Gray et. al conducted an ecological and observational study with nearly 5000 uncircumcised, HIV- men between the ages 15-49 in Uganda to determine whether or not male circumcision could help to prevent the spread of HIV in men. The men were placed in two groups: immediate circumcision (n=2474) or delayed circumcision by 24 months (n=2522). These men were followed up at 6, 12, and 24 months and tested for HIV. In the immediate circumcision group the incidence rate was 0.66 cases per 100 people while in the delayed circumcision group the incidence rate was 1.33 cases per 100 people. HIV transmission rates were clearly lower in the immediate circumcision group and suggests that male circumcision can help prevent STD transmission. Males contract STDs such as the immunodeficiency virus when it comes in contact with the urethra or foreskin. The components of an uncircumcised penis include the penile shaft, glans, urethra, foreskin and the frenulum. The outside of the penis, the shaft and outer foreskin, are keratinised, which provides a barrier against HIV. The inner foreskin, however, does not have keratin which allows for the presence of Langerhan’s cells (dendritic cells of the epidermis). These cells allow for the infection of the virus. During intercourse, the foreskin is pulled back, exposing the inner non-keratinized portion of the foreskin to the viaginal wall and thus providing HIV a surface to infect another person. Circumcised men lack a foreskin, which removes the foreskin that lacks keratin, do not have a microbiome in the genital mucosa which may attract HIV-susceptible cells and have dry glans after intercourse. The wetness/microbiome under the foreskin may play a role in HIV acquisition by providing an anoxic microenvironment which supports pro-inflammatory anaerobes. This activates Langerhan’s cells, which may accelerate the process of infection. Circumcised men have a significant difference in microbiota, particularly a decrease in anaerobic bacterial families, which may help decrease transmission. Mechanistically, HIV requires a specific CD4 receptor and a chemokine receptor, CCR5 to infect a host. The HIV protein envelop (env) has a glycoprotein gp120 which binds to CD4 of the host cell. Next gp120 undergoes a conformational change which allows it to bind to another surface cell receptor, CCR5. This binding to the coreceptor causes a conformational change in gp41 on the surface of the virus, ultimately leading to the fusion of HIV with the host cell.