The document summarizes hepatitis E virus (HEV), including its virology, epidemiology, transmission, clinical presentation, diagnosis, management, and prevention. HEV is an RNA virus endemic in Asia and causes acute, self-limiting hepatitis but can develop into acute liver failure, especially in pregnant women. It is transmitted primarily through contaminated food or water. Acute hepatitis E presents with jaundice and liver enzyme abnormalities and typically resolves within 1-6 weeks, though complications can include acute liver failure, chronic hepatitis may occur in immunosuppressed patients. Pregnant women are at higher risk for more severe outcomes. Management involves supportive care and chronic hepatitis may be treated with antivirals.

1. HEPATITIS E

2. OBJECTIVES
Hepatitis E virus
• Virology and epidemiology
• Transmission
A. Acute Hepatitis E
B. Chronic Hepatitis E
• Diagnosis
• Management

3. HEPATITIS E
• Hepatitis E is caused by an RNA virus which is endemic in India and
the Middle East
• The clinical presentation and management of hepatitis E are similar to
that of hepatitis A
• it presents as a self-limiting acute hepatitis and does not cause chronic
liver disease
• Hepatitis E differs from hepatitis A in that infection during pregnancy
is associated with the development of acute liver failure, which has a
high mortality

4. VIROLOGY (HEV)
• Hepviridae family
• Icosahedral , non-enveloped single stranded + RNA virus
• Has 3 open reading frames (ORF) (genes):
• ORF1- codes non-structural protein, involved in replication
• ORF2- codes for viral capsid protein
• ORF3- codes for viroporin (help release of infectious virions
frominfected cell)
• Among five known genotypes, Four are infectious to human
(Genotypes differ in geographic region and route of transmission)

5. EPIDEMIOLOGY
Global distribution (20 million new cases/year and over 55,000
deaths/year)
• Genotypes 1 and 2 – Asia, India , and North America
• Genotypes 2- Mexico and west Africa
• Genotypes 3 – Western countries, Asia and North America
• Genotypes 4 – Asian and European Countries
• More common in developing countries (10-70% Vs. 1-20%)

6. TRANSMISSION
1. Contaminated food and water
a. water borne infection - HEV genotype 1 and 2
b. Zoonotic Transmission – HEV Genotypes 3 and 4
- selfish consumption and
- animal exposure(swine, rodents, cow milk
(HEV-4)
2. Blood Transfusion
3. Perinatal transmission
4. Transmission in breast milk – though insufficient data , not suggested to
breastfeed

7. A. Acute Hepatitis

8. ACUTE HEAPTITIS E
• Though self-limited HEV, some may develop acute hepatic failure
Clinical features:
• asymptomatic (majority)
• jaundice, accompanied by - malaise, anorexia, nausea, vomiting,
abdominal pain, fever, and hepatomegaly
• less common features include diarrhea, arthralgia, pruritus, and
urticarial rash

9. Extrahepatic findings
• Hematologic abnormalities including thrombocytopenia, hemolysis, and
aplastic anaemia
• Acute thyroiditis
• Membranous glomerulonephritis
• Acute Pancreatitis
• Neurological disease
(e.g. Acute transverse myelitis, Aseptic meningitis,
Cranial nerve palsies, peripheral neuropathy )

10. INVESTIGATIONS
Lab Findings :
• Increase – serum bilirubin, ALT, and AST
• Symptoms coincide with a sharp rise in serum ALT levels, which may rise
up into the thousands and return to normal during convalescence
• Resolution of the abnormal biochemical tests generally occurs within one
to six weeks after the onset of the illness
Liver histology : bile stasis in canaliculi and gland-like transformation of
hepatocytes

11. COMPLICATIONS:
No complications in majority but few as –
1. Acute Hepatic Failure (0.5 to 4%)
• More likely in pregnancy, malnourished and pre-existing liver disease
• characterized by hepatic encephalopathy, elevated aminotransferases (often with
abnormal bilirubin and alkaline phosphatase levels), and impaired synthetic
function (international normalized ratio ≥1.5)
• High mortality rate

12. 2. Cholestatic Hepatitis
• Prolonged cholestasis (> 3 Months) in up to 60 % of patients with
acute HEV
• May present with pruritus,
• Resolves spontaneously (weeks-months) with no sequel
3. Chronic heaptitis E

13. B. Chronic heaptitis E

14. • Detection of HEV RNA in serum or stool for longer than six
months
• Exclusively occurs in immunosuppressed patients
• ( HIV infection, following solid organ or bone marrow
transplantation)
• Caused by HEV genotype 3 and genotype 4 (transplant

15. PREGNANT WOMEN
• Acute hepatic failure more common in pregnancy (3rd trimester )
• Acute HEV infection during pregnancy has been associated with
a mortality rate of 15 to 25 percent

16. • The outbreak (Niger)January 2017
WHO reported 282 suspected cases, including 27 deaths
among pregnant women

17. Effects on pregnancy :
• Increased risk of abortion, preterm labour & stillbirth
• Increased incidence of
• Primary pulmonary HTN
• Hemorrhagic manifestation
• Hepatic coma

18. HEV AND HORMONAL FACTORS IN PREGNANCY
• May be related to one of several host factors, such as differences in immune,
hormonal factors (during pregnancy), genetic and environmental factors
• Progesterone, estrogen and human chorionic gonadotropin (HCG) are shown to
have suppressive effect on the cell-mediated immunity
• Decrease in bone marrow B cell production due to increase in estrogen and
progesterone during pregnancy
• Steroid hormones (high in pregnancy) may influence viral replication

19. INVESTIGATIONS
• CBC/Hct
• Liver function test
• ALT & AST – variably increase
during prodormal phase
• Does not correlate well with
degree of liver cell damage
• Rise in bilirubin
• Prolonged prothrombin time
Viral serology
-detection of serum IgM
and IgG antibodies by
ELISA
-RT-PCR assay for HEV
RNA in serurm or stool
(require specialised
laboratory facilities)
• USG
• Liver biopsy – rarely
indicated

20. MANAGEMENT
• Depends on immune status and stage of disease (Acute Vs Chronic)
Goal of therapy
• Maintenance of fluid balance
• Support of circulation and respiration
• Control of bleeding—FFP (no role of Vit. K)
• Correction of hypoglycemia
• Treatment of other complications of the comatose state in anticipation of
liver regeneration and repair

21. • Rivaverin monotherapy (C/I pregnancy) - In pt. with
immunosuppressive therapy and chronic liver dz

22. PREVENTION
# Travelling in endemic area :
avoidance of water of unknown purity, food from street vendors, raw or
undercooked seafood, meat or pork products, and raw vegetables.
# Vaccine : HEV vaccination (12 month protection with 96% efficacy)
# Immune Globulin: The efficacy of pre- or post-exposure immune globulin
prophylaxis for the prevention of HEV has not been established

23. REFERENCES
• Casper et al, Harrison’s Principles of Internal
Medicine, 19th edition.
• Up to Date, last updated: Aug 21, 2017

24. •Thank you