Factors associated with self-reported unprotected anal sex among male sex workers in Mombasa, Kenya

To identify social and behavioral characteristics associated with sexual risk behaviors among male sex workers who sell sex to men in Mombasa, Kenya.

Using time-location sampling, 425 men who had recently sold, and were currently willing to sell sex to men were invited to participate in a cross-sectional survey. A structured questionnaire was administered using handheld computers. Factors associated with self-reported unprotected anal sex with male clients in the past 30 days were identified and subjected to multivariate analysis.

Thirty-five percent of respondents did not know HIV can be transmitted via anal sex, which was a significant predictor of unprotected anal sex [adjusted odds ratio (AOR) 1.92; 95% confidence interval (95% CI), 1.16-3.16]. Other associated factors included drinking alcohol 3 or more days per week (AOR, 1.63; 95% CI, 1.05-2.54), self-report of burning urination within the past 12 months (AOR, 2.07; 95% CI, 1.14-3.76), and having never been counseled or tested for HIV (AOR, 1.66; 95% CI, 1.07-2.57). Only 21.2% of respondents correctly knew that a water-based lubricant should be used with latex condoms.

Male sex workers who sell sex to men in Mombasa are in acute need of targeted prevention information on anal HIV and STI transmission, consistent condom use, and correct lubrication use with latex condoms. HIV programs in Africa need to consider and develop specific prevention strategies to reach this vulnerable population.

To evaluate the utility of Total Lymphocyte Count (TLC) as a surrogate marker for CD4 + T cell count in antiretroviral (ARV) treatment initiation in a Kenyan population of HIV seropositive patients at Kenyatta National Hospital.

Kenyatta National Hospital, HIV treatment and follow-up outpatient facility; Comprehensive Care Centre, Nairobi, Kenya.

Two hundred and twenty five HIV Elisa positive, ARV naive patients visiting the Comprehensive Care Centre between January 2006 to March 2006.

A significant linear correlation was found between TLC and CD4 cell count for the whole group with a Spearman rank correlation of 0.761 (p < 0.01); and was also independently observed in the four WHO clinical stages. The classification utility of TLC 1200 cells/mm3 cut-off was suboptimal; sensitivity 37% specificity of 99% and the NPV of 56%. The receiver operator characteristics (ROC) curve generated an optimal TLC cut-off of 1900 cells/mm3 cut-off to be of greatest utility with a sensitivity of 81.1%, specificity of 90.3%, PPV of 90.8% and NPV of 80.2%. This implies that a TLC cut-off of 1900 cells/mm3 correctly classify eight out of ten HIV positive patients as having a CD4 < 200 cells/mm3 and only misclassify two such patients. Serial CD4 testing can then be performed on the minority of patients who despite a TLC > or = 1900 cells/mm3 are, on basis of clinical data, suspect of more advanced disease warranting ARV therapy. This would reduce the number of patients tested for and focus the application of CD4 testing and thus reduce attendant cost in care provision in CD4 resource poor settings.

Our data showed a good positive correlation between TLC and CD4 cell count, however the WHO recommended TLC cuto-ff of 1200/mm3 was found to be of low sensitivity in classifying patients as having a CD4 counts < 200 cells/mm3. This would result in underestimation of advanced stage of disease and to withholding ARVs treatment to persons who need treatment. We recommend a TLC cut-off of 1900 cells/mm3 for our population to classify patients as either above or below the CD4 count cut-off of 200 cells/mm3 as an indicator of when to start antiretroviral therapy.

Patterns of transmission of HIV are different among different regions of the world and change over time within regions. In order to adapt prevention strategies to changing patterns of risk, we need to understand the behaviours that put people at risk of infection and how new infections are distributed among risk groups.

A model is described to calculate the expected incidence of HIV infections in the adult population by mode of exposure using the current distribution of prevalent infections and the patterns of risk within different populations. For illustration the model is applied to Thailand and Kenya.

New infections in Kenya were mainly transmitted through heterosexual contact (90%), while a small but significant number were related to injecting drug use (4.8%) and men who have sex with men (4.5%). In Thailand, the epidemic has spread over time to the sexual partners of vulnerable groups and in 2005 the majority of new infections occurred among the low risk heterosexual population (43%). Men having sex with men accounted for 21% and sex work (including sex workers, clients, and partners of clients) for 18% of new infections. Medical interventions did not contribute significantly to new infections in either Kenya or Thailand.

