Beruflich Dokumente
Kultur Dokumente
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
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
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).
EPIDEMIOLOGY
DIAGNOSIS
MICROSCOPY.
SEROLOGICAL TECHNIQUES.
-ELISA.
MOLECULAR TECHNIQUE.
- PCR.
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.
THANKS FOR
LISTENING