Table 1.

Conventional view of immunity to gonorrhea^*.

Postulate	Evidence for	Evidence against
Neisseria gonorrhoeae induces immune responses in infected subjects	Infected (and many uninfected) humans have serum antibodies against gonococcal antigens	Little or no increase in antibody levels after infection, or in subjects with previous infection
Specific antibodies are rendered ineffective by antigenic variation	Most major gonococcal surface molecules undergo extensive variation through:	Partial serovar-specific immunity reported in one study
	allelic polymorphism genetic recombination phase–variable expression horizontal gene exchange	Anti-Opa antibodies may be associated with resistance to salpingitis
N. gonorrhoeae avoids complement-mediated destruction	N. gonorrhoeae inhibits complement activation (C4BP, RMP, LOS sialylation, factor H binding) and resists bacteriolysis	Serum bactericidal assay taken as an index of immunity
N. gonorrhoeae resists phagocytic destruction	N. gonorrhoeae invades neutrophils and partially survives within vacuoles	Resistance to intracellular killing is partial
Hence N. gonorrhoeae can survive whatever the immune system develops against it

*For discussion and references, see text.