Hepatitis E Virus

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University of Oklahoma Study Abroad Microbiology in Arezzo, Italy[1]



NCBI: [2] Genome: [3]

genus: Hepevirus


Hepatitis E virus (HEV) was first discovered and accurately documented as a large acute outbreak in New Delhi around 1955. At the time they just called it enteric non-A, non-B hepatitis.[8] it wasn't until the 90s when its genome was cloned, studied and identified that it was named Hepatitis E.[9] is a non-enveloped, positive-sense, single-stranded ribonucleic acid (RNA) virus.[1] It is also the only virus within the genus Hepevirus and the family Hepeviridae.[2] 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. HEV is unique in that it displays different clinical and epidemiologic characteristics depending on where the infection is acquired which is mainly due to the four viral genotypes of HEV that have been identified.[3] 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.[4]



HEV has been found in all regions but has been more prevalently identified in certain parts of the world. The main factor identified in the transmission of HEV is through contaminated water and food. Hence, HEV outbreaks are common in developing countries that lack water supply and environmental sanitation. Although uncommon, cases of hepatitis E caused by HEV have been found in developed countries such as the United States ,usually by individuals who have traveled to areas where HEV is commonly an issue.[3] HEV can rarely happen in single cases or also in large epedemics. The epedemics occurs in areas where lots of people are using a common source of fecally contaminated water.

Infectious dose, incubation, and colonization

virulence factor

No specific virulence factor has been associated with the human or animal strains of HEV.[5]


HEV has four distinct types of genotypes that different epidemiological and clinical characteristics.
Genotype one: is found in Africa and Asian. It's transmitted through water-borne fecal- oral and also person-to-person. Although person-to-person transmission of HEV is is extremely uncommon there is a few studies that show its possibility in genotype one. The occurrence of outbreak of the genotype one is common.
Genotype two: genotype is found in Mexico and and West Africa. It too is transmitted through water-borne fecal- oral. The occurrence of genotype two is smaller scale outbreaks.
Genotype three geographic location is in developed countries. The route of transmission is food-borne. The occurrence of genotype three is very uncommon. Genotype three: is the only one of the four that can cause chronic infection.
Genotype four: occurs in China, Taiwan, and Japan. Its transmission route is also food-borne and its occurrence is rare (like genotype three). There is studies also suggesting that geonotype three and four can be passed between humans and animals. So these two genotypes could have the ability of zoonotic spread of the virus. This was concluded from a study in whichHEV RNA (genotypes 3 and 4) had been extracted from pork, boar, and deer meat. Infection could occur in the consumption of infected animals.[3]

Clinical features

The clinical symptoms are typically of acute viral hepatitis including jaundice, malaise, weight-loss and loss of appetite, nausea, abdominal pain, fever and hepatomegaly(enlarged liver).



Hepatitis E is self-limiting and doesn't result in chronic hepatitis.[6] This means it will resolve on its own and have no long term effect. Therefore treatment should be supportive to provide management of the symptoms.


Several vaccines for HEV are under development. A vaccine for HEV that uses recombinant baculoviruses was developed and clinically tested on human with a 95% success rate.[7] There is no information on when this vaccine will be in the market. Until a vaccine is approved for use, prevention includes not consuming contaminated food and water, avoiding travel to areas where HEV is prevalent and sustaining a general sanitary environment. When water contamination seems to be the cause of an epidemic measures to filter the water of HEV include chlorination of water supplies. Also Iodinated disinfectants or autoclaving destroys the virus.[6

Host immune response


1."Hepatitis E." WHO. Web. 25 July 2015. < http://www.who.int/mediacentre/factsheets/fs280/en/>
2. Purcell, R.H. and Emerson, S.U. Hepatitis E: an emerging awareness of an old disease. J Hepatol. 2008; 48: 494–503
3."Hepatitis E FAQs for Health Professionals." Centers for Disease Control and Prevention. Centers for Disease Control and Prevention, 31 May 2015. Web. 25 July 2015. <http://www.cdc.gov/hepatitis/hev/hevfaq.htm>.
4..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
5.Fayer R, Orlandi P, Perdue ML. 2009. Virulence factor activity relationships for hepatitis E and Cryptosporidium. J. Water Health 7(Suppl 1):S55–S63 doi:10.2166/wh.2009.044 [PubMed]
6. Smith J L 2001 A review of hepatitis E virus; J. Food. Prot. 64 572–586
7. Shrestha M P, Scott R M, Joshi D M, Mammen M P, Thapa G B, Thapa N, Myint K S, Fourneau M, et al 2007 Safety and efficacy of a recombinant hepatitis E vaccine. N. Engl. J. Med. 356 895–903 <http://www.ncbi.nlm.nih.gov/pubmed/17329696>
8. Vishwanathan R 1957 Infectious hepatitis in Delhi (1955–56). A critical study: epidemiology; Indian J. Med. Res. 45 49–58
9.ReyesGR,PurdyMA,KimJP,LukKC,YoungLM,FryK E and Bradley D W 1990 Isolation of a cDNA from the virus responsible for enterically transmitted non-A, non-B hepatitis; Science 247 1335–1339 <http://www.ncbi.nlm.nih.gov/pubmed/2107574>
10. Ticehurst JR. Hepatitis E Virus. In: Murray PR, Baron EJ, Pfaller MA, Tenover FC, and Yolken RH, eds. Manual of Clinical Microbiology, 7th ed. Washington DC, American Society for Microbiology Press, 1999:1053-1069.