The model provides a simple tool to inform the planning of effective, appropriately targeted, country specific intervention programmes. However, better surveillance systems are needed in countries to obtain more reliable biological and behavioural data in order to improve the estimates of incidence by risk group.

Low vitamin E levels are often found in HIV-1 infection, and studies have suggested that higher levels may decrease the risk of disease progression. However, vitamin E supplementation has also been reported to increase CCR5 expression, which could increase HIV-1 replication. We hypothesized that vitamin E levels at HIV-1 acquisition may influence disease progression.

Vitamin E status was measured in stored samples from the last pre-infection visit for 67 Kenyan women with reliably estimated dates of HIV-1 acquisition. Regression analyses were used to estimate associations between pre-infection vitamin E and plasma viral load, time to CD4 count <200 cells/muL, and mortality.

After controlling for potential confounding factors, each 1 mg/L increase in pre-infection vitamin E was associated with 0.08 log10 copies/mL (95% CI -0.01 to +0.17) higher set point viral load and 1.58-fold higher risk of mortality (95% CI 1.15-2.16). The association between higher pre-infection vitamin E and mortality persisted after adjustment for set point viral load (HR 1.55, 95% CI 1.13-2.13).

Higher pre-infection vitamin E levels were associated with increased mortality. Further research is needed to elucidate the role vitamin E plays in HIV-1 pathogenesis.

To demonstrate the value of routine, basic sexually transmitted infection (STI) screening at enrolment into an HIV-1 vaccine feasibility cohort study and to highlight the importance of soliciting a history of receptive anal intercourse (RAI) in adults identified as "high risk".

Routine STI screening was offered to adults at high risk of HIV-1 upon enrolment into a cohort study in preparation for HIV-1 vaccine trials. Risk behaviours and STI prevalence were summarised and the value of microscopy assessed. Associations between prevalent HIV-1 infection and RAI or prevalent STI were evaluated with multiple logistic regression.

Participants had a high burden of untreated STI. Symptom-directed management would have missed 67% of urethritis cases in men and 59% of cervicitis cases in women. RAI was reported by 36% of male and 18% of female participants. RAI was strongly associated with HIV-1 in men (adjusted odds ratio (aOR) 3.8; 95% CI 2.0 to 6.9) and independently associated with syphilis in women (aOR 12.9; 95% CI 3.4 to 48.7).

High-risk adults recruited for HIV-1 prevention trials carry a high STI burden. Symptom-directed treatment may miss many cases and simple laboratory-based screening can be done with little cost. Risk assessment should include questions about anal intercourse and whether condoms were used. STI screening, including specific assessment for anorectal disease, should be offered in African research settings recruiting participants at high risk of HIV-1 acquisition.

To determine whether observed changes in HIV prevalence in countries with generalised HIV epidemics are associated with changes in sexual risk behaviour.

A mathematical model was developed to explore the relation between prevalence recorded at antenatal clinics (ANCs) and the pattern of incidence of infection throughout the population. To create a null model a range of assumptions about sexual behaviour, natural history of infection, and sampling biases in ANC populations were explored to determine which factors maximised declines in prevalence in the absence of behaviour change. Modelled prevalence, where possible based on locally collected behavioural data, was compared with the observed prevalence data in urban Haiti, urban Kenya, urban Cote d'Ivoire, Malawi, Zimbabwe, Rwanda, Uganda, and urban Ethiopia.

Recent downturns in prevalence observed in urban Kenya, Zimbabwe, and urban Haiti, like Uganda before them, could only be replicated in the model through reductions in risk associated with changes in behaviour. In contrast, prevalence trends in urban Cote d'Ivoire, Malawi, urban Ethiopia, and Rwanda show no signs of changed sexual behaviour.

Changes in patterns of HIV prevalence in urban Kenya, Zimbabwe, and urban Haiti are quite recent and caution is required because of doubts over the accuracy and representativeness of these estimates. Nonetheless, the observed changes are consistent with behaviour change and not the natural course of the HIV epidemic.

To determine the association of DQ antigens with resistance and susceptibility to HIV-1.

Despite repeated exposure to HIV-1, a subset of women in the Pumwani Sex Worker cohort established in Nairobi, Kenya in 1985 have remained HIV-1 negative for at least 3 years and are classified as resistant. Differential susceptibility to HIV-1 infection is associated with HIV-1 specific CD4 and CD8 T cell responses. As human leukocyte antigen-DQ antigens present viral peptides to CD4 cells, we genotyped human leukocyte antigen -DQ alleles for 978 women enrolled in the cohort and performed cross-sectional and longitudinal analyses to identify associations of human leukocyte antigen -DQ with resistance/susceptibility to HIV-1.

DQA1 and DQB1 were genotyped using taxonomy-based sequence analysis. SPSS 13.0 was used to determine associations of DQ alleles/haplotypes with HIV-1 resistance, susceptibility, and seroconversion rates.

Several DQB1 alleles and DQ haplotypes were associated with resistance to HIV-1 infection. These included DQB1*050301 (P = 0.055, Odds Ratio = 12.77, 95% Confidence Interval = 1.44-112), DQB1*0603 and DQB1*0609 (P = 0.037, Odds Ratio = 3.25, 95% Confidence Interval = 1.12-9.47), and DQA1*010201-DQB1*0603 (P = 0.044, Odds Ratio = 17.33, 95% Confidence Interval = 1.79-168). Conversely, DQB1*0602 (P = 0.048, Odds Ratio = 0.68, 95% Confidence Interval = 0.44-1.05) and DQA1*010201-DQB1*0602 (P = 0.039, Odds Ratio = 0.64, 95% Confidence Interval = 0.41-1.03) were overrepresented in the HIV-1 infected population. DQA1*0504-DQB1*0201, DQA1*010201-DQB1*0201, DQA1*0402-DQB1*0402 and DQA1*0402-DQB1*030101 genotypes were only found in HIV-1 positive subjects (Odds Ratio = 0.30-0.31, 95% Confidence Interval = 0.03-3.70), and these women seroconverted rapidly. The associations of these DQ alleles and haplotypes with resistance and susceptibility to HIV-1 were independent of the previously reported human leukocyte antigen-DRB*01, human leukocyte antigen A2/6802, and human leukocyte antigen-A*2301.

The associations of DQ alleles and haplotypes with resistance and susceptibility to HIV-1 emphasize the importance of human leukocyte antigen-DQ and CD4 in anti-HIV-1 immunity.

HIV-neutralizing immunoglobulin A (IgA) and HIV-specific cellular immunity have been described in highly exposed, persistently seronegative (HEPS) individuals, but well controlled studies have not been performed. We performed a prospective, nested case-control study to examine the association of genital IgA and systemic cellular immune responses with subsequent HIV acquisition in high-risk Kenyan female sex workers (FSWs).

A randomized trial of monthly antibiotic prophylaxis to prevent sexually transmitted disease/HIV infection was performed from 1998 to 2002 in HIV-uninfected Kenyan FSWs. After the completion of trial, FSWs who had acquired HIV (cases) were matched 1: 4 with persistently uninfected controls based on study arm, duration of HIV-seronegative follow-up, and time of cohort enrolment. Blinded investigators assayed the ability at enrolment of genital IgA to neutralize primary HIV isolates as well as systemic HIV-specific cellular IFNgamma-modified enzyme-linked immunospot and proliferative responses.

The study cohort comprised 113 FSWs: 24 cases who acquired HIV and 89 matched controls. Genital HIV-neutralizing IgA was associated with reduced HIV acquisition (P = 0.003), as was HIV-specific proliferation (P = 0.002), and these associations were additive. HIV-specific IFNgamma production did not differ between case and control groups. In multivariable analysis, HIV-neutralizing IgA and HIV-specific proliferation each remained independently associated with lack of HIV acquisition. Genital herpes (HSV2) was associated with increased HIV risk and with reduced detection of HIV-neutralizing IgA.

Genital HIV-neutralizing IgA and systemic HIV-specific proliferative responses, assayed by blinded investigators, were prospectively associated with HIV nonacquisition. The induction of these immune responses may be an important goal for HIV vaccines.

To study demographic, social, behavioral, and biological variables as risk factors for HIV infection among men and women in Kenya.

Data from the cross-sectional, population-based 2003 Kenya Demographic and Health Survey were used. During the course of survey fieldwork, 3,273 women aged 15 to 49 years and 2,941 men aged 15 to 54 years gave consent to have a few drops of blood taken for anonymous testing. HIV serostatus data for men and women were analyzed for their relationships to key characteristics using bivariate and multivariate techniques to determine factors associated with being HIV-positive.