Viral hepatitis

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Viral hepatitis
Ground glass hepatocytes high mag cropped 2.jpg
Micrograph showing ground glass hepatocytes, which are seen in chronic hepatitis B infections (a type of viral hepatitis), and represent accumulations of viral antigen in the endoplasmic reticulum. H&E stain.
SymptomsNone, fever, tiredness, abdominal pain, vomiting, dark urine, yellowish skin[1]
ComplicationsCirrhosis, liver failure, liver cancer[2]
DurationShort or long-term[2]
CausesHepatitis A, B, C, D, E, X[2]
Diagnostic methodBlood tests[3]
PreventionVaccination, sanitation[1][4]
TreatmentSupportive, medications, liver transplant[1]
FrequencyShort-term: >10 million[5][6]
Long-term: 325 million[7]

Viral hepatitis is liver inflammation (hepatitis) due to a viral infection.[2] It may present as a short-term (acute) or long-term (chronic) infection.[2][1] Symptoms may vary from none, to fever, tiredness, abdominal pain, vomiting, dark urine, and yellowish skin.[1] The long-term form can result in cirrhosis, liver failure, or liver cancer.[2]

Most commonly it occurs due to five unrelated viruses hepatitis A, B, C, D, or E.[2] Hepatitis A and E typically spread through food and water that have been contaminated with stool.[2] Hepatitis B, C, and D are typically spread through contact with infected blood.[2] Cases were the cause is not clear may be called non-A–E hepatitis or hepatitis X.[2] A number of other viruses, such as herpes simplex, have been implicated.[8] Diagnosis is by blood tests.[3]

Hepatitis A and B can be prevented by vaccination, while hepatitis A and E can be prevented by improvements in sanitation.[1][4] Hepatitis A and E will often resolve on their own.[2][1] Effective treatments for long-term hepatitis C are available but costly.[9][10] Medications may also be used for long-term hepatitis B.[11] Liver transplant may be required to address complications.[1]

Long-term viral hepatitis affects about 325 million people globally (257 million with hepatitis B and 71 million with hepatitis C).[7][4] Outbreaks of hepatitis A and E occur worldwide, affecting at least 10 million people a year, mostly in developing countries.[4][5][6] It is the most common cause of liver inflammation.[1] In 2013, about 1.5 million people died from viral hepatitis, most commonly due to hepatitis B and C.[12] East Asia and South Asia are the most commonly affected regions.[12] Infectious hepatitis was first determined in the 1940s.[5]


The most common cause of hepatitis is viral. Although the effects of various viruses are all classified under the disease hepatitis, these viruses are not all related.

Hepatitis viruses
Hepatitis A (HAV) Hepatitis B (HBV) Hepatitis C (HCV) Hepatitis D (HDV) Hepatitis E (HEV)
Viral species Hepatovirus A Hepatitis B virus Hepacivirus C Hepatitis delta virus Orthohepevirus A
Viral family Picornaviridae Hepadnaviridae Flaviviridae Incertae sedis Hepeviridae
Genome (+)ssRNA dsDNA-RT (+)ssRNA (−)ssRNA (+)ssRNA
Antigens HBsAg, HBeAg Core antigen Delta antigen
Transmission Enteral Parenteral Parenteral Parenteral Enteral
Incubation period 20–40 days 45–160 days 15–150 days 30–60 days 15–60 days
Severity/Chronicity[13] Mild; acute Occasionally severe; 5–10% chronic Subclinical; 70% chronic Exacerbates symptoms of HBV; chronic with HBV Mild in normal patients; severe in pregnant women; acute
Vaccine 10 year protection 3 injections, lifetime protection None available None available Investigational (approved in China)

Hepatitis A

Hepatitis A or infectious jaundice is caused by hepatitis A virus (HAV), a picornavirus transmitted by the fecal-oral route often associated with ingestion of contaminated food. It causes an acute form of hepatitis and does not have a chronic stage. The patient's immune system makes antibodies against HAV 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 HAV infection 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 HAV 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),[14] 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.[15]

Hepatitis A[16]
Marker Detection Time Description Significance
Faecal HAV 2–4 weeks or 28 days Early detection
Ig M anti HAV 4–12 weeks Enzyme immunoassay for antibodies During acute Illness
Ig G anti HAV 5 weeks–persistent Enzyme immunoassay for antibodies Old infection or reinfection

Hepatitis B

Hepatitis B is caused by the hepatitis B virus, a hepadnavirus that can cause both acute and chronic hepatitis. Chronic hepatitis develops in the 15% of adults who are unable to eliminate the virus after an initial infection. Identified methods of transmission include contact with blood, blood transfusion (now rare), unsanitary tattoos, sex (through sexual intercourse or contact with bodily fluids), or mother-to-child by breast feeding;[citation needed] there is 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 the virus, but not enough to clear the infected liver cells. The continued production of virus and countervailing antibodies is a likely cause of the immune complex disease seen in these patients. A vaccine is available to prevent infection 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 eight treatment options approved by the U.S. Food and Drug Administration (FDA) available for persons with a chronic hepatitis B infection: alpha-interferon, pegylated interferon, adefovir, entecavir, telbivudine, lamivudine, tenofovir disoproxil and tenofovir alafenamide with a 65% rate of sustained response.

