Hepatitis E pathophysiology: Difference between revisions
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==Associated Conditions== | ==Associated Conditions== | ||
===HIV Patients=== | |||
===Organ Transplant Recipients=== | |||
==Gross Pathology== | ==Gross Pathology== | ||
Revision as of 11:10, 27 August 2014
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Hepatitis E Microchapters |
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Risk calculators and risk factors for Hepatitis E pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]
Overview
Pathogenesis
The cellular receptor for HEV and the mode of entry of the virus into the host cell are yet to be identified.[1] However, heparin sulfate proteoglycans are known to be required for the attachment to target cells and infection. A proposed theory for the replication of the virus is that, once within the host cell, HEV exposes its RNA which is then translated into proteins (ORF1) that will be responsible for the production of a negative-strand RNA. This newly produced strand will serve as a template for new genomic and subgeneric RNAs.[2]
Transmission
The hepatitis E virus is transmitted mainly through the fecal-oral route, due to fecal contamination of drinking water.
Other transmission routes have been identified, including:
- Foodborne transmission from ingestion of products derived from infected animals
- Transfusion of infected blood products
- Vertical transmission from a pregnant woman to her fetus
- Ingestion of raw or uncooked shellfish has also been identified as the source of sporadic cases in endemic areas.
Although humans are considered the natural host for the hepatitis E virus, antibodies to the hepatitis E virus or closely related viruses have been detected in primates and several other animal species, suggesting infection by the virus.
Hepatitis E is a waterborne disease. Contaminated water or food supplies have been implicated in major outbreaks.
Associated Conditions
HIV Patients
Organ Transplant Recipients
Gross Pathology
Microscopic Pathology
Patients who develop chronic liver disease often have changes in liver histology. These may include:[2]
- Portal hepatitis
- Lymphocytic infiltrate
- Necrosis
- Fibrosis
In severe cases, these changes may evolve to fibrosis and cirrhosis.[2][3]
References
- ↑ Kalia M, Chandra V, Rahman SA, Sehgal D, Jameel S (2009). "Heparan sulfate proteoglycans are required for cellular binding of the hepatitis E virus ORF2 capsid protein and for viral infection". J Virol. 83 (24): 12714–24. doi:10.1128/JVI.00717-09. PMC 2786843. PMID 19812150.
- ↑ 2.0 2.1 2.2 Aggarwal R, Jameel S (2011). "Hepatitis E." Hepatology. 54 (6): 2218–26. doi:10.1002/hep.24674. PMID 21932388.
- ↑ Gérolami R, Moal V, Colson P (2008). "Chronic hepatitis E with cirrhosis in a kidney-transplant recipient". N Engl J Med. 358 (8): 859–60. doi:10.1056/NEJMc0708687. PMID 18287615.