In HPTN 061, a study of Black Men Who Have Sex with Men (MSM), we evaluated the association of healthcare-specific racial discrimination with healthcare utilization and HIV testing among 1167 HIV-negative participants. Median age was 38 years, 41% were uninsured, and 38% had an annual household income < $10,000. Overall, 19% reported healthcare-specific racial discrimination directed toward family, friend, or self; 61% saw a healthcare provider in the previous 6 months and 81% HIV tested within the past year. Healthcare-specific racial discrimination was positively associated with seeing a provider (adjusted odds ratio (AOR)=1.4 [1.0, 2.0]) and HIV testing (AOR=1.6 [1.1, 2.4]) suggesting that barriers other than racial discrimination may be driving health disparities related to access to medical care and HIV testing among Black MSM. These results contrast with previous studies, possibly due to measurement or cohort differences, strategies to overcome discrimination, or because of greater exposure to healthcare.

During a course of human immunodeficiency virus (HIV-1) infection, the viral load usually increases sharply to a peak following infection and then drops rapidly to a steady state, where it remains until progression to AIDS. This steady state is often referred to as the viral set point. It is believed that the HIV viral set point results from an equilibrium between the HIV virus and immune response and is an important indicator of AIDS disease progression. In this paper, we analyze a real data set of viral loads measured before antiretroviral therapy is initiated, and propose two-phase regression models to utilize all available data to estimate the viral set point. The advantages of the proposed methods are illustrated by comparing them with two empirical methods, and the reason behind the improvement is also studied. Our results illustrate that for our data set, the viral load data are highly correlated and it is cost effective to estimate the viral set point based on one or two measurements obtained between 5 and 12 months after HIV infection. The utility and limitations of this recommendation will be discussed.

We used baseline data from a study of Black MSM/MSMW in 6 US cities to examine the association of female partnership types with disease prevalence and sexual behaviors among the 555 MSMW participants. MSMW reported more than three times as many total and unprotected sex acts with each primary as they did with each non-primary female partner. We compared MSMW whose recent female partners were: (1) all primary (“PF only”, n = 156), (2) both primary and non-primary (“PF & NPF”, n = 186), and (3) all non-primary (“NPF only”, n = 213). HIV/STI prevalence did not differ significantly across groups but sexual behaviors did. The PF only group had the fewest male partners and was the most likely to have only primary male partners; the PF & NPF group was the most likely to have transgender partners. PF & NPF men reported the most sex acts (total and unprotected) with females; NPF only men reported the fewest. Implications for HIV risk and prevention are discussed.

e15065 Background: CD133 identifies intestinal stem cells and colon CSC, the putative culprit of cancer initiation, progression and resistance. Elevated CD133 levels at protein & mRNA levels predict poor outcomes in patients (pts) with colon cancer. Given that celecoxib reduces colon polyp and only maintenance capecitabine plus celecoxib lead to paradoxically high complete remission (CR) in colon cancer pts who had no resection or positive margin resection of metastases (ASCO 2007), we hypothesized that celecoxib could modulate CD133 and other stemness genes/signaling pathways. Methods: we studied the effects of celecoxib versus 5-FU on CD133, Wnt and other stemness genes/pathways using flow cytometry, immunoflurorescence, real time RT-PCR, western blot, TOP-Flash for Wnt, limiting dilution assay, and Affymetrix in colon cancer cell lines and primary colon cancer spheres. Results: Celecoxib or 5FU inhibited the growth of COX-2+ HT29 or COX-2- DLD1 that express CD133 at 80% and 30% respectively. Only celecoxib down-regulated CD133 expression at the mRNA, and protein levels in a dose and time dependent manner. This effect could not be rescued with PGE2 and may be due to Wnt inhibition. Microarray showed 4 folds down-regulation of CD133 and other stemness genes e.g. CD24, ABC transporters, and LGR4/5, findings of colon cancer sphere under differentiation. Celecoxib affected several key stem cells signaling pathway, restored RB and promote cell cycle progression (P < 0.05). In contrast, 5FU affected G2M transition but had no effects on stemness genes/pathways (p < 0.05). Celecoxib resulted in 6–10 folds reduction in colony size and number with 5.6–36 folds down-regulation of CD133 mRNA in primary colon cancer spheres. Pts with confirmed radiographic CR who had received >6 months of maintenance capecitabine and celecoxib reached 5-year survival > 90% comparable to pts who achieved pathological CR (12/19). Conclusions: Targeting colon CSC with capecitabine and celecoxib may lead to durable CR and survival and deserves further investigation. No significant financial relationships to disclose.