Hepatitis E historical perspective

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

The hepatitis E virus (HEV) was discovered in 1980 by a soviet researcher. Its most recent ancestor is thought to have evolved between 536 and 1344 years ago. It has evolved into two initial clades, that lately would be classified and divided in 4 different genotypes. Genotypes 1, 3 and 4 have seen their effective population sizes increased during the 20th century.

Historical Perspective

In 1980, the hepatitis E virus was discovered 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.

In 1983, the virus particle was first visualised.[3]

In 1990, hepatitis E virus was only molecularly cloned.[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, the 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, while genotypes 3 and 4 have only began to increase their population sized in the late 19th century.

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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