Hepatitis E pathophysiology: Difference between revisions
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===Transmission=== | ===Transmission=== | ||
Hepatitis E is mainly transmitted through the fecal-oral route. In developing countries this occurs mostly from the ingestion of contaminated water.<ref name="pmid22549046">{{cite journal| author=Kamar N, Bendall R, Legrand-Abravanel F, Xia NS, Ijaz S, Izopet J et al.| title=Hepatitis E. | journal=Lancet | year= 2012 | volume= 379 | issue= 9835 | pages= 2477-88 | pmid=22549046 | doi=10.1016/S0140-6736(11)61849-7 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22549046 }} </ref> | |||
Other transmission routes have been identified, including: | Other transmission routes have been identified, including: | ||
* Foodborne [[transmission]] from [[ingestion]] of products derived from [[infected]] animals | * Foodborne [[transmission]] from [[ingestion]] of products derived from [[infected]] animals | ||
* [[Transfusion]] of infected [[blood]] products | * [[Transfusion]] of infected [[blood]] products | ||
* Vertical [[transmission]] from a pregnant woman to | * Vertical [[transmission]] from a pregnant woman to the [[fetus]] | ||
* [[Ingestion]] of raw or uncooked shellfish has also been identified as the source of sporadic cases in [[endemic]] areas. | * [[Ingestion]] of raw or uncooked shellfish has also been identified as the source of sporadic cases in [[endemic]] areas. | ||
==Associated Conditions== | ==Associated Conditions== | ||
Revision as of 12:41, 27 August 2014
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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
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 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. The new RNAs, are translated to ORF2 and ORF3. The ORF proteins will then transport the RNA into new virions that will use cellular lipids and ORF3 for their formation.[2][3]
Similarly to other hepatitis viruses, HEV is not cytopathic. The host's immune response to the infection is the cause of liver injury.[2]
Although the pathogenesis behind the increased mortality of infected pregnant women is not completely understood, it is thought to be related to hepatocyte injury mediated by endotoxins, and greater T-cell type 2 response.[4]
Transmission
Hepatitis E is mainly transmitted through the fecal-oral route. In developing countries this occurs mostly from the ingestion of contaminated water.[5] 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 the fetus
- Ingestion of raw or uncooked shellfish has also been identified as the source of sporadic cases in endemic areas.
Associated Conditions
HIV Co-Infection
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][6]
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 2.3 Aggarwal R, Jameel S (2011). "Hepatitis E." Hepatology. 54 (6): 2218–26. doi:10.1002/hep.24674. PMID 21932388.
- ↑ Nagashima S, Takahashi M, Tanaka T, Yamada K, Nishizawa T; et al. (2011). "A PSAP motif in the ORF3 protein of hepatitis E virus is necessary for virion release from infected cells". J Gen Virol. 92 (Pt 2): 269–78. doi:10.1099/vir.0.025791-0. PMID 21068219.
- ↑ Pal R, Aggarwal R, Naik SR, Das V, Das S, Naik S (2005). "Immunological alterations in pregnant women with acute hepatitis E." J Gastroenterol Hepatol. 20 (7): 1094–101. doi:10.1111/j.1440-1746.2005.03875.x. PMID 15955220.
- ↑ 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.
- ↑ 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.