BackgroundAt the individual level, higher HIV viral load predicts sexual transmission risk. We evaluated San Francisco's community viral load (CVL) as a population level marker of HIV transmission risk. We hypothesized that the decrease in CVL in San Francisco from 2004–2008, corresponding with increased rates of HIV testing, antiretroviral therapy (ART) coverage and effectiveness, and population-level virologic suppression, would be associated with a reduction in new HIV infections.Methodology/Principal FindingsWe used San Francisco's HIV/AIDS surveillance system to examine the trends in CVL. Mean CVL was calculated as the mean of the most recent viral load of all reported HIV-positive individuals in a particular community. Total CVL was defined as the sum of the most recent viral loads of all HIV-positive individuals in a particular community. We used Poisson models with robust standard errors to assess the relationships between the mean and total CVL and the primary outcome: annual numbers of newly diagnosed HIV cases. Both mean and total CVL decreased from 2004–2008 and were accompanied by decreases in new HIV diagnoses from 798 (2004) to 434 (2008). The mean (p = 0.003) and total CVL (p = 0.002) were significantly associated with new HIV cases from 2004–2008.Conclusions/SignificanceReductions in CVL are associated with decreased HIV infections. Results suggest that wide-scale ART could reduce HIV transmission at the population level. Because CVL is temporally upstream of new HIV infections, jurisdictions should consider adding CVL to routine HIV surveillance to track the epidemic, allocate resources, and to evaluate the effectiveness of HIV prevention and treatment efforts.

Highly active antiretroviral therapy (HAART) has dramatically reduced the incidence of acquired immunodeficiency syndrome (AIDS) and increased AIDS survival time, but little is known about its impact on cancer. Data from adults in the San Francisco, California, AIDS surveillance registry were computer matched with the California Cancer Registry. Age-, sex-, and race-adjusted standardized incidence ratios (SIRs) were computed, and proportional hazards models evaluated the effect of HAART use on cancer incidence and cancer survival time. Among 14,210 adults with AIDS diagnosed in 1990-2000, 482 non-AIDS-defining cancers were diagnosed. Compared with rates for the general population, significantly increased cancer incidence rates were observed for anal (SIR = 13.4), Hodgkin's lymphoma (SIR = 11.5), liver (SIR = 3.6), oral cavity and pharynx (SIR = 2.6), respiratory (SIR = 2.6), leukemia (SIR = 2.4), skin melanoma (SIR = 2.4), and prostate (SIR = 1.7) cancers. Risk of liver cancer was lower with HAART use (relative hazard (RH) = 0.32). Risk of anal cancer increased after 1995 (RH = 2.9). Respiratory cancer (RH = 0.40) and Hodgkin's lymphoma (RH = 0.17) showed increased cancer survival time with HAART use, while anal cancer survival may have been slightly decreased (RH = 1.4). The impact of HAART on non-AIDS-defining cancer incidence rates and survival is not uniform, and the mechanism(s) responsible for these differences should be investigated further.

The reasons for recent declines in AIDS incidence and mortality may include advances in treatment, but these may be confounded by earlier declines in the incidence of human immunodeficiency virus (HIV) infection. To determine whether the declines in AIDS and mortality may, in part, stem from wider use of combination antiretroviral therapy, 622 HIV-positive men with well-characterized dates of seroconversion were followed. In this group, combination therapy came into widespread use in only 1996. In a Cox proportional hazards model, the 1996 calendar period was significantly associated with slower progression to AIDS (relative hazard [RH]=0. 19, 95% confidence interval [CI], 0.05-0.69, P=.01) and death (RH=0. 45, 95% CI, 0.21-0.95, P=.04). Declines in incidence of HIV infection, changes in HIV virulence, and end-point underreporting cannot fully explain the decline in AIDS and death in 1996. The introduction of combination antiretroviral therapy as the standard of care may already have had measurable effects.

Strategies to prevent HIV for urban MSM should focus on new predictors of HIV transmission.

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Socioeconomic resources and age, not race or gender, are associated with disparities in engagement in HIV care in San Francisco.

Steps can be taken to minimize potential social harms and to mobilize diverse communities to enroll in trials. Statements of hypothetical willingness to participate in future trials may overestimate true enrollment.

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