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A

SEMINAR PRESENTATION
ON
HEPATITIS E VIRUS INFECTION
BY
OLADIPUPO, OLUWAFEMI TOSIN
08/55EJ121
MARCH, 2012

OUTLINE

INTRODUCTION
CHARACTERISTICS
PATHOGENESIS
CLINICAL MANIFESTATION
EPIDEMIOLOGY
DIAGNOSIS
PREVETION AND CONTROL
REFERENCES

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).

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)

Plate 1: Electron micrograph of hepatitis E Virus


(Brooks et al., 2007).

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.

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 (30100%).
Icteric phase symptoms include: Jaundice, dark urine, light
coloured stool (20-40%), urticarial rash, diarrhea, pruritus
(50%), malaise (95-100%) (Lagrand et al., 2011).

Plate 2: Jaundiced patient with


Hepatitis E virus

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).

DIAGNOSIS
MICROSCOPY.
SEROLOGICAL TECHNIQUES.
-ELISA.
MOLECULAR TECHNIQUE.
- PCR.

PREVENTION AND CONTROL

Proper sanitation.
Higher standards for public water supply.
Vaccination (Shrestha et al., 2007).

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.

REFERENCE

Brooks, G.F., Carroll, K..C., Butel, J.S., and Morse, S.A. (2007). Hepatitis virus. Jawetz, Melnick
and Adelbergs Medical Microbiology, 24th Edition. McGraw Hill, New York,
p 467.
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: 81824.
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): 895903.
WHO. "Global Alert and Response (GAR); Hepatitis E". Retrieved 26 January, 2012.

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, nonhepatitis virus aetiology. Lancet 2:876-9.

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