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The purpose of this study was to assess humoral antibody responses as a function of disease progression (DP) in a well-defined HIV + cohort. We quantified antibodies to HIV-1 gp120, Gag, and CD4 receptor by enzyme-linked immunosorbent assay in sera from a cohort of 97 HIV + subjects at defined stages of DP. We also measured antibody-dependent cellular cytotoxicity (ADCC) as a function of the clinical status of the patients. We purified antibodies to CD4 and gp120 and assessed them for specificity, ability to block gp120 binding to target cells, ability to block virus infection, and ability to facilitate ADCC. All of the HIV + patient samples were positive for antibodies to HIV gp120 and p24 and 80% showed evidence of hypergammaglobulinemia. Approximately 10% of cohort members were positive for antibodies to CD4, but we noted no significant correlation relevant to DP. There were statistically significant differences between the groups concerning the level of humoral response to gp120 and Gag. However, we observed no distinction in ability of anti-gp120 antibodies purified from each group to neutralize infection. In addition, there was a statistically significant difference in ADCC, with elite controllers exhibiting significantly lower levels of ADCC than the other five groups. We detected IgA anti-gp120 antibodies, but did not correlate their presence with either DP or ADCC levels. The results are consistent with the interpretation that the humoral antibody response to the antigens assessed here represents a signature of the level of viremia but does not correlate with clinical status of HIV infection., Competing Interests: Author Disclosure Statement No competing financial interests exist.

Objectives As socioeconomic factors may impact the risk of chronic kidney disease ( CKD), we evaluated the incidence and risk factors of incident CKD among an HIV-infected cohort with universal access to health care and minimal injecting drug use ( IDU). Methods Incident CKD was defined as an estimated glomerular filteration rate (eGFR) <60 ml/min/1.73 m2 for ≥ 90 days. eGFR was calculated using the Chronic Kidney Disease Epidemiology Collaboration ( CKD-EPI) equation. Rates were calculated per 1000 person-years ( PY). Associations with outcomes were assessed using two separate Cox proportional hazard models, adjusting for baseline and time-updated covariates. Results Among 3360 participants [median age 29 years; 92% male; 44% African American ( AA)] contributing 23 091 PY of follow-up, 116 developed incident CKD [5.0/1000 PY; 95% confidence interval ( CI) 4.2-6.0/1000 PY]. The median first eGFR value was 97.0 mL/min/1.73 m2 [interquartile range ( IQR) 85.3-110.1 mL/min/1.73 m2]. Baseline factors associated with CKD included older age, lower CD4 count at HIV diagnosis [compared with CD4 count ≥ 500 cells/μL, hazard ratio ( HR) 2.1 (95% CI 1.2-3.8) for CD4 count 350-499 cells/μL; HR 3.6 (95% CI 2.0-6.3) for CD4 count 201-349 cells/μL; HR 4.3 (95% CI 2.0-9.4) for CD4 count ≤ 200 cells/μL], and HIV diagnosis in the pre-highly active antiretroviral therapy ( HAART) era. In the time-updated model, low nadir CD4 counts, diabetes, hepatitis B, hypertension and less HAART use were also associated with CKD. AA ethnicity was not associated with incident CKD in either model. Conclusions The low incidence of CKD and the lack of association with ethnicity observed in this study may in part be attributable to unique features of our cohort such as younger age, early HIV diagnosis, minimal IDU, and unrestricted access to care. Lower baseline CD4 counts were significantly associated with incident CKD, suggesting early HIV diagnosis and timely introduction of HAART may reduce the burden of CKD. [ABSTRACT FROM AUTHOR]

HIV and syphilis are often seen as co-infections since they share a common mode of transmission. During episodes of syphilis, CD4 counts transiently decrease and HIV viral loads increase; however, the effect of syphilis co-infection on HIV disease progression (time to AIDS or death) is unclear. We analysed prospectively collected information on 2239 persons with estimated dates of HIV seroconversion (205 [9.2%] with confirmed syphilis and 66 [2.9%] with probable syphilis) in order to determine the effect of syphilis co-infection on HIV disease progression. In multivariate models censored at highly active antiretroviral therapy (HAART) initiation or last visit, adjusting for CD4 count, age, race, gender, and hepatitis B and C status, syphilis (confirmed + probable) was not associated with increased hazard of AIDS or death (hazard ratio 0.99, 95% CI 0.73-1.33). Treating HAART as a time-varying covariate or limiting the analysis to only confirmed syphilis cases did not significantly alter the results. Despite transient changes in CD4 counts and viral loads, syphilis does not appear to affect HIV disease progression. [ABSTRACT FROM AUTHOR]