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Figure 1. Representation of a virosome with HAV. (A) HAV virus adsorbed on its surface and (B) electron microscopy of a virosomal preparation. HAV: Hepatitis A virus.
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Figure 2. Mechanism of action of hepatitis A virosomal vaccine. After intramuscular injection, formalin-inactivated HAV adsorbed on the surface of a virosome are taken up by immunocompetent cells (e.g., macrophage) via influenza HA-mediated endocytosis (1) . Exposure to the low pH (5) of the cell endosome (2) causes conformational changes in HA, resulting in fusion (3) of the virosome and endosome membranes. Within the endosome, the virus antigen is proteolysed (4) to antigenic peptides. Thereafter, the antigen-containing endosomes join (5) with vacuoles containing MHC II molecules. The resulting MHC II-antigen complex is transported to the surface of the cell (6) where it initiates either a specific humoral response and/or a cellular immune response. HA: Hemagglutin; HAV: Hepatitis A vius.
(Figure omitted. See article PDF.)
Hepatitis A vaccines have been available for approximately 15 years [1]. Following their introduction, they were primarily targeted to individuals at increased risk for hepatitis A, particularly international travelers, long-term expatriates, and military personnel [2]. While this strategy efficiently prevented hepatitis A in these groups, it had little impact on the overall incidence of hepatitis A virus (HAV) infections in most countries.
Humans are the only natural hosts of HAV, which is a picornavirus first visualized by electron microscopy in 1973. HAV consists of one ssRNA molecule associated with capsid proteins, forming a roughly cubic or icosahedric structure of 27-32-nm diameter. In the environment, the virus can remain stable for several months; it is resistant to low pH and moderate temperatures (-20-70°C) and is inactivated by high temperature (85°C for 1 min or higher), formalin and chlorine. Only one serotype of HAV has been demonstrated by neutralization assays.
The incubation period lasts approximately 28 days (range: 15-50 days) following the ingestion of contaminated food or water or close contact with an infected host [3]. Transmission can also occur through blood or blood products of donors who were in their viremic phase. The illness has an abrupt onset of fever, malaise, anorexia, nausea, abdominal discomfort, dark urine and jaundice, and resolves in general within 2 months. The likelihood of...