin (HBIG) to newborns. We analyzed the rate of HBV infection among children born to hepatitis B surface antigen (HBsAg)-positive mothers and whether HBIG administration reduces transmission. We analyzed data from 2356 children born to HBsAg-positive mothers, identified through prenatal maternal screens. In addition to HBV vaccines, HBIG was given to all 583 children with hepatitis B e antigen (HBeAg)-positive mothers and to 723 of 1773 children with HBeAg-negative mothers. Serology tests for HBV were performed from 2007 to 2009, when children were 0.5-10 years old. A significantly greater percentage of children with HBeAg-positive mothers tested positive for antibodies against the hepatitis B core protein (16.76%) and HBsAg (9.26%) than children with HBeAg-negative mothers (1.58% and 0.29%, respectively; P < .0001 and <.001). Among the HBV-infected children, the rate of chronicity also was higher among children with HBeAg-positive mothers than children with HBeAg-negative mothers (54% vs 17%; P = .002). Similar rates of antibodies against the hepatitis B core protein (0.99% and 1.88%; P = .19) and HBsAg (0.14% and 0.29%; P = .65) were noted in children born to HBeAg-negative mothers who were or were not given HBIG. Infantile fulminant hepatitis developed in 1 of 1050 children who did not receive HBIG (.095%). Children born to HBeAg-positive mothers are at greatest risk for chronic HBV infection (9.26%), despite immunization. Administration of HBIG to infants born to HBeAg-negative mothers did not appear to reduce the rate of chronic HBV infection, but might prevent infantile fulminant hepatitis. Screening pregnant women for HBsAg and HBeAg might control mother-to-infant transmission of HBV. Copyright © 2012 AGA Institute. Published by Elsevier Inc. All rights reserved.

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Hepatitis B vaccines: WHO position paper – July 2017.

(2017)

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Author and article information

Contributors

O Babatunde: Role: ND

H Smuts: Role: ND

B Eley: Role: ND

S Korsman: Role: ND

R de Lacy: Role: ND

D R Hardie: Role: ND

Journal

Journal ID (publisher-id): samj

Title: SAMJ: South African Medical Journal

Abbreviated Title: SAMJ, S. Afr. med. j.

Publisher: Health and Medical Publishing Group (Cape Town, Western Cape Province, South Africa )

ISSN (Print): 0256-9574

ISSN (Electronic): 2078-5135

Publication date (Print and electronic): May 2018

Volume: 108

Issue: 5

Pages: 389-392

Affiliations

[02] orgnameUniversity of Cape Town orgdiv1Faculty of Health Sciences orgdiv2Department of Paediatrics and Child Health South Africa

[11] Cape Town orgnameGroote Schuur Hospital orgdiv1National Health Laboratory Service South Africa

[12] Cape Town orgnameRed Cross War Memorial Children's Hospital orgdiv1Paediatric Infectious Diseases Unit South Africa

[10] orgnameUniversity of Cape Town orgdiv1Department of Paediatrics and Child Health South Africa

[01] Cape Town orgnameRed Cross War Memorial Children's Hospital orgdiv1Paediatric Infectious Diseases Unit South Africa

[13] orgnameUniversity of Cape Town orgdiv1Faculty of Health Sciences orgdiv2Department of Paediatrics and Child Health South Africa

[03] Cape Town orgnameGroote Schuur Hospital orgdiv1National Health Laboratory Service South Africa

[05] Cape Town orgnameRed Cross War Memorial Children's Hospital orgdiv1Paediatric Infectious Diseases Unit South Africa

[04] orgnameUniversity of Cape Town orgdiv1Faculty of Health Sciences orgdiv2Department of Pathology South Africa

[08] orgnameUniversity of Cape Town orgdiv1Faculty of Health Sciences orgdiv2Department of Pathology South Africa

[06] orgnameUniversity of Cape Town orgdiv1Faculty of Health Sciences orgdiv2Department of Paediatrics and Child Health South Africa

[09] Cape Town orgnameRed Cross War Memorial Children's Hospital orgdiv1Gastroenterology Unit South Africa

[07] Cape Town orgnameGroote Schuur Hospital South Africa

Article

Publisher ID: S0256-95742018000500012

DOI: 10.7196/samj.2018.v108i5.13017

SO-VID: ef5b705f-f14d-4077-92d8-0ddee9509d5b

License:

This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

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Figures: 0, Tables: 0, Equations: 0, References: 25, Pages: 4

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SciELO South Africa

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