Hepatitis E Virus: Difference between revisions
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==References== | ==References== | ||
1."Hepatitis E." WHO. Web. 25 July 2015. < http://www.who.int/mediacentre/factsheets/fs280/en/> <br> | 1."Hepatitis E." WHO. Web. 25 July 2015. < http://www.who.int/mediacentre/factsheets/fs280/en/> <br> | ||
2.Rein DB, Stevens GA, Theaker J, Wittenborn JS, Wiersma ST. The Global Burden of Hepatitis E Virus Genotypes 1 and 2 in 2005. Hepatology, Vol. 55, No. 4, 2012: 988-997 | 2.Rein DB, Stevens GA, Theaker J, Wittenborn JS, Wiersma ST. The Global Burden of Hepatitis E Virus Genotypes 1 and 2 in 2005. Hepatology, Vol. 55, No. 4, 2012: 988-997 | ||
Revision as of 13:51, 25 July 2015
[[Category:Pages edited by students of Tyrrell Conway at the University of Oklahoma]]
Etiology/Bacteriology
Taxonomy
Description
Hepatitis E virus (HEV) is a non-enveloped, positive-sense, single-stranded ribonucleic acid (RNA) virus.[1] HEV is one of the five identified hepatitis viruses (A,B,C,D, E) . Hepatitis E is most similar to hepatitis A, in that they are both transmitted through contaminated food or water. The other types of hepatitis(B,C,D) are transmitted through infected blood, sexual contact and from mother to child. HEV is the causative agent of the infectious disease Hepatitis E. Every year there are 20 million hepatitis E infections, with over 3 million symptomatic cases of hepatitis E, and 56 600 hepatitis E-related deaths.[2]
Pathogenesis
Clinical features
Diagnosis
Treatment
Prevention
Host immune response
References
1."Hepatitis E." WHO. Web. 25 July 2015. < http://www.who.int/mediacentre/factsheets/fs280/en/>
2.Rein DB, Stevens GA, Theaker J, Wittenborn JS, Wiersma ST. The Global Burden of Hepatitis E Virus Genotypes 1 and 2 in 2005. Hepatology, Vol. 55, No. 4, 2012: 988-997
