H. pylori colonizes the human stomach where it can cause a variety of diseases, including peptic ulcer disease, chronic gastritis, and gastric cancer. Flagellum-mediated motility and chemotaxis are essential for host colonization by H. pylori. I examined three genes involved in motility and chemotaxis in H. pylori - flhF, cheA, and flgV. The H. pylori flhF deletion mutant has defects in motility, flagellation, and flagellar localization, consistent with previous reports. The H. pylori cheA deletion mutant exhibits aberrant cell morphologies, in addition to the expected chemotaxis defect. Deletion of H. pylori flgV, a previously uncharacterized gene, results in defects in motility and flagellation. I identified an allele of fliF (encodes the MS ring protein) that suppresses the motility and flagellation defects of an flhF deletion mutant. I also found that FlgV has roles in both motor function and flagellum assembly, and forms a novel ring structure in the flagellar motor.