mBio: Mutations in key molecules can stop gonorrhea infections

Researchers at Georgia State University's Institute of Biomedical Sciences say that making a mutation that inhibits the way the bacterial pathogen Neisseria gonorrhoeae causes gonorrhea, could provide a new way
to prevent and treat gonorrhea.

The researchers found that mutations in key parts of the outer membrane transporters that Neisseria gonorrhoeae use to hijack human immune proteins and strip their metals may help prevent gonorrhea infections
.

Gonorrhea affects more than 80 million people worldwide each year and is a global threat to public health due to the increasing incidence of antimicrobial resistance, rising costs of treatment and the lack of protective vaccines
.

Due to the evolution of resistance to existing drugs, effective treatment options for gonorrhoea are decreasing
.

To overcome the nutritional immunity of the host, Neisseria gonorrhoeae deploys tonb-dependent transporters (tdt) to its outer membrane, binds to the host's nutritional immune proteins, and strips its metals
.

A TdT called TdfJ can recognize human S100A7, a zinc-binding protein that can inhibit replication
of pathogens by hiding zinc.

"The prospect of untreatable gonococcal infections has prompted efforts to identify targets for new therapeutic and prevention strategies, and members of the outer membrane metal transporter family that rely on tonb have become promising candidate genes because they play a key role
in identifying infections.

The study describes the binding interaction between the zinc-input protein TdfJ and its human zinc source S100A7, and identifies key regions where
TdfJ mediates this interaction.

"For the first time, we described in detail the binding interaction
of gonococcal TdfJ and its human ligand S100A7.

Co-authors of the study include Stavros A.

The study was funded
by the National Institutes of Health (NIH).

Journal Reference:

1. Stavros A.