Is there a role for viruses in triggering autoimmune hepatitis?

Research output: Contribution to journalReview article

45 Citations (Scopus)

Abstract

A role for viruses in autoimmune hepatitis (AH) has been repeatedly proposed but convincing evidence links only two viruses, hepatitis A and Epstein-Barr virus, to the type 1 form of the disease, and only in those rare cases where a genetic predisposition exists and the viral infection occurs at the right time, i.e. when other unknown factors are cooperating. In spite of an impressive amount of information conclusively showing molecular mimicry between cytochrome P450IID6 (the target autoantigen of autoantibodies characteristic of AH type 2) sequences and viral (hepatitis C virus, herpes simplex virus 1, cytomegalovirus, human T lymphotropic viruses 1 and 2) or bacterial (Salmonella typhimurium) antigens, no infectious agent is clearly able to induce this second form of the disease. In conclusion, the molecular mimicry theory has so far found little clinical evidence in its support and many more clinical observations are needed in order to unreveal possible links between viruses and AH.

Original languageEnglish
Pages (from-to)61-69
Number of pages9
JournalAutoimmunity Reviews
Volume3
Issue number1
DOIs
Publication statusPublished - Jan 2004
Externally publishedYes

Fingerprint

Autoimmune Hepatitis
Molecular Mimicry
Viruses
Human T-lymphotropic virus 2
Hepatitis A virus
Human T-lymphotropic virus 1
Autoantigens
Human Herpesvirus 1
Virus Diseases
Salmonella typhimurium
Cytochromes
Genetic Predisposition to Disease
Cytomegalovirus
Human Herpesvirus 4
Hepacivirus
Autoantibodies
Antigens

Keywords

  • Autoimmune hepatitis
  • Epstein-Barr virus
  • Hepatitis A virus
  • Measles virus
  • Suppressor T lymphocytes

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy

Cite this

Is there a role for viruses in triggering autoimmune hepatitis? / Vento, Sandro; Cainelli, Francesca.

In: Autoimmunity Reviews, Vol. 3, No. 1, 01.2004, p. 61-69.

Research output: Contribution to journalReview article

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