the first 6 months of exposure averaging 90 days from exposure to jaundice and 60 days to abnormal serum alanine aminotransferase (ALT) levels indicating liver injury (Krugman et al., 1979).
Approximately 95 percent of all hepatitis B infections among otherwise healthy adults resolve without sequelae, and the recovered individual possesses lifelong immunity to HBV infection (CDC, 2006). In the other 5 percent, chronic infection develops (CDC, 2006). Chronic HBV infection may lead to liver cirrhosis, liver failure, hepatocellular carcinoma, or death (Mast and Ward, 2008). These outcomes are thought to be the result of the constant activity of the immune system and not a direct consequence of damage caused by the virus itself (Ganem and Prince, 2004). The likelihood of chronic hepatitis B disease is inversely related to the age of the individual at the time of HBV infection (Beasley et al., 1983; Edmunds et al., 1993). Among infants perinatally infected with HBV, 80–90 percent develop chronic disease; among children infected postnatally through 5 years of age, 30 percent; and among adults, fewer than 5 percent (Hyams, 1995). The risk of chronic disease may be higher in the immunocompromised and diabetics dependent on finger-stick monitoring devices (CDC, 2006; Polish et al., 1992).
HBV transmission through blood and blood products was first evidenced in 1883 after an outbreak of hepatitis among shipyard workers following smallpox vaccination in Bremen, Germany (Mast and Ward, 2008). In 1965, Blumberg and Alter (Blumberg and Alter, 1965) discovered the Australia antigen (Au), which was later determined to be hepatitis B surface antigen (HBsAg) (Prince, 1968). Research performed in the early 1970s showed that HBV could be heat-inactivated and that inoculation with inactivated serum provided resistance to or modification of the virus (Krugman, 1974; Krugman and Giles, 1973).
In the early 1980s, several groups developed preliminary HBV vaccines (Coutinho et al., 1983; McLean et al., 1983; Purcell and Gerin, 1975). The vaccines consisted of inactivated, alum-adsorbed, 22-nm HBsAg particles recovered and purified from individuals with chronic hepatitis B infection (Coutinho et al., 1983; McLean et al., 1983; Purcell and Gerin, 1975). With the development of DNA recombinant technologies and the ability to obtain HBsAg from other sources such as Saccharomyces cerevisiae (baker’s yeast), DNA recombinant vaccines replaced plasma-derived vaccines in the United States (Mast and Ward, 2008). In 1991, the Centers for Disease Control and Prevention (CDC) and the American Academy of Pediatrics recommended HBV vaccination for all infants and adults (CDC, 1991).
Currently, hepatitis B vaccines are available in single- and multiantigen formulations (CDC, 2005). The two single-antigen vaccines are Recombivax HB (Merck & Co., Inc.) and Engerix-B (GlaxoSmithKline Biologicals) (CDC, 2005). Of the three licensed combination vaccines, Comvax (Merck) and Pediarix (GlaxoSmithKline) are used for infant and child