Hepatitis A virus is culturable in primate cell lines – but wild type strains are difficult to culture and generally do not produce cell changes, and so are not easy to identify by culture alone. It will not grow in food or water.
HAV is very stable, shows high resistance to chemical and physical agents such as heat, acid and solvents and has been shown to survive in the environment for over 3 months.
HAV integrity and infectivity were retained after 60 min incubation at 60°C and the virus was only partially inactivated after 10-12 hours at 56°C. Infectivity was retained after 10 min at 80°C in 1M MgCl2 but for only 5 min in phosphate buffered saline. HAV heat resistance is reported to be greater in foods and shellfish. HAV inoculated into oysters was not fully inactivated after heating in a can for 19 min at 60°C. MAFF recommend a heat treatment of 1.5 min at 90ºC to inactivate HAV in cockles. Under refrigeration and freezing conditions the virus remains intact and infectious for several years.
Stable at acid pH. At pH 1.0 and 25°C, HAV retained high infectivity after 2 hours and was still infectious after 5 hours. So, not killed by stomach acid.
Infectious for >1 month at 25°C and 42% humidity. Greater resistance to inactivation at low humidity and temperatures.
Sanitisers / Disinfectants
Infectivity is decreased by exposure to 70% alcohol. Resistant to chloroform, Freon, Arklone and 20% ether. Not inactivated by 300mg/l perchloroacetic acid or 1g/l chloramine at 20°C for 15min. HAV is inactivated by chlorine: 99.99% reduction in 6.5 min at pH6 and 49.6 min at pH10 (estimated Ct values under conditions described are 1.8 and 12.3 respectively). Hypochlorite: 3-10mg/l at 20°C for 5 -15min. Iodine: 3 mg/l for 5 min at 20°C Formalin: 1:4000 for 72 hours at 37°C or 3% for 5 min at 25°C.
Inactivated by UV irradiation after 1 min exposure to 1.1W or 197μW/cm2 for 4 min. Gamma irradiation has not been found to be effective for inactivation of HAV on fresh fruits and vegetables.
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2-6 weeks, average 28 days. Symptoms Initially non-specific symptoms – fever, headache, fatigue, anorexia, nausea and vomiting, then viraemia, jaundice and hepatitis symptoms appear 1-2 weeks later. Virus is present in the blood at weeks 2- 4, and is shed in faeces (>106 particles/g) from the latter 2 weeks of the incubation period for up to 5 weeks. Jaundice is usually evident from weeks 4 to 7, and virus shedding generally continues throughout this period. Overall debility lasting several weeks is common and relapses may occur. Acute hepatitis is usually self-limiting but can occasionally cause fulminant disease that results in death. Estimated hospitalisation rate is 13%.
HAV infects hepatocytes, causes elevation of liver enzymes and inflammation of the liver. The cytotoxic T cell immune response destroys infected liver cells. Virus particles are released into the bile duct and excreted in faeces. The virus is believed to initially enter the liver via the bloodstream and it is not clear if intestinal replication occurs. The gastrointestinal tract is not a required route for infection.
None produced in foods.
At Risk Groups
All age-groups. The disease is milder in young children under 6 years than older children and adults. Case-fatality risk increases with age so risks are higher for unexposed older people.
Long Term Effects
As an illustration overall case fatality rates in the US are 0.3% (0.003 per 100,000) and range between 0.004% for 5-14 years to 2.7% in people > 49 years. HAV has not been associated with chronic liver disease.
Rest and an appropriate low-fat diet. Post-exposure prophylaxis may be recommended for certain groups such as day-care centre staff, military and food industry staff. Prevention is possible via HAV vaccination for at-risk groups including overseas travellers and for food handlers when situations warrant it.
Human faeces are the major reservoir. Coprophagy is not recommended.
HAV infects primates including chimps and some species of monkeys. Non-primates are also infected but disease is milder. Transmission via these hosts is unlikely.
Contaminated bivalve shellfish, salads, fresh fruits and vegetables, water, and any manually prepared food products. HAV survived in cream-filled biscuits for >1 day at 21ºC. Poor hygiene practices and poor sanitation are major risk factors. Pre-symptomatic food handlers excreting HAV pose a risk. Food is rarely available for post hoc analysis because of the long incubation period.
Survival of HAV in the environment (fresh and seawater, wastewater, marine sediments, soils and shellfish), is prolonged (>12 weeks) at 25°C. Excreta from infected humans may contaminate soil or water. Human faecal pollution from sewage discharges, septic tank leachates and boat discharges has caused contamination of shellfish beds, recreational water, irrigation water and drinking water.
The faecal/oral route is the established route of transmission and infection occurs following ingestion of faecally-contaminated food and water. Viral contamination of fresh fruits and salad vegetables through the global marketplace is becoming a significant route of exposure, especially in countries with low levels of hepatitis A. Person to person transmission is also important especially among young children in overcrowded living conditions, day-care centres or institutions. Parenteral transmission occurs in the drug-using population and via contaminated blood products.
Most cases of disease are outbreak-related. Large outbreaks have been reported in developed countries where there is little immunity. Secondary transmission may account for 20% of cases in an outbreak.