Poster Presentation Australian Society for Microbiology Annual Scientific Meeting 2023

4CMenB vaccine-induced immune response to Neisseria gonorrhoeae. (#219)

Valentin Slesarenko 1 , S. Eskandari 1 , Taha Taha 1 , C. Thng 1 2 , E. A. Semchenko 1 , K. L. Seib 1
  1. Griffith University, Labrador, QLD, Australia
  2. Gold Coast Sexual Health, Southport Community Health Precinct, Gold Coast, QLD, Australia

Introduction:

Gonorrhea is a sexually transmitted infection caused by Neisseria gonorrhoeae that remains a significant concern with ~100 million cases per year worldwide. There is currently no gonococcal vaccine, however observational studies indicate that the 4CMenB vaccine against the closely related bacteria Neisseria meningitidis may provide protection against N. gonorrhoeae. Here we investigate antibody responses to N. gonorrhoeae following 4CMenB vaccination in patients with high risk of gonorrhoea.

Methods:

As part of a clinical trial, 20 participants received 4CMenB and the other 20 received a placebo. Western Blot analysis was used to investigate cross-reactive proteins. Enzyme-linked immunosorbent assay (ELISA) was used to detect and quantify total IgG antibody responses in the vaccinated and unvaccinated human serum to whole-cell N. gonorrhoeae and the vaccine component NHBA.

Results:

Comparison of baseline (unvaccinated) vs 6 months (3 months post 2nd vaccine dose) by Western blot showed cross reactive proteins in all samples at both timepoints. The cross reactivity at baseline may be due to past N. gonorrhoeae infections in participants. ELISA showed an increased antibody response post vaccination to whole-cell N. gonorrhoeae in 20% of the participants, and to NHBA in 45% of the participants.

Conclusion:

We demonstrated that vaccination with 4CMenB leads to an increased antibody response to whole-cell N. gonorrhoeae and NHBA. Future work to investigate specific proteins from 4CMenB involved in the immune response will enable identification of possible targets and mechanisms of cross-protection.