Hepatitis A: Old and New

Abstract

The hepatitis A virus (HAV), a picornavirus, is a common cause of hepatitis worldwide. Spread of infection is generally person to person or by oral intake after fecal contamination of skin or mucous membranes; less commonly, there is fecal contamination of food or water. Hepatitis A is endemic in developing countries, and most residents are exposed in childhood. In contrast, the adult population in developed countries demonstrates falling rates of exposure with improvements in hygiene and sanitation. The export of food that cannot be sterilized, from countries of high endemicity to areas with low rates of infection, is a potentially important source of infection. After ingestion and uptake from the gastrointestinal tract, the virus replicates in the liver and is excreted into the bile. Cellular immune responses to the virus lead to destruction of infected hepatocytes with consequent development of symptoms and signs of disease. Humoral immune responses are the basis for diagnostic serologic assays. Acute HAV infection is clinically indistinguishable from other causes of acute viral hepatitis. In young children the disease is often asymptomatic, whereas in older children and adults there may be a range of clinical manifestations from mild, anicteric infection to fulminant hepatic failure. Clinical variants include prolonged, relapsing, and cholestatic forms. Management of the acute illness is supportive, and complete recovery without sequelae is the usual outcome. Research efforts during World War II led to the development of passive immunoprophylaxis. Pooled immune serum globulin is efficacious in the prevention and attenuation of disease in exposed individuals. More recently, active immunoprophylaxis by vaccination has been accomplished. Future eradication of this disease can now be contemplated

Identification of hepatitis A virus mimotopes by phage display, antigenicity and immunogenicity

“…Both IgG and IgM isotypes have been shown to neutralize HAV (Lemon and Binn, 1983). The IgG response to HAV is delayed compared with the IgM response but is long-lived and accounts for resistance to reinfection (Cuthbert, 2001). …”

“…The etiological agent is Hepatitis A virus (HAV), classified in the genus Hepatovirus within the Picornaviridae family (Cuthbert, 2001). …”

Infección por el virus de la hepatitis A: epidemiología y diversidad genética

“…Y P2 y P3, que comprenden proteínas no estructurales con funciones bioquímicas que soportan la replicación viral, como la 2A que interviene en la morfogénesis de la cápside, la 2C con función helicasa, la 3C con función proteasa y la 3D como ARN polimerasa (tabla1) (8,23). El virus se une al receptor celular HAVcr-1 (por la sigla en inglés de Hepatitis A virus cellular receptor 1), una glicoproteína integral de membrana clase I caracterizada por dominios similares a los de mucinas e inmunoglobulinas (5,20,24,25). Sin embargo, se propone que otros receptores deben intervenir en el proceso de unión y entrada del virus a la célula puesto que HAVcr-1 está presente en otras poblaciones celulares además de los hepatocitos (24,25).…”

“…Las partículas del VHA son estables en el medio ambiente, permanecen de días a meses en suelos, fuentes de agua, sedimento marino y ostras (5,(26)(27)(28)(29)(30). Son resistentes al pH en un rango de 3 a 10; se requiere un pH superior a 10 para inactivarlas.…”

Análisis filogenético de las cepas de rotavirus y virus de la hepatitis A encontradas en agua de consumo en el municipio de Quibdó, Chocó

“…El virus de la hepatitis A pertenece a la familia Picornaviridae, género Hepatovirus; se ha descrito un solo serotipo y siete genotipos cuya presencia se ha asociado a zonas geográficas. Por pertenecer a esta familia, se encuentra genéticamente relacionado con el virus de la poliomielitis y el de la fiebre aftosa (4)(5)(6)(7). La infección por este virus puede no producir síntomas, lo que lleva a subestimar su presencia y a encontrar un porcentaje alto de la población con títulos positivos de anticuerpos en edad adulta (4).…”