Viral hepatitis

Viral hepatitis

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Viral hepatitis is the cause of most cases of acute hepatitis. Types include Hepatitis A, Hepatitis B, Hepatitis C, Hepatitis B with D, Hepatitis E, Hepatitis F virus (existence unknown), and Hepatitis G or GBV-C.

In addition to the hepatitis viruses, other viruses can also cause hepatitis, including cytomegalovirus, Epstein-Barr virus, yellow fever, etc.

Hepatitis A

Hepatitis A or infectious jaundice is caused by a picornavirus transmitted by the fecal-oral route, often associated with ingestion of contaminated food or with anal/oral sex. It causes an acute form of hepatitis and does not have a chronic stage. The patient's immune system makes antibodies against hepatitis A that confer immunity against future infection. People with hepatitis A are advised to rest, stay hydrated and avoid alcohol. A vaccine is available that will prevent infection from hepatitis A for up to 10 years. Hepatitis A can be spread through personal contact, consumption of raw sea food or drinking contaminated water. This occurs primarily in third world countries. Strict personal hygiene and the avoidance of raw and unpeeled foods can help prevent an infection. Infected people excrete the hepatitis A virus with their feces two weeks before and one week after the appearance of jaundice. The time between the infection and the start of the illness averages 28 days (ranging from 15 to 50 days), [cite web | title = CDC Hepatitis A FAQ | url=http://www.cdc.gov/ncidod/diseases/hepatitis/a/faqa.htm#general | accessdate = 2008-03-03] and most recover fully within 2 months, although approximately 15% of sufferers may experience continuous or relapsing symptoms from six months to a year following initial diagnosis. [cite web | title = CDC Hepatitis A Fact Sheet | url=http://www.cdc.gov/ncidod/diseases/hepatitis/a/fact.htm | accessdate = 2008-03-03]

Hepatitis B

Hepatitis B is caused by a hepadnavirus, which can cause both acute and chronic hepatitis. Chronic hepatitis develops in the 15% of patients who are unable to eliminate the virus after an initial infection. Identified methods of transmission include blood (blood transfusion, now rare), tattoos (both amateur and professionally done), sexually (through sexual intercourse or through contact with blood or bodily fluids), or via mother to child by breast feeding (minimal evidence of transplacental crossing). However, in about half of cases the source of infection cannot be determined. Blood contact can occur by sharing syringes in intravenous drug use, shaving accessories such as razor blades, or touching wounds on infected persons. Needle-exchange programmes have been created in many countries as a form of prevention.

Patients with chronic hepatitis B have antibodies against hepatitis B, but these antibodies are not enough to clear the infection that establishes itself in the DNA of the affected liver cells. The continued production of virus combined with antibodies is a likely cause of the immune complex disease seen in these patients. A vaccine is available that will prevent infection from hepatitis B for life. Hepatitis B infections result in 500,000 to 1,200,000 deaths per year worldwide due to the complications of chronic hepatitis, cirrhosis, and hepatocellular carcinoma. Hepatitis B is endemic in a number of (mainly South-East Asian) countries, making cirrhosis and hepatocellular carcinoma big killers. There are six FDA-approved treatment options available for persons with a chronic hepatitis B infection: alpha-interferon, pegylated interferon adefovir, entecavir, telbivudine and lamivudine. About 65% of persons on treatment achieve a sustained response.

Hepatitis C

Hepatitis C (originally "non-A non-B hepatitis") is caused by a virus with an RNA genome that is a member of the Flaviviridae family. It can be transmitted through contact with blood (including through sexual contact if the two parties' blood is mixed) and can also cross the placenta. Hepatitis C may lead to a chronic form of hepatitis, culminating in cirrhosis. It can remain asymptomatic for 10-20 years. Patients with hepatitis C are susceptible to severe hepatitis if they contract either hepatitis A or B, so all hepatitis C patients should be immunized against hepatitis A and hepatitis B if they are not already immune, and avoid alcohol. The virus can cause cirrhosis of the liver. HCV viral levels can be reduced to undetectable levels by a combination of interferon and the antiviral drug ribavirin. The genotype of the virus determines the rate of response to this treatment regimen. Genotype 1 is more resistant to interferon therapy than other HCV genotypes.

Hepatitis C is the most common bloodborne infection in the United States.

Hepatitis D

Hepatitis D is caused by hepatitis delta agent, which is similar to a viroid as it can only propogate in the presence of the Hepatitis B virus.

Hepatitis E

Hepatitis E produces symptoms similar to hepatitis A, although it can take a fulminant course in some patients, particularly pregnant women; it is more prevalent in the Indian subcontinent.

Hepatitis F virus

Hepatitis F virus is a hypothetical virus linked to hepatitis. Several hepatitis F virus candidates emerged in the 1990s; none of these reports have been substantiated.

Hepatitis G, now called GB virus C

Another potential viral cause of hepatitis, initially identified as hepatitis G virus, [cite journal |author=Linnen J, Wages J, Zhang-Keck ZY, "et al" |title=Molecular cloning and disease association of hepatitis G virus: a transfusion-transmissible agent |journal=Science (journal) |volume=271 |issue=5248 |pages=505–8 |year=1996 |pmid=8560265 |doi=10.1126/science.271.5248.505 |url=http://www.sciencemag.org/cgi/pmidlookup?view=long&pmid=8560265] is probably spread by blood and sexual contact. [cite journal
author = Stark J, "et al"
year =1996
title = Detection of the hepatitis G virus genome among injecting drug users, homosexual and bisexual men, and blood donors
journal =J. Infect. Dis.
volume = 174
issue = 6
pages = 1320–3
pmid = 8940225
] There is very little evidence that this virus causes hepatitis, as it does not appear to replicate primarily in the liver. [cite journal |author=Pessoa MG, Terrault NA, Detmer J, "et al" |title=Quantitation of hepatitis G and C viruses in the liver: evidence that hepatitis G virus is not hepatotropic |journal=Hepatology |volume=27 |issue=3 |pages=877–80 |year=1998 |pmid=9500722 |doi=10.1002/hep.510270335 |url=] It is now classified as GB virus C. [cite web |url=http://phene.cpmc.columbia.edu/Ictv/fs_flavi.htm#Genus0 |title=00.026. Flaviviridae - ICTVdB Index of Viruses |format= |work= |accessdate=]

References


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