Hepatitis E virus Virology

1. HEPATITIS E PRESENTED BY:
ZOHAIB PERVEZ
ROLL NO. 04

2. .
“Hepatitis E is characterized by the inflammation of the liver caused by infection
with the hepatitis E virus (HEV).”
• TRANSMISSION: HEV is the majorally transmitted by the fecal oral route.
• OCCURANCE: It is the common cause of water borne epidemics of hepatitis
in Asia, Africa, India and Mexico.
• CLINICAL: The disease resembles hepatitis A with high mortality rate in
pregnant women specially in 3rd trimester due to fulminant hepatitis.

3. .
• STRUCTURE: HEV is a single stranded RNA virus,
having icosahedral shape belonging to the
HEPEVIRIDAE family. Its genome has 3 ORF (open
reading frame) i.e., ORF 1, ORF 2, ORF3.
• VIRULENCE: It is a noncytopathic virus.
• GENETIC DIVERSITY: HEV exhibits genetic diversity
and is classified into 4 major genotypes i.e., 1,2,3,4.
• Genotype 1 and 2 primarily infect humans.
• Genotypes 3 and 4 infect both humans and animals,
including pigs, wild boars and deer.

4. .
• FECAL ORAL ROUTE: HEV is primarily
transmitted via the fecal-oral route.
-CONTAMINATED WATER: HEV can survive in
water for extended periods, making it a significant
risk factor for infection.
-CONTAMINATED FOOD: Consumption of raw or
undercooked shellfish, pork, or meat that are
contaminated with HEV. Proper cooking and
handling of food can help reduce the risk.
• Person to person transmission: HEV can also be
transmitted through person-to-person contact,
particularly in settings such as households or
healthcare facilities where there is close contact
with infected individuals.

5. .
• Acute Infection: HEV infection typically manifests as an acute
illness characterized by jaundice, fatigue, nausea, vomiting,
abdominal pain, and sometimes fever. Most cases of HEV resolve on
their own within a few weeks to months.
• Fulminant hepatitis: While most cases of HEV infection are self-
limiting, but a small proportion of individuals, particularly pregnant
women and those with pre existing liver disease, can develop
fulminant hepatitis, which is a severe and potentially life-threatening
form of liver failure.
• Chronic infection: Although rare, HEV infection can sometimes lead
to chronic hepatitis in immunocompromised individuals, such as
organ transplant recipients or these with HIV infection.

7. • ATTACHEMENT & ENTRY: HEV attaches to the
enterocytes integrin a3 with the help of heparan sulfate.
• PENETRATION: It enters the cell as whole and gets
surrounded by membrane to form a vesicle.
• UNCOATING: The coats gets removed and viral genome
is released into the cell.

8. NOTE: HEV IS A NONCYTOPATHIC VIRUS
• REPLICATION: The process of translation occurs with the
help of RNA polymerase and produces structural proteins.
• ORF1 & ORF 3 encode for nonstructural proteins whereas
ORF 2 encodes for capsid of the virus.
• ASSEMBLY: All of the structural and nonstructural proteins
assemble to form a new virus.
• RELEASE: New viruses are released without damaging the
cell wall of the host cell.

10. .
• VIRAL TRANSMISSION: HEV is transmitted primarily
through the fecal oral route, typically via contaminated water
or food.
• VIRAL REPLICATION: After ingestion the virus enters the
gastrointestinal tract and infects enterocytes, which are cells
lining the intestine. HEV then replicates within these cells.
• DISSEMINATION: The virus can spread from the intestine to
liver through the bloodstream. It infects hepatocytes, the main
cells of the liver where it continues to replicate. It might enter
GIT through bile.

11. • IMMUNE RESPONSE: The immune system recognizes the
presence of the virus and mounts as immune response, this response
can lead to inflammation of the liver (hepatitis). You can detect virus
in liver by this time i.e., 7 days after transmission.
• LIVER DAMAGE: The ongoing immune response, along with viral
replication, can cause damage to hepatocytes, leading to liver
inflammation and dysfunction
• EXTRAHEPATITIC MANIFESTATIONS : In addition to liver
involvement, HEV infection can sometimes lead to neurological
symptoms, acute pancreatis, and kidney injury, although these are
relatively rare.

12. .
• Initial phase includes symptoms like:
• Fever
• Fatigue
• Vomiting
• Abdominal pain or discomfort
• Jaundice
• Dark urine
• Pale stools
• Sometimes itching
• Rarely, acute liver failure or fulminant hepatitis especially in
pregnant women or individuals with pre existing liver conditions.
• Symptoms may vary person to person

13. • The incubation period for HEV is 2-9 weeks.
• Since clinically the symptoms of hepatitis E are not distinguishable
from the other types of acute viral hepatitis, so diagnosis can only be
done by testing the presence of anti-HEV, IgM and IgG through rapid
testing assays or through PCR.

14. .
• There is no specific treatment for altering the course of hepatitis E. It
is usually self-limiting, hospitalization is generally not required. It is
important to avoid unnecessary medications that can adversely affect
liver function, e.g. acetaminophen, paracetamol.
• 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 antiviral drugs.

15. .
Preventions for hepatitis E include:
• Maintaining quality standards for
public water supplies.
• Establishing proper disposal systems.
• Maintaining hygienic practices.
• Avoiding water and ice of unknown
purity.

16. .
• In 1996, hepatitis G virus (HGV) was isolated from
patients with post transfusion hepatitis, HGV is a member
of the flavivirus family, as is HCV. It can cause a chronic
infection lasting for decades. Approximately 60% to 70%
of those infected clear the virus and develop antibodies.
• HGV is transmitted via sexual intercourse and blood.
Patients confected with HIV and HGV have a lower
mortality rate and have less HIV in their blood than those
infected with HIV alone. It is hypothesized that HGV
may interfere with the replication of HIV.

17. THE END 
• REFERENCE: Wikipedia, Byju’s & YouTube