Human antibody responses to A and C capsular polysaccharides, IgA1 protease and transferrin-binding protein complex stimulated by infection with Neisseria meningitidis of subgroup IV-1 or ET-37 complex
N. Brieske et al., Human antibody responses to A and C capsular polysaccharides, IgA1 protease and transferrin-binding protein complex stimulated by infection with Neisseria meningitidis of subgroup IV-1 or ET-37 complex, VACCINE, 17(7-8), 1999, pp. 731-744
The protein sequences of the IgA1 protease, TbpA and TbpB proteins differ b
etween meningococci representative of serogroup A, subgroup IV-1 from epide
mic disease in The Gambia and serogroup C, ET-37 complex from endemic disea
se in Mali. The uniformity of restriction endonuclease sites was determined
for the iga, tbpA and tbpB genes among strains of both clonal lineages. Ra
re isolates had acquired a variant tbpAB operon by horizontal genetic excha
nge but all other strains were uniform within each clonal lineage. The quan
titative levels of IgG to capsular polysaccharide, IgA1 protease and TBP co
mplex were measured in paired acute phase and convalescent phase sera from
The Gambia and from Mali using antigens from the homologous clonal lineages
. IgG levels to these antigens were also measured in paired sera from healt
hy Gambians who permanently carried meningococci in the nasopharynx or did
not. The results showed that disease stimulated IgG to each antigen in Mall
and to all but TBP complex in The Gambia. Similarly, higher levels of IgG
were found in sera from permanent carriers than in sera from permanent non-
carriers. Acute phase sera from Mall contained low levels of IgG to C capsu
lar polysaccharide (geometric mean value of 0.3 mu g ml(-1)) while such ser
a from The Gambia contained higher and potentially protective levels of IgG
to A polysaccharide (geometric mean of 5.5 mu g ml(-1)). The concentration
s of IgG to TBP complex in acute phase sera were higher and IgG to IgA1 pro
tease was even higher, suggesting that intermediate levels of IgG to these
proteins do not protect against disease. (C) 1999 Elsevier Science Ltd. All
rights reserved.