Exploring HIV-Related Stigma as a Determinant of Engagement in HIV Care by African American Women.

Engagement in HIV care reduces HIV-related health disparities that persist across racial/ethnic and gender lines; yet, African American (AA) women face multiple challenges to remaining engaged in care, including HIV-related stigma. We analyzed longitudinal data from 239 participants in the Unity Health Study to estimate associations between HIV-related stigma and engagement in care among AA women linked to HIV care. In adjusted Poisson regression analyses, engagement in care was not associated with HIV-related stigma but was associated with older age (incidence rate ratio [IRR] = 1.01, 95% confidence interval [CI] = [1.00-1.01], p = .01), higher levels of education (IRR = 1.18, 95% CI = [1.02-1.35], p = .03), and higher levels of social support (IRR = 1.05, 95% CI = [1.01-1.09], p = .04). Our findings suggest the need for targeted interventions to enhance engagement in care and to incorporate social support into health promotion programming for AA women living with HIV.

HIV stigma and viral load among African-American women receiving treatment for HIV.

OBJECTIVE: African-American women are more likely than other women in the United States to experience poor HIV-related health; HIV stigma may contribute to these outcomes. This study assessed the relationship between HIV stigma and viral load, over time, among a sample of African-American women receiving treatment for HIV, and explored social support and depressive symptoms as mediators. DESIGN: Secondary analysis of longitudinal data. METHODS: Data came from a randomized trial of an intervention to reduce HIV stigma among African-American women in HIV care in Chicago, Illinois and Birmingham, Alabama. Sociodemographic and psychosocial data were collected at up to six study visits over 14 months. Viral loads were extracted from medical records during the study period. Generalized linear mixed effects models were used to estimate associations among overall, internalized, and enacted HIV stigma and viral load over time. Mediation analyses were used to estimate indirect effects via social support and depressive symptoms. RESULTS: Data from 234 women were analyzed. Overall HIV stigma was significantly associated with subsequent viral load (adjusted ß = 0.24, P = 0.005). Both between-subject (adjusted ß = 0.74, P < 0.001) and within-subject (adjusted ß = 0.34, P = 0.005) differences in enacted stigma were associated with viral load. Neither social support nor depressive symptoms were statistically significant mediators. CONCLUSION: Ongoing experiences of HIV stigmatization may contribute to increased viral load among African-American women in primary HIV care. Interventions should aim to alleviate the consequences of stigma experienced by patients and prevent future stigmatization.

A matched cross-sectional study of the association between circulating tissue factor activity, immune activation and advanced liver fibrosis in hepatitis C infection.

BACKGROUND: Tissue factor (TF) is a protein that mediates the initiation of the coagulation cascade. TF expression is increased in patients with poorly-controlled HIV, and may be associated with increased immune activation that leads to cardiovascular morbidity. The role of TF in immune activation in liver disease in hepatitis C virus (HCV)-monoinfection and HIV/HCV-coinfection has not been explored. METHODS: Fifty-nine patients were stratified: A) HIV-monoinfection (N = 15), B) HCV-monoinfection with chronic hepatitis C (CHC) (N = 15), C) HIV/HCV-coinfection with CHC (N = 14), and D) HIV/HCV-seropositive with cleared-HCV (N = 15). All HIV+ patients had undetectable HIV viremia. Whole blood was collected for CD4/CD8 immune activation markers by flow cytometry and plasma was assayed for microparticle TF (MPTF) activity. Subjects underwent transient elastography (TE) to stage liver fibrosis. Undetectable versus detectable MPTF was compared across strata using Fisher's Exact test. RESULTS: MPTF activity was more frequently detected among patients with HCV-monoinfection (40%), compared to HIV-monoinfection and HIV/HCV-seropositive with cleared HCV (7%) and HIV/HCV-coinfection with CHC (14%) (p = 0.02). Mean TE-derived liver stiffness score in kPa was higher in patients with detectable MPTF (12.4 ± 8.5) than those with undetectable MPTF (6.4 ± 3.0) (p = 0.01). Mean CD4 + HLADR+ and CD4 + CD38-HLADR+ expression were higher in those with detectable MPTF (44 ± 9.8% and 38 ± 8.7%, respectively) than those with undetectable MPTF (36 ± 11% and 31 ± 10.4% respectively) (p = 0.05 and 0.04 respectively). CONCLUSIONS: HCV-monoinfection and HIV/HCV-coinfection with CHC were associated with MPTF activity. MPTF activity is also associated with advanced liver fibrosis and with CD4 + HLADR+ immune activation.

Characterization of CD4⁺ T-cell immune activation and interleukin 10 levels among HIV, hepatitis C virus, and HIV/HCV-coinfected patients.

