3. INTRODUCTION• Hepatitis is a general term meaning inflammation of the liver and can be
caused by a variety of different viruses such as hepatitis A, B, C, D and E.
• Hepatitis E is a non-enveloped, icosahedral, single stranded positive-sense
RNA virus, with a diameter of 30-32nm.
• It is a sole member of the genus Hepevirus (Brooks, et al., 2004).
• It was first discovered in India in 1955 when a newly developed assays for
hepatitis A and B showed a high prevalence for anti-HAV IgG but no sign
of acute hepatitis A or B. This means there is another enterically
transmitted non-A, non-B hepatitis (ET-NANB) (Khuroo,1980; Wong,
1980).
• Hepatitis E virus (HEV) has three large open reading frames (ORFs) of the
positive-sense RNA of HEV. The largest ORF consists of 1,693 codons
which encodes for non-structural proteins responsible for the processing
and replication of the virus, the other two ORFs (660 and 123 codons,
respectively) encode for structural protein.
• HEV has four genotypes, with genotypes 1 and 2 affecting developing
regions of Asia, Africa and South America and countries like Mexico,
Chad and Nigeria respectively. Genotypes 3 and 4 has been found in cases
of autochthonous hepatitis E in many developed countries and
industrialized regions of Asia respectively.
• Genotypes of HEV 1 and 2 are confined to only humans while 3 and 4 to
swines and wild animals (Lu, 2006).
4. TABLE 1: CHARACTERISTICS of HEPATITIS E VIRUS
Family Unclassified
Genus Hepevirus
Virion 30-32nm, icosahedral
Envelope None
Genome ssRNA
Genome size 7.6kb
Stability Heat-stable
Transmission Fecal-oral
Prevalence Regional
Fulminant disease In pregnancy
Chronic disease Never
Oncogenic No
(Brooks et al., 2007)
5. Plate 1: Electron micrograph of hepatitis E Virus
(Brooks et al., 2007).
6. PATHOGENESIS
• The virus gets into the host through the oral route into the
gastrointestinal tract.
• The virus then reaches the liver through the portal vein, then
replicates and released into the bile and blood stream
(Krawczynski, 1989).
• Infectious viral particles present in the bile, faeces and blood
stream during the late incubation phase (32 days) of hepatitis
E which persist for a week or two before the onset of clinical
diseases (Chauhan, 1993).
• Anti HEV antibodies of the IgA, IgG and IgM types appear in
the blood during the course of the disease.
7. CLINICAL MANIFESTATION
• The disease may range in severity from sub-clinical to
fulminant liver failure and causes death in pregnant women
(Herrera, 1993).
• After an incubation period of 15-60 days, the infected patient
develops symptoms and clinical signs that resembles those
seen with other forms of acute viral hepatitis.
• These symptoms has 2 phases:
Prodromal phase symptoms include: Myalgia, arthralgia,
Fever with mild temperature (25-97%), Nausea/vomiting (30-
100%).
Icteric phase symptoms include: Jaundice, dark urine, light
coloured stool (20-40%), urticarial rash, diarrhea, pruritus
(50%), malaise (95-100%) (Lagrand et al., 2011).
9. EPIDEMIOLOGY
• Genotypes 1 and 2 occurs in countries with poor
sanitary conditions, while genotypes 3 and 4 infect
humans, pigs and other animal species (Satou and
Nishura, 2007).
• The incidence of hepatitis E is highest in juveniles
and adults between ages 15 and 40 (WHO, 2012).
• Hepatitis E virus is most prevalent in developing
regions and countries; Asia, central Africa, India and
central America.
• In 2011, in Mumbai, six pregnant women died to
hepatitis E virus infection (Nurul, 2011).
• Pregnant women, especially those in the third
trimester, suffer an elevated mortality rate of around
20% (WHO, 2012).
11. PREVENTION AND CONTROL
• Proper sanitation.
• Higher standards for public water supply.
• Vaccination (Shrestha et al., 2007).
12. CONCLUSION
• It can be concluded that hepatitis E virus infection is
implicated in the inflammation of the liver, jaundice and
deaths in humans. This is due to faecal contamination of food
and water with hepatitis E virus.
• The proper screening of animals, like swine, should also be
put into consideration before consumption as they are
reservoirs of hepatitis E virus.
13. REFERENCEBrooks, G.F., Carroll, K..C., Butel, J.S., and Morse, S.A. (2007). Hepatitis virus. Jawetz,
Melnick and Adelberg’s Medical Microbiology, 24th
Edition. McGraw Hill, New York,
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Chauhan, A. (1993) Hepatitis E virus transmission to a volunteer. Lan Pub.Med. 6:149-150.
Herrera, J.L. (1993). Hepatitis E as a cause of acute non-A, non-B hepatitis. Arch Intern Med.
153: 773-5.
Khuroo, M.S.(1980). Study of an epidemic of non-A, non-B hepatitis. Possibility of another
human hepatitis virus distinct from post-transfusion non-A, non-B type. Am J Med.
68: 818-24.
Krawczynski, K. and Bradley, D.W. (1989). Enterically transmitted non-A, non-B hepatitis:
identification of virus- associated antigen in experimentally infected cynomolgus
macaques. J Infect Dis. 159: 1042-1049.
Legrand-Abravanel F., Kamar N. and Sandres-Saune K. (2011). Heparecipientstitis E virus
infection without reactivation in solid-organ transplant, France. Emerg Infect Dis.s
17(1):30-7.
Lu, L., Li, C. and Hagedorn, C.H. (2006). Phylogenetic analysis of global hepatitis E virus
sequences:genetic diversity, subtypes and zoonosis. Rev Med Virol; 16: 5-36.
Shresthan, M.P., Scott, R.M. and Joshi, D.M. (2007). "Safety and efficacy of a recombinant
hepatitis E vaccine". N. Engl. J. Med. 356 (9): 895–903.
WHO. "Global Alert and Response (GAR); Hepatitis E". Retrieved 26 January, 2012.
14. REFERNCES (continued)
Wong, D.C., Purcell, R.H., Sreenivasan, M.A., Prasad, S.R and Pavri, K.M. (1980).
Epidemic and endemic hepatitis in India: evidence for a non-A, non-
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