As noted previously, the distribution of the MDA in the collection of disease isolates was not uniform by age of patient. While the prevalence of the MDA was approximately 88% in the patients aged beween 2�C12 or older than 28 years, it was overrepresented in the 13�C28 year age band but underrepresented in those patients aged less than 2 years. These findings suggest that the major part of the effect of the MDA on increased invasive potential of meningococci is manifested in young adults but not in infants. This is interesting in light of the fact that young children are relatively unprotected by circulating antibody, no longer being protected by maternally-derived antibodies and not yet having acquired natural immunity by carriage of non-virulent meningococci and other commensal Neisseria. It is possible that MDA promotes disease in immunologically mature individuals, whereas its effect is not apparent in young children who are susceptible to strains of lesser virulence lacking MDA. The means by which the bacteriophage could increase the virulence of the host strains of meningococcus remain to be determined, in contrast to some other cases where disease symptoms are largely determined by phage-carried toxin genes. In the case of the meningococcus, one possibility is that genomic rearrangements induced by the element might lead to changes in gene expression, hence disturbing the normal, nonpathogenic relationship between bacterium and human. This notion is in agreement with recent results from genome comparisons between pathogenic Neisserial strains and between pathogens and carriage isolates. In conclusion, comparative genomic analysis followed by verification in a large-scale epidemiolgical survey shows that the MDA phage is associated with TPPB invasiveness in meningococci in the age group of young adults. The study highlights the power of combining comparative genomics with human disease data collected in the community, particularly as an Kaempferol alternative to classical techniques in the study of specifically human diseases, where laboratory assays of pathogenicity correlates are not entirely representative.