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T helper cells and efficacy of Haemophilus influenzae type b conjugate vaccination

Immunological background to the use of conjugate vaccines

Immunity acquired against encapsulated bacteria such as H influenzae type b (Hib) and certain viruses including polio depends, as far as we know, entirely on antibodies. Vaccines against these agents need to induce protective levels of antibody, and in many cases probably do so by more than one means. The antibody may be made simply in response to the original doses of vaccine and continually produced over a period of time. This is termed “sterile immunity”, since the antibody wipes out the

Memory response to the Hib vaccine

In evaluating protective efficacy, the critical issue is whether boosting with plain polysaccharide elicits sufficiently rapidly a protective level of antibody, particularly in children whose antibody levels from the original vaccination have fallen below the protective level. Two studies, both in children who had been primed by conjugate vaccine using the standard three-dose infant regimen, clearly demonstrated rising antibody titres following a dose of Hib polysaccharide in the 2nd year of

The factors responsible for vaccine failure

Before the introduction of widespread immunisation, children between the ages of 6 months and 2 years were susceptible to invasive Hib infections, with the age-specific incidence falling thereafter to become rare after 5 years of age.⁵ Much of this early susceptibility was attributed to the relative hyporesponsiveness of infants to the Hib capsular polysaccharide PRP due to immaturity of the B cell compartment, as demonstrated following exposure to oropharyngeal carriage,⁶ invasive infection,⁷

Implications

The most obvious additional case to which this analysis is relevant is the meningococcal C conjugate vaccine, also administered at 2, 3, and 4 months without a booster dose. This vaccine, introduced routinely as a primary infant course in late 1999, is required to provide protection well into the second decade of life when there is a peak in morbidity and mortality due to serogroup C meningococcus.²⁵ The implication of the present hypothesis is that if vaccine failures occur (ie, infection in

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