Abnormal Development - Hepatitis Virus

Introduction

Hepatitis A virions (CDC)

Hepatitis B virions (CDC)

Hepatitis (inflammation of the liver) is caused in humans by one of 7 viruses (A, B, C, D, E) with the 2 additional F has not been confirmed as a distinct genotype; and G is a newly described flavivirus. CDC states that all of these viruses can cause an acute disease with symptoms lasting several weeks including yellowing of the skin and eyes (jaundice); dark urine; extreme fatigue; nausea; vomiting and abdominal pain. It can take several months to a year to feel fit again.

An estimated 400 million people worldwide are living with chronic hepatitis B infection.

Virus particles measure 42nm in overall diameter and contain a 27nm diameter DNA-based core.

| Liver Development | Liver Histology

Some Recent Findings

Update on childhood and adolescent immunizations: selected review of US recommendations and literature: part 2 "Vaccine coverage is relatively static or improving for the vaccines included in the 2010 annual harmonized immunization schedules. Providers should be reviewing patients' immunization records at each visit to take advantage of any opportunity to administer indicated, age-appropriate vaccines. There have been infectious disease outbreaks among highly immunized populations, although unvaccinated or undervaccinated individuals continue to play large roles in the spread of disease. Infants, many of whom are too young to be vaccinated, continue to bear a large disease burden, which underscores the importance of cocooning and, in some cases, vaccination of pregnant women. Influenza, measles, mumps, and rubella, varicella, hepatitis A, meningococcal conjugate, human papillomavirus, diphtheria and tetanus toxoids and acellular pertussis, and tetanus and diphtheria toxoids and acellular pertussis vaccines are reviewed in this second of two articles."

Hepatitis Transmission Risk to the Fetus

Hepatitis A

• Fetal transmission of virus occurs with extreme rarity.

Hepatitis B

• Can occur as a consequence of intrapartum exposure, transplacental transmission, and breastfeeding.
• 20% - 30% of HBsAg-positive/HbeAg-negative women will transmit virus to their infants.
• 90% of HBsAg- and HBeAg-positive women will transmit virus to their infants.
• Immunoprophylaxis at birth with both HBIG and Hepatitis B vaccine within 12 hours of birth decreases the risk of transmission.
• Passive (HBIG) and active immunization is 85-95% effective in preventing neonatal HBV infection.
• Chronic infection occurs in almost all children who are infected with hepatitis B during the perinatal period and in up to 50% of children who become infected between 1 and 5 years of age.

Hepatitis C

• The overall risk of transmission is approximately 2-6% with unknown maternal viral titers.
• All pregnant women with HCV should have viral titers performed.
• The placenta appears to act as an immunological organ providing antiviral protection against hepatitis C viral transmission in the majority of cases.
• Children and adolescents with chronic infection generally have no symptoms.
• Breast-feeding does not appear to transmit virus.

Data Sources

Hepatitis E virions (CDC)

Adult Hepatitis B Treatment

Women who are HBsAg-positive have a very high risk for vertical transmission to their infants. NIH currently recommends that infants of HBsAg-positive women receive hepatitis B immunoglobulin and hepatitis B vaccination within 12 hours of birth and receive a complete set of 3 vaccinations and long-term follow-up. This has been shown to substantially reduce the risk for perinatal transmission.

U.S. Food and Drug Administration have approved 7 agents, used as monotherapy or in combination, for use in the treatment of adults with Hepatitis B.

• interferons (interferon-α2b and peginterferon-α2a)
  • Interferon use has a defined self-limited course.
• nucleoside or nucleotide analogues (lamivudine, adefovir, entecavir, tenofovir, and telbivudine)
  • therapy can be long-term or indefinite treatment.

Liver Damage

Sequelae of chronic Hepatitis C infection are progressive liver fibrosis leading to cirrhosis, end-stage liver disease, and Hepatocellular Carcinoma (HCC).

References

Textbooks

• Medical Microbiology. 4th edition. Baron S, editor. Galveston (TX): University of Texas Medical Branch at Galveston; 1996.
  • Chapter 55 Togaviruses: Rubella Virus

• Molecular Biology of the Cell. 4th edition. Alberts B, Johnson A, Lewis J, et al. New York: Garland Science; 2002.
  • Viruses Exploit Host Cell Machinery for All Aspects of Their Multiplication
  • Some Viruses Use Transpositional Site-specific Recombination to Move Themselves into Host Cell Chromosomes

Search Pubmed

Search PubMed: term = Hepatitis Virus teratology | embryo infection | fetal infection | neonatal infection

External Links

External Links Notice - The dynamic nature of the internet may mean that some of these listed links may no longer function. If the link no longer works search the web with the link text or name. Links to any external commercial sites are provided for information purposes only and should never be considered an endorsement. UNSW Embryology is provided as an educational resource with no clinical information or commercial affiliation.

• International Committee on Taxonomy of Viruses
• Australian Government The Australian Immunisation Handbook 9th Edition 2008
• NIH (USA) Consensus Development Conference Management of Hepatitis B October 20–22, 2008 Bethesda, Maryland | Management of Hepatitis C: 2002 June 10-12, 2002

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Glossary Links

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Cite this page: Hill, M.A. (2024, May 6) Embryology Abnormal Development - Hepatitis Virus. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Abnormal_Development_-_Hepatitis_Virus

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