BACKGROUND: HIV/hepatitis C virus (HCV)-coinfected patients have accelerated liver disease compared with HCV monoinfection. In HIV-positive patients with viral suppression, data comparing inflammatory cytokines and immune activation between HIV/HCV coinfection with chronic hepatitis C (CHC) to HIV/HCV-seropositive patients with cleared HCV are limited. METHODS: Fifty-nine age- and sex-matched patients were stratified: (1) HIV monoinfection (n = 15); (2) HCV monoinfection with CHC (n = 15); (3) HIV/HCV coinfection with CHC (n = 14); and (4) HIV/HCV seropositive with cleared HCV (n = 15). All HIV-positive patients had undetectable HIV viremia, and median CD4 was 420 cells per microliter. Liver fibrosis was assessed in each subject using transient elastography. Cells were collected for CD4 and CD8 immune activation (CD38/HLA-DR) markers via flow cytometry and plasma for luminex-multiplex cytokine assays. RESULTS: CD38⁺HLA-DR⁺ expression on CD4⁺ T cells was significantly increased in HIV/HCV coinfection with CHC (7%) versus HCV monoinfection (4%) (P = 0.012). CD4⁺ total HLA-DR⁺ expression was significantly increased in HIV/HCV coinfection with CHC (43%) versus HIV monoinfection (31%) (P = 0.010) and HIV/HCV seropositive with cleared HCV (38%) (P = 0.046). Total CD4⁺CD38⁺ and CD4⁺CD38⁺HLA-DR⁻ expression was significantly higher in HIV monoinfection (23% and 18%) than HCV moninfection (13%, P = 0.002% and 9%, P = 0.001, respectively). Interleukin 10 levels were significantly lower in HIV monoinfection versus HIV/HCV coinfection with CHC (P = 0.0002). In multivariate analysis, severe fibrosis was associated with lower expression of CD4⁺CD38⁺HLA-DR⁺ and CD4⁺ total CD38⁺ than mild-moderate fibrosis (P = 0.03 and 0.03, respectively). CONCLUSIONS: CD4 immune activation with HLA-DR⁺ expression in HIV/HCV coinfection with well-controlled HIV may arise from chronic HCV viremia. Conversely, CD4⁺CD38⁺ expression may be driven by underlying HIV infection. CD4 immune activation was unexpectedly found to be associated with decreased liver fibrosis.

Multiplex immunoassay of lower genital tract mucosal fluid from women attending an urban STD clinic shows broadly increased IL1ß and lactoferrin.

BACKGROUND: More than one million new cases of sexually transmitted diseases (STDs) occur each day. The immune responses and inflammation induced by STDs and other frequent non-STD microbial colonizations (i.e. Candida and bacterial vaginosis) can have serious pathologic consequences in women including adverse pregnancy outcomes, infertility and increased susceptibility to infection by other pathogens. Understanding the types of immune mediators that are elicited in the lower genital tract by these infections/colonizations can give important insights into the innate and adaptive immune pathways that are activated and lead to strategies for preventing pathologic effects. METHODOLOGY/PRINCIPAL FINDINGS: 32 immune mediators were measured by multiplexed immunoassays to assess the immune environment of the lower genital tract mucosa in 84 women attending an urban STD clinic. IL-3, IL-1ß, VEGF, angiogenin, IL-8, ß2Defensin and ß3Defensin were detected in all subjects, Interferon-α was detected in none, while the remaining mediators were detected in 40% to 93% of subjects. Angiogenin, VEGF, FGF, IL-9, IL-7, lymphotoxin-α and IL-3 had not been previously reported in genital mucosal fluid from women. Strong correlations were observed between levels of TNF-α, IL-1ß and IL-6, between chemokines IP-10 and MIG and between myeloperoxidase, IL-8 and G-CSF. Samples from women with any STD/colonization had significantly higher levels of IL-8, IL-3, IL-7, IL-1ß, lactoferrin and myeloperoxidase. IL-1ß and lactoferrin were significantly increased in gonorrhea, Chlamydia, cervicitis, bacterial vaginosis and trichomoniasis. CONCLUSIONS/SIGNIFICANCE: These studies show that mucosal fluid in general appears to be an environment that is rich in immune mediators. Importantly, IL-1ß and lactoferrin are biomarkers for STDs/colonizations providing insights into immune responses and pathogenesis at this mucosal site.

HIV-infected adults from minority ethnic groups are willing to participate in research if asked.

HIV-infected ethnic minorities are underrepresented in HIV research. We sought to better understand the reasons for the low participation rates. An anonymous 1-page survey was administered to HIV-infected patients attending primary care clinics at the CORE Center in Chicago during 8 weeks in 2007. Four hundred seventeen HIV-infected patients (mean age, 43 years; 60% male, 65% African American, 21% Hispanic) completed the survey. Forty percent had previously participated in research but only 29% had ever been asked by their primary care provider (PCP) to participate. The strongest predictor of participation was being asked (RR 3.0; p < 0.001). The majority of patients would agree (65%) or consider (30%) participating in a study if recommended by their PCP. Being treated like a "guinea pig" was the most common (40%) concern of patients. However, despite this concern, patients would still agree to participate if recommended by their PCP. In our urban cohort of HIV-infected patients, the majority were willing to participate in HIV research studies if asked, highlighting the important role of primary providers in improving research participation.

Metabolic syndrome in older HIV-infected patients: data from the CORE50 cohort.

Metabolic abnormalities and cardiovascular disease are increasingly recognized in HIV-infected patients. While HIV-infected patients older than 50 years of age account for up to 25% of HIV cases in the United States, there are limited data on these individuals. To determine the prevalence and predictors of the metabolic syndrome among a cohort of older, HIV-infected patients and to calculate their 10-year Framingham cardiac risk (FCR) score a cross-sectional study of HIV patients older than 50 years of age was conducted at the CORE Center, Chicago, Illinois, between May 2005 and February 2006. There were 121 HIV-infected patients with a median age of 54 years, of whom 79% were male, 83% African American, 9% Hispanic, and 6% Caucasian. Thirty-four percent of patients had the metabolic syndrome, 49% had a moderate-high (>10%) 10-year FCR, and 13% had a high (>20%) 10-year FCR. Patients with the metabolic syndrome were significantly more likely to have a greater than 20% 10-year FCR. Sixty-five percent of all patients were current smokers and 55% of patients with the metabolic syndrome were current smokers. There were significant differences in the components of the metabolic syndrome by gender with women having significantly more components related to insulin resistance such as elevated waist circumference and diabetes, while men were more likely to have low high-density lipoprotein (HDL) levels. This study shows a high prevalence of the metabolic syndrome in older HIV-infected patients and an association between the metabolic syndrome and FCR in our study population. As the HIV population ages, attention to modifiable cardiac risk factors will become increasingly important.