Complete information about hepatitis E Virus - structure, epidemiology, replication, pathogenesis, transmission, treatment, vaccine and prevention.

1. HEPATITIS (E)VIRUS
PREPARED
BY:-
SOURABH
GROUP 323-A

2. STRUCTURE OF THEVIRUS
• The virus is non enveloped (naked).
• Icosahedral symmetry
• 27-30 nm diameter.
• The genome is single stranded RNA genome
• With positive polarity and measure about 7.2 kb in length.

3. STRUCTURE OF THE HEPATITIS EVIRUS

4. EPIDEMIOLOGY
• The HEV infection was first reported from the Indian
subcontinent and subsequently from other parts of Asia,
the Middle East, Central and South America, Africa, Central
Europe and Russia.
• People travelling to countries with high prevalence are
therefore at risk of acquiring infection during their travel.
• Adult populations in endemic areas are generally
susceptible and there is a high infection rate in epidemics.

6. REPLICATION OF THEVIRUS
• The HEV capsid protein is believed to bind to a cellular receptor to initiate viral entry and
replication.
• ORF2 peptide-binding experiments suggested that the C-terminal region of ORF2 may mediate
virus entry by binding to heat shock cognate protein 70 (HSC70) on the cell surface.
• Additionally, HSPGs have been identified as attachment receptors that are located on the cell
surface.
• After virus entry into permissive cells, the HEV genomic RNA is uncoated by unknown
mechanisms.
• After uncoating, virion releases the positive-sense genomic RNA into the cytoplasm of the cell.

7. REPLICATION OF THEVIRUS
• The positive-sense genomic viral RNA serves as the template to translate the ORF1
nonstructural polyprotein in the cytoplasm.
• The viral RdRp synthesizes an intermediate, replicative negative-sense RNA from the
positive-sense genomic RNA that serves as the template for the production of positive-
sense, progeny viral genomes.
• The ORF2 and ORF3 proteins are translated from the subgenomic, positive-stranded RNA,
and the ORF2 capsid protein packages the genomic viral RNA and assembles new virions.
• The nascent virions are transported to the cell membrane.
• The ORF3 protein facilitates the trafficking of the virion, and the nascent virions are
released from the infected cells by lysis.

9. TRANSMISSION OF THEVIRUS
• The hepatitis E virus is transmitted mainly through the faecal-
oral route due to faecal contamination of drinking water or via
Ingestion of undercooked meat or meat products derived from
infected animals.
• Other transmission route includes: vertical transmission from a
pregnant woman to her fetus and transfusion of infected blood
products.

10. PATHOGENESIS OF THEVIRUS
• Since HEV is presumably transmitted by the fecal-oral route, it is unclear
how the virus reaches the liver.
• There is an extra-hepatic site of virus replication.
• The virus could replicate in the intestinal tract before reaching the liver.
• Negative strands of HEV RNA, indicating virus replication, have been
detected in the small intestine, lymph nodes, colon, and liver of pigs,
indicating extra-hepatic HEV replication.
• HEV then replicates in the cytoplasm of hepatocytes and is released into
both blood and bile.

11. PATHOGENESIS OF THEVIRUS
• The liver damage induced by HEV infection may be immune-mediated by cytotoxic
T cells and natural killer (NK) cells since HEV is not cytopathic.
• The virus is shed in the stool.
• A serological anti-HEV response is generally detected in patients at the time of
onset of illness.
• Anti-HEV IgMs are detected in the early phase of clinical illness, and can persist for
several months.
• Anti-HEV IgG appears shortly after the IgM response and can last several years.
• Cross protection is possible due to the existence of only one serotype.

13. LABORATORY DIAGNOSIS OF THE HEPATITIS E
VIRUS
• Specimens: Blood, serum, stool
• Definitive diagnosis of hepatitis E infection is usually based
on the detection of specific IgM and IgG antibodies to the
virus in a person’s blood.
• Additional tests include reverse transcriptase polymerase
chain reaction (RT-PCR) to detect the hepatitis E virus RNA
in blood and/or stool.

14. TREATMENT OFTHE HEPATITIS EVIRUS
• There is no specific treatment capable of altering the course of acute
hepatitis E.
• The disease is usually self-limiting.
• Hospitalization is required for people with fulminant hepatitis, and
should also be considered for symptomatic pregnant women.
• Immunosuppressed people with chronic hepatitis E benefit from specific
treatment using ribavirin, an antiviral drug.
• In some specific situations, interferon has also been used successfully.

15. VACCINE FORTHEVIRUS
• HEV is preventable by
vaccination. HEV239 (Hecolin) is a
recombinant HEV vaccine against
genotype 1 and 4 that has shown
to have more than 95%
protection against the virus and
to be safe in pregnancy. This
vaccine is now available in China”.

16. PREVENTIONAND CONTROL OF THEVIRUS
• At the population level, transmission of HEV and hepatitis E disease can
be reduced by:
• Maintaining quality standards for public water supplies.
• Establishing proper disposal systems for human feces.
• On an individual level, infection risk can be reduced by:
• Maintaining hygienic practices such as hand-washing with safe water,
particularly before handling food.
• Avoiding consumption of water and/or ice of unknown purity, and
adhering to WHO safe food practices.

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