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Hepatitis and Liver Cancer: A National Strategy for Prevention and Control of Hepatitis B and C
sis (March 2001–July 2002), pneumococcal conjugate (September 2001– March 2003 and February 2004–September 2004), measles–mumps–rubella (October 2001–July 2002), and varicella (October 2001–August 2002) (Jacobson et al., 2006).
Although there has not been a national shortage of the hepatitis B vaccine, temporary supply problems occurred with this vaccine in 2008 (adult and dialysis formulations of Recombivax HB) and 2009 (pediatric formulations of Recombivax HB and Pediatric Engerix-B) (CDC, 2009a). A shortage was avoided because other manufacturers were able to provide an adequate supply of the vaccine in adult and dialysis formulations, and CDC released doses of pediatric vaccine from its stockpile.
Recommendation 4-6. The federal government should work to ensurean adequate, accessible, and sustainable hepatitis B vaccine supply.
HEPATITIS C VACCINE
Efforts are going on to develop a vaccine for hepatitis C, and several candidates are in phase I and phase II clinical trials (Inchauspe and Michel, 2007). Although some vaccines are being developed to treat people with chronic HCV infection (that is, therapeutic vaccines), this section focuses on vaccines to prevent chronic HCV infection. An incomplete understanding of how chronic HCV infection is spontaneously controlled in some people and antigenic variability of the virus remain barriers to development of a vaccine to prevent chronic hepatitis C.
Feasibility of Preventing Chronic Hepatitis C
The outcomes of HCV infections in humans and chimpanzees suggest that it may be possible to develop a vaccine to prevent HCV infection. Spontaneous clearance of the virus in 15–45% of persons after acute HCV infection demonstrates that immunity can prevent chronic infection and its long-term consequences, such as cirrhosis and hepatocellular carcinoma (HCC) (Alter et al., 1992; Barrera et al., 1995; Villano et al., 1999; Vogt et al., 1999). It also seems that immunity can be conditioned by prior exposure: humans and chimpanzees that recover from HCV infection appear to control a second infection better (the peak of viremia is lower than in the initial infection, and the chance of recovery is greater compared with that in persons not previously infected) (Lanford et al., 2004; Major et al., 2002; Mehta et al., 2002). In addition, IDUs who recovered from earlier HCV infections and have continuing HCV exposure have substantially less viremia than those who have similar exposure but had no earlier infection