Hepatitis A Virus

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Hepatitis A Virus (HAV) is simply an enteric RNA virus that causes Hepatitis A, a liver disease [1][2][3]. Identification of the virus occurred in 1973. This event could be achieved by the help of electron microscope because of HAV’s small sizes, it has 27-32 nm range of diameter. It is composed of 70% viral protein and 30% RNA [4][5][6]. Its RNA is positive sense single stranded. Because of that it can translate its genetic material directly into protein. HAV differs from other members of the family, that it belongs to, in terms of:

  • Replication rate and adaptation duration in cell culture
  • Rare production of cytopathic effect [7][8]
  • Unique composition
  • Ability to navigate itself to specific tissue
  • Genetic differences

Uniqueness of this organism leads to formation of a new genus, called Hepatovirus, under the family Picornavaridae [9][10].

An individual infected by this virus is very lucky after overcome the infection. Because HAV includes only one serotype, one infection is enough to get lifelong immunity. However, it is reported that genetic variation occurs in Hepatitis A virus [11]. Seven HAV genotype exist. They are I, II, III, IV, V, VI and VII. Four of them are able to infect human. Among four of them, I is the most common one [12].

Severity of HAV infection differs in terms of the type. Infection may include no symptom or may lead to formation of hepatic failure which can result in death [13]. The virus is mainly threatening young children and chronic liver diseased old adults [14].

Most infections caused by the virus have fecal-oral route. General transmission way are the direct contact with infected individual and consumption of contaminated water or food. The most encouraged sources of foodborne HAV are vegetables, fruits and shellfish, which is able to be counted as major source among the others [15]. The organism infects liver of, not only, humans and other primates, too. It is possible to acquire HAV from non-human infected primates in slavery, via close contact [16]. The organism is very resistance. It can be understood from:

  • Its durability to purification process [17][18].
  • It is able to live more than 1 mount in seawater [19].
  • HAV is stable against to acid as other enteric viruses are (It can maintain its infectivity below pH 3)
  • Resistance to heating and freezing [20]
  • Resistance against ether, chloroform and alcohol (because of non-lipid envelop) [21][22] [23].

Although it has very strong sides, chlorination, is the most commonly used disinfection method, can partially inactivate HAV while ionizing radiation, usage of phenol and formaldehyde are providing total inactivation [24].

Wild type of the virus has low rate of reproduction. Rate of reproduction increases after long term adaptation. This adaptation induces emergence of persistent infection of HAV. After infection, the virus loses its strong effect [25].

Fetal Rhesus monkey kidney and Africa green monkey kidney cells mainly used for culturing HAV though another cell types are available [26]. In cell culture systems, some HAVs, that cause cytopathic effect, are observed. It is observed that these strains of HAV reproduce faster. Because of that more viral load formed than non-cytopathic strains produced [27]. Average time needed for incubation of HAV is 30 days, however, it ranges from 2 weeks to 6 weeks [28].

It is a mystery what exact story of viral activity inside the host is. But it is known that as HAV is reproducing in host cell, organelles work synchronized. As a result of this collaboration, non-lytic quit of viruses from host occurs. Progeny of the virus released to bile and transported to fecces.

It is supposed that viral activity is much related with membranes produced from Endoplasmic Reticulum. And a recent study demonstrated that mature virions are stored in lysosome. Therefore, lysosome plays key role on non-lytic secretion of progenies [29]. HAV is distributed over all around the World. However, this distribution is not uniform because regions includes low level of sanitation disrupt uniformness [30].

Sweden was the first victim of outbreak of Hepatitis A in 1955. This outbreak occurred because of ingestion of raw oysters [31]. Such a good new, just 629 victims was part of the outbreak. But in following years larger scaled outbreaks experienced like outbreak in Shanghai, China in 1987. In this outbreak 300 000 people suffered from Hepatitis A and its source was contaminated clams [32].

