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Published online November 23, 2009
PEDIATRICS Vol. 124 No. 6 December 2009, pp. 1633-1641 (doi:10.1542/peds.2008-3645)
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STATE-OF-THE-ART REVIEW ARTICLE

Booster Vaccinations: Can Immunologic Memory Outpace Disease Pathogenesis?

Michael E. Pichichero, MD

Rochester General Research Institute, Rochester General Hospital, Rochester, New York

ABSTRACT

Almost all current vaccines work by the induction of antibodies in serum or on the mucosa to block adherence of pathogens to epithelial cells or interfere with microbial invasion of the bloodstream. However, antibody levels usually decline after vaccination to undetectable amounts if further vaccination does not occur. Persistence of vaccine-induced antibodies usually goes well beyond the time when they should have decayed to undetectable levels because of ongoing "natural" boosting or other immunologic mechanisms. The production of memory B and T cells is of clear importance, but the likelihood that a memory response will be fast enough in the absence of a protective circulating antibody level likely depends on the pace of pathogenesis of a specific organism. This concept is discussed with regard to Haemophilus influenzae type b, Streptococcus pneumoniae, and Neisseria meningitidis; hepatitis A and B; diphtheria, tetanus, and pertussis; polio, measles, mumps, rubella, and varicella; rotavirus; and human papilloma virus. With infectious diseases for which the pace of pathogenesis is less rapid, some individuals will contract infection before the memory response is fully activated and implemented. With infectious diseases for which the pace of pathogenesis is slow, immune memory should be sufficient to prevent disease.


Key Words: vaccines • immunologic memory • pathogenesis • Neisseria meningitidesHaemophilus influenzae type b • human papilloma virus

Abbreviations: TLR—Toll-like receptor • Hib—Haemophilus influenzae type b • DTaP—diphtheria-tetanus-acellular pertussis • HPV—human papilloma virus


Accepted Jun 15, 2009.


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