Hepatitis C

Drawing of the hepatitis C virus

Hepatitis C (originally "non-A non-B hepatitis") is caused by hepatitis C virus (HCV), an RNA virus of the family Flaviviridae. HCV 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 usually leads to chronic hepatitis, culminating in cirrhosis in some people. It usually remains asymptomatic for decades. Patients with hepatitis C are susceptible to severe hepatitis if they contract either hepatitis A or B, so all persons with hepatitis C should be immunized against hepatitis A and hepatitis B if they are not already immune, and avoid alcohol. HCV can lead to the development of hepatocellular carcinoma, however, only a minority of HCV-infected individuals develop cancer (1-4% annually), suggesting a complex interplay between viral gene expression and host and environmental factors to promote carcinogenesis. The risk is increased two-fold with active HBV coinfection and a 21% increase in mortality compared to those with latent HBV and HCV.[17] HCV viral levels can be reduced to undetectable levels by a combination of interferon and the antiviral drug ribavirin. The genotype of the virus is the primary determinant of the rate of response to this treatment regimen, with genotype 1 being the most resistant.

Hepatitis C is the most common chronic blood-borne infection in the United States.[18]

Hepatitis C[19]
Marker Detection Time Description Significance Note
HCV-RNA 1–3 weeks or 21 days PCR Demonstrates presence or absence of virus Results may be intermittent during course of infection. Negative result is not indicative of absence.
anti-HCV 5–6 weeks Enzyme Immunoassay for antibodies Demonstrates past or present infection High false positive in those with autoimmune disorders and populations with low virus prevalence.
ALT 5–6 weeks Peak in ALT coincides with peak in anti-HCV Fluctuating ALT levels is an indication of active liver disease.

Hepatitis D

Hepatitis D is caused by the hepatitis D virus (HDV), or hepatitis delta virus; it belongs to the genus Deltavirus. It is similar to a viroid as it can only propagate in the presence of the hepatitis B virus, depending on the helper function of HBV for its replication and expression. It has no independent life cycle, but can survive and replicate as long as HBV infection persists in the host body. It can only cause infection when encapsulated by hepatitis B virus surface antigens.

Hepatitis E

Hepatitis E is caused by the Hepatitis E virus (HEV), from the family Hepeviridae; it produces symptoms similar to hepatitis A, although it can take a fulminant course in some patients, particularly pregnant women (mortality rate about 20%); chronic infections may occur in immune-compromised patients. It is more prevalent in the Indian subcontinent. The virus is feco-orally transmitted and usually is self-limited.

Hepatitis F

Hepatitis F virus (HFV) is a hypothetical virus linked to certain cases of hepatitis. Several hepatitis F virus candidates emerged in the 1990s, but none of these reports have been substantiated.

GB virus C

The GB virus C is another potential viral cause of hepatitis that is probably spread by blood and sexual contact.[20] It was initially identified as Hepatitis G virus.[21] There is very little evidence that this virus causes hepatitis, as it does not appear to replicate primarily in the liver.[22] It is now classified as GB virus C.[23]

Hepatitis C and liver cancer

Hepatitis C causes acute and chronic infections that is a major cause of hepatocellular carcinoma (HCC), advanced hepatic fibrosis and cirrhosis.

A major cause of death in HCC patients with chronic HCV infection. The pathogenesis of HCC associated with HCV, that virus play direct and indirect roles.[24]

A major risk for the development of HCC is persistent infection with HCV and the highest risk for HCC development is associated with co-infection of HBV with HDV, HCV or HIV.[25]

The risk factors lead to development of HCC in chronic HCV is synchronous liver diseases, viral genotype, lifestyle factors and presence of obesity and diabetes mellitus. The lifestyle factors such as smoking, alcohol use and coffee drinking accelerated progression to HCC in HCV.

The purpose of HCV treatment is to eliminate the infection, reduce the transmission to other people and decrease the risk of HCC development.[citation needed]

Other viruses

The virus first known to cause hepatitis was the yellow fever virus, a mosquito-borne flavivirus. Other viruses than can cause hepatitis include:

KIs-V is a virus isolated in 2011 from four patients with raised serum alanine transferases without other known cause; a causal role is suspected.[34]


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