Phase and Antigenic Variation of Pili and Outer Membrane Protein II of Neisseria gonorrhoeae

ology and the clinical implications of antigenic variation in a number of microorganisms, including Neisseria gonorrhoeae. Among a number of gonococcal surface antigens under intense scrutiny because of their postulated roles in pathogenesis are two that undergo both phase and antigenic variations: pili (or fimbriae) and an outer membrane protein designated P.II. Pili are surface fibrils made up of multiple subunits of r',19 kDa that function to increase adherence to a number of cell types [1]. P.II is a family of heat-modifiable proteins of 24-30 kDa, the presence of which is associated with increased intercellular adhesion between gonococci, and also with increased attachment to certain cells [2]. Phase variation or phase switching generally refers to reversible switches between alternative states, such as pilus-expressing (P+) or pilus nonexpressing (P-) and P.II expressing (PM+) or P.II nonexpressing (P.II-). The switch between these phases in vitro is a relatively high-frequency event. The P+ to 13phase variation occurs at an estimated frequency of ,N,10-2-10-3/cell per generation; the reverse switch from 13to P+ occurs at variable frequency from >10-2 to essentially undetectable. The phase variation between P.II+ and P.IIoccurs at f\40-2-10-3/cell per generation, apparently with equal rates in both directions [3]. These rates are too high to be explained by classical mutation events. Antigenic variation refers to alterations in structure that are accompanied by detectable alterations