Using a more sensitive technical approach, Ruff et al. reported

in nine children that archival wild-type HIV-1 persisted in a replication-competent form in resting CD4 T cells despite up to 10 years of continuous antiretroviral exposure [4]. Interestingly, among the 86 virologically controlled patients enrolled in the ANRS 106-WINDOW trial, 31% had cellular Torin 1 manufacturer HIV DNA mutations, which were associated with longer of treatment duration exposition [14]. Firstly, the lower resistance found in DNA could be a consequence of the fact that sequence amplifications in DNA failed for 24% and 8% of RT and PR sequences, respectively. Secondly, it is important to underline the point that our analysis is based on routine assays, such as population-based sequencing, which does not detect minor variants, and that total DNA was extracted from whole blood. Cloning or single

genome sequencing would probably have detected more archived mutations [5, 15, 16], as would sequencing of DNA from selected latent T cells, the main cellular HIV reservoir [4]. However, these methods are too costly and complex for routine clinical use. It should also be noted that we analysed the cumulative number selleck products of RNA mutations. As recently reported, a single plasma genotypic test tends to underestimate the level of resistance in heavily pretreated patients with a history of treatment failures [17]. Undetected drug-resistant minority variants are known to persist when antiretroviral therapy is discontinued or changed, and the rapid reappearance of these mutations on treatment resumption has been extensively documented [18-21]. This difference in resistance mutations between the plasma and cellular compartments suggests that plasma viruses at the time of treatment failure are enriched for resistant viruses, leading to a better Tyrosine-protein kinase BLK capture of the resistant genotypes than in the mononuclear cells which may have a large library of archival variants, the bulk of which may be lacking resistance mutations. Verhofstede et al. suggested that the probability of finding a resistant variant within the cellular reservoir depended, at least in part, on the period

during which this variant was able to replicate [5]. Thus, delays in changing a failing therapeutic regimen may favour mutant archiving. Interestingly, a longitudinal analysis has shown that resistance mutations emerge in plasma HIV-1 more than 1 year before they are found in peripheral blood mononuclear cells (PBMCs) [2, 22]. In contrast, because genetic changes in cellular proviruses occur more slowly than in plasma viruses, which are more sensitive to selective pressure, mutations persisted longer in proviral DNA [6, 11, 14]. Another hypothesis is that, in patients on effective HAART, cells infected by archived resistant provirus could be diluted by more recent uninfected cells and therefore be less readily detectable.

The risk of death from each specific cause was higher in IDUs than non-IDUs, with particularly marked increases in risk for liver-related deaths, and those from violence and non-AIDS infection. While liver-related deaths and deaths from direct effects of substance abuse appear to explain much of the excess mortality in IDUs, they are at increased risk for many other causes of death, which may relate to suboptimal management of HIV disease in these

individuals. Injecting drug use (IDU) is one of the most frequent routes of HIV transmission in Venetoclax purchase many industrialized countries [1] and is responsible for up to one-third of HIV transmission globally, outside of sub-Saharan Africa [2]. Since the introduction of combination antiretroviral therapy (cART) in 1996, mortality rates related to HIV infection have significantly decreased [3–9]. Rates of morbidity and mortality subsequent to initiation of cART are higher in HIV-positive IDUs than in other HIV-positive persons [10–13], although some studies found only

limited evidence for this effect [6,14,15]. Several factors may contribute to the relatively poor response to treatment observed in HIV-positive patients who have a history of IDU. They have been shown to have decreased access to HIV care and treatment [16,17], more comorbid conditions associated with drug use and addiction [such as hepatitis C virus (HCV) coinfection], poorer adherence to treatment [18], and more adverse drug interactions [19,20]. They are also more likely to come from click here particular ethnic or racial groups that have historically been disadvantaged with respect

to health outcomes [21]. In some studies, immunological or virological responses to cART appeared to be lower in HIV-positive IDUs than in other patients [11,22]. However, it is important to distinguish between those who are and are not actively injecting Cobimetinib mouse drugs, as the former will have additional risks from overdose, accidents and violence. Given the high prevalence of IDU among HIV-positive individuals receiving cART, it is important to understand what factors affect disease progression and death in this group: for example, in order to design programmes to reduce disparities in health outcomes between IDUs and non-IDUs receiving cART. We examined determinants of disease progression and death among IDUs and non-IDUs initiating cART in participants in a large multinational collaboration of HIV treatment programmes, and compared causes of death in IDU and non-IDU populations. The Antiretroviral Therapy Cohort Collaboration (ART-CC) is a multinational collaboration of HIV cohort studies. The collaboration has been described in detail elsewhere [12,23,24]. In brief, it was established in 2001, updated in 2004, 2006 and 2008, and includes cohort studies from Canada, Europe and the USA.

The risk of death from each specific cause was higher in IDUs than non