Hepatitis E historical perspective

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]

Overview

Historical Perspective

The virus of hepatitis E was discovered in 1980, during the occupation of Afghanistan by the soviet troops. The virus was responsible for an outbreak of the disease among the troops. In order to make the discovery, a member of the research team ingested fecal extract from the affected soldiers, and became sick. The virus was then detected in the stool of the researcher by electron microscopy. [1]

After this discovery, the HEV was identified as responsible for many endemic cases of hepatitis in developing countries. Today, HEV is the most common global cause of viral hepatitis. [1]

The most recent common ancestor of Hepatitis E evolved between 536 and 1344 years ago.[2] It diverged into two clades—an anthropotropic and an enzootic form - which subsequently evolved into genotypes 1 and 2 and genotypes 3 and 4 respectively. The divergence dates for the various genotypes are as follows: Genotypes 1/2 367–656 years ago; Genotypes 3/4 417–679 years ago. For the most recent common ancestor of the various viruses themselves: Genotype 1 between 87 and 199 years ago; Genotype 3 between 265 and 342 years ago; and Genotype 4 between 131 and 266 years ago. The anthropotropic strains (genotypes 1 and 2) have evolved more recently than the others suggesting that this virus was originally a zoonosis.

The virus particle was first visualised in 1983[3] but was only molecularly cloned in 1990.[4]

The use of an avian strain confirmed the proposed topology of the genotypes 1–4 and suggested that the genus may have evolved throughout the years.[2] The use of a rat sequence also confirmed this topology and estimated that the date of divergence from the swine/human strains was 7.44×104 years ago (range 2.1×104 to 1.4×105 years ago). Since this date is approximately coincident with the advent of agriculture, this virus may have originally infected rats and subsequently spread to pigs and then to humans. Additional work is required to support or refute this possibility, as very few sequences have been isolated from species other than humans and suids.

Genotypes 1, 3 and 4 have all increased their effective population sizes in the 20th century.[2] The population size of genotype 1 increased noticeably in the last 30–35 years. Genotypes 3 and 4 population sizes began to increase in the late 19th century up to 1940–1945.

References

  1. 1.0 1.1 Kamar N, Bendall R, Legrand-Abravanel F, Xia NS, Ijaz S, Izopet J; et al. (2012). "Hepatitis E." Lancet. 379 (9835): 2477–88. doi:10.1016/S0140-6736(11)61849-7. PMID 22549046.
  2. 2.0 2.1 2.2 Tavis, John E.; Purdy, Michael A.; Khudyakov, Yury E. (2010). "Evolutionary History and Population Dynamics of Hepatitis E Virus". PLoS ONE. 5 (12): e14376. doi:10.1371/journal.pone.0014376. ISSN 1932-6203.
  3. Balayan MS, Andjaparidze AG, Savinskaya SS; et al. (1983). "Evidence for a virus in non-A, non-B hepatitis transmitted via the fecal-oral route". Intervirology. 20 (1): 23–31. PMID 6409836.
  4. Reyes GR, Purdy MA, Kim JP; et al. (1990). "Isolation of a cDNA from the virus responsible for enterically transmitted non-A, non-B hepatitis". Science. 247 (4948): 1335–9. doi:10.1126/science.2107574. PMID 2107574.

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