The Hepatitis virus (HAV) is a Picornavirus; it is non-enveloped and contains a single-stranded RNA packaged in a protein shell.[8] There is only one serotype of the virus, but multiple genotypes exist.

Following ingestion, HAV enters the bloodstream through the epithelium of the oropharynx or intestine.[10] The blood carries the virus to its target, the liver, and multiplies within hepatocytes and Kupffer cells (i.e., liver macrophages). There is no apparent virus-mediated cytotoxicity, and liver pathology is likely immune-mediated. Virions are secreted into the bile and released in stool. HAV is excreted in large quantities approximately 11 days prior to appearance of symptoms or anti-HAV IgM antibodies in the blood. The incubation period is 15–50 days, and mortality is less than 0.5%.

Hepatitis A does not have a chronic stage, is not progressive, and does not cause permanent liver damage. Following infection, the immune system makes antibodies against HAV that confer immunity against future infection. The disease can be prevented by vaccination, and hepatitis A vaccine has been proven effective in controlling outbreaks worldwide.

Transmission
The virus spreads by the fecal-oral route and infections often occur in conditions of poor sanitation and overcrowding. Hepatitis A can be transmitted by the parenteral route but very rarely by blood and blood products. Food-borne outbreaks are not uncommon,[19] and ingestion of shellfish cultivated in polluted water is associated with a high risk of infection.[23] Approximately 40% of all acute viral hepatitis is caused by HAV.[10] Infected individuals are infectious prior to onset of symptoms, roughly 10 days following infection. The virus is resistant to detergent, acid (pH 1), solvents (e.g., ether, chloroform), drying, and temperatures up to 60oC. It can survive for months in fresh and salt water. Common-source (e.g., water, restaurant) outbreaks are typical. Infection is common in children in developing countries, reaching 100% incidence, but following infection there is life-long immunity. HAV can be inactivated by: chlorine treatment (drinking water), formalin (0.35%, 37oC, 72 hours), peracetic acid (2%, 4 hours), beta-propiolactone (0.25%, 1 hour), and UV radiation (2 μW/cm2/min).

Symptoms can return over the following 6–9 months and include:[7]

Fatigue
Fever
Abdominal pain
Nausea
Diarrhea
Appetite loss
Depression
Jaundice, a yellowing of the skin or whites of the eyes
Sharp pains in the right-upper quadrant of the abdomen
Weight loss
Itching
Bile is removed from blood stream and excreted in urine giving a dark amber colour
Feces tend to be light in colour due to lack of bilirubin in bile

Hepatitis E is a viral hepatitis (liver inflammation) caused by infection with a virus called hepatitis E virus (HEV). HEV is a positive-sense single-stranded RNA icosahedral virus with a 7.5 kilobase genome. HEV has a fecal-oral transmission route. Infection with this virus was first documented in 1955 during an outbreak in New Delhi, India.[1]
Domestic animals have been reported as a reservoir for the hepatitis E virus, with some surveys showing infection rates exceeding 95% among domestic pigs.[3] Transmission after consumption of wild boar meat and uncooked deer meat has been reported as well.[4] The rate of transmission to humans by this route and the public health importance of this are however still unclear.[5]
A number of other small mammals have been identified as potential reservoirs: the lesser bandicoot rat (Bandicota bengalensis), the black rat (Rattus rattus brunneusculus) and the Asian house shrew (Suncus murinus).[6] A new virus designated rat hepatitis E virus has been isolated.[7]
An avian virus has been described that is associated with Hepatitis-Splenomegaly syndrome in chickens. This virus is genetically and antigenically related to mammalian HEV and probably represents a new genus in the family.
Replicative virus has been found in the small intestine, lymph nodes, colon as well as the liver of experimentally infected pigs.
The incidence of hepatitis E is highest in juveniles and adults between the ages of 15 and 40. Though children often contract this infection as well, they less frequently become symptomatic. Mortality rates are generally low, for Hepatitis E is a “self-limiting” disease, in that it usually goes away by itself and the patient recovers. However, during the duration of the infection (usually several weeks), the disease severely impairs a person’s ability to work, care for family members, and obtain food. Hepatitis E occasionally develops into an acute severe liver disease, and is fatal in about 2% of all cases. Clinically, it is comparable to hepatitis A, but in pregnant women the disease is more often severe and is associated with a clinical syndrome called fulminant hepatic failure. Pregnant women, especially those in the third trimester, suffer an elevated mortality rate from the disease of around 20%.