References

  1. ↑ Krugman, S., et al. (1967). "Infectious hepatitis: Evidence for two distinctive clinical, epidemiological, and immunological types of infection." Jama 200(5): 365-373.
  2. ↑ Rueckert, R. R. and E. Wimmer (1984). "Systematic nomenclature of picornavirus proteins." Journal of virology 50(3): 957.
  3. ↑ Melnick, J. (1992). "Properties and classification of hepatitis A virus." Vaccine 10: S24-26.
  4. ↑ Lemon, S. M. (1994). Hepatitis A virus. Encyclopedia of Virology. R. G. W. a. A. Granoff. London, Academic Press Ltd.
  5. ↑ Stapleton, J. T., and S.M. Lemon (1994). Hepatitis A and hepatitis E. Infectious Diseases. M. C. J. P.D. Hoeprich, and A.R. Ronald. Philadelphia, Lippincott Co.: 790-797.
  6. ↑ Koff, R. S. (1998). "Hepatitis a." Lancet 341(16439.29).
  7. ↑ Cromeans, T., et al. (1987). "Development of a plaque assay for a cytopathic, rapidly replicating isolate of hepatitis A virus." Journal of medical virology 22(1): 45-56.
  8. ↑ Lemon, S. M. (1992). "Hepatitis A virus: current concepts of the molecular virology, immunobiology and approaches to vaccine development." Reviews in Medical Virology 2(2): 73-87.
  9. ↑ Rueckert, R. R. and E. Wimmer (1984). "Systematic nomenclature of picornavirus proteins." Journal of virology 50(3): 957.
  10. ↑ Melnick, J. (1992). "Properties and classification of hepatitis A virus." Vaccine 10: S24-26.
  11. ↑ Jansen, R. W., et al. (1990). "Molecular epidemiology of human hepatitis A virus defined by an antigen-capture polymerase chain reaction method." Proceedings of the National Academy of Sciences 87(8): 2867-2871.
  12. ↑ Arauz‐Ruiz, P., et al. (2001). "Presumed common source outbreaks of hepatitis A in an endemic area confirmed by limited sequencing within the VP1 region." Journal of medical virology 65(3): 449-456.
  13. ↑ Ross, B. C. and D. A. Anderson (1991). "Characterization of hepatitis A virus capsid proteins with antisera raised to recombinant antigens." Journal of virological methods 32(2-3): 213-220.
  14. ↑ Akriviadis, E. A. and A. G. Redeker (1989). "Fulminant hepatitis A in intravenous drug users with chronic liver disease." Annals of Internal Medicine 110(10): 838-839.
  15. ↑ Cliver, D. (1985). "Vehicular transmission of hepatitis A." Public health reviews 13: 235-292.
  16. ↑ Andrew, J. B., et al. (2016). "Naturally Circulating Hepatitis A Virus in Olive Baboons, Uganda." Emerging Infectious Disease journal 22(7): 1308.
  17. ↑ Siegl, G., et al. (1984). "Stability of hepatitis A virus." Intervirology 22(4): 218-226.
  18. ↑ Biziagos, E., et al. (1988). "Long-term survival of hepatitis A virus and poliovirus type 1 in mineral water." Applied and Environmental Microbiology 54(11): 2705-2710.
  19. ↑ Callahan, K. M., et al. (1995). "Comparative survival of hepatitis A virus, poliovirus and indicator viruses in geographically diverse seawaters." Water Science and Technology 31(5-6): 189-193.
  20. ↑ Siegl, G., et al. (1984). "Stability of hepatitis A virus." Intervirology 22(4): 218-226.
  21. ↑ Lemon, S. M. (1994). Hepatitis A virus. Encyclopedia of Virology. R. G. W. a. A. Granoff. London, Academic Press Ltd.
  22. ↑ Stapleton, J. T., and S.M. Lemon (1994). Hepatitis A and hepatitis E. Infectious Diseases. M. C. J. P.D. Hoeprich, and A.R. Ronald. Philadelphia, Lippincott Co.: 790-797.
  23. ↑ Koff, R. S. (1998). "Hepatitis a." Lancet 341(16439.29).
  24. ↑ Siegl, G., et al. (1984). "Stability of hepatitis A virus." Intervirology 22(4): 218-226.
  25. ↑ Feinstone, S., et al. (1982). "Live attenuated vaccine for hepatitis A." Developments in biological standardization 54: 429-432.
  26. ↑ Weitz, M., et al. (1986). "Detection of a genome-linked protein (VPg) of hepatitis A virus and its comparison with other picornaviral VPgs." Journal of virology 60(1): 124-130.
  27. ↑ Cromeans, T., et al. (1987). "Development of a plaque assay for a cytopathic, rapidly replicating isolate of hepatitis A virus." Journal of medical virology 22(1): 45-56.
  28. ↑ Pal, S., et al. (2016). "An outbreak of hepatitis A virus among children in a flood rescue camp: A post-disaster catastrophe." Indian Journal of Medical Microbiology 34(2): 233-236.
  29. ↑ Seggewiß, N., et al. (2016). "Lysosomes serve as a platform for hepatitis A virus particle maturation and nonlytic release." Archives of virology 161(1): 43-52.
  30. ↑ Hadler, S. (1991). "Global impact of hepatitis A virus infection: changing patterns." Viral hepatitis and liver disease. Baltimore: Williams & Wilkins.
  31. ↑ Roos, R. (1956). "Hepatitis epidemic conveyed by osyters " 53: 989-1003.
  32. ↑ Halliday, M. L., et al. (1991). "An epidemic of hepatitis A attributable to the ingestion of raw clams in Shanghai, China." Journal of Infectious Diseases 164(5): 852-859.
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