Grant: Project Grant

The two basic elements of successful Human Immunodeficiency Virus (HIV) transmission are a viable virus and a susceptible target host cell. Activated immune cells are more susceptible to HIV infection than resting cells and, once infected, they produce up to 1000 times more virus. It is known that inflammation brings activated HIV target cells to the site of irritation. Most of biomedical prevention approaches focus on either keeping HIV away (condom use) or neutralizing it once it is present in the genital tract (antiviral drugs, microbicides, vaccines). However, what has not been a focus of HIV prevention efforts, is trying to limit the availability of susceptible HIV-target cells at the genital tract. We conducted a pilot study to determine if a common anti-inflammatory drug acetylsalicylic acid (ASA or Aspirin) could decrease inflammation among low-risk Kenya women. The results showed ASA reduced the number of HIV target cells in the female genital tract by 35%. In this current study, we build on those finding using detailed molecular studies to determine the molecular mechanism(s) involved in ASA's effect on the recruitment of HIV target cells in the genital tract. We will also determine if daily administration of ASA will reduce HIV target cells numbers at the genital tract Kenyan female sex workers who are at high risk of acquiring HIV. We will also determine which dose of ASA is most effective, the duration of the effect and whether there are any side-effects on the vaginal microbiome. The long-term goal of this study is to provide a novel HIV-prevention approach that is both readily available and non-stigmatizing. If we can demonstrate that ASA is able to reduce HIV target cells among women at high risk of acquiring HIV, then we will be one step closer to a much needed novel HIV prevention.