It appears incontestable that there is a link between genital ulcer disease and HIV infection. On the one hand the natural history and response to therapy of syphilis, HSV-2, and chancroid are all modified by the immunosuppressive effects of HIV infection. On the other hand, HIV transmission is probably facilitated by the disruption of the normal epithelial barriers of the genital organs caused by these ulcerative infections. Information is somewhat less convincing that a similar association exists between the nonulcerative STDs (trichomonas, gonorrhea, chlamydial infections) and HIV. Conceptually, the mucosal inflammation associated with these infections might serve as a focus for HIV transmission. The available data, though suggestive, do not strongly support this contention. Theoretically though, even a small risk might potentially result in significant HIV transmission given the prevalence of nonulcerative STDs. These infectious processes do not appear to be markedly altered by HIV induced immunosuppression. The ability of HPV to cause dysplastic changes in cervical and anal tissue did not require the AIDS epidemic to come to light. In HIV infection, disruptions of immunoregulatory processes, which might ordinarily control the progression of potentially malignant cell lines, have created fertile ground for an increasing incidence of premalignant and malignant cytologic changes. The mutual impact these processes have or may have on one another requires that clinicians who care for patients with either HIV infection or with STDs should be thoroughly familiar with both and not consider them somehow exclusive of one another. Efforts toward the prevention and control of STDs should be considered important in the control and prevention of HIV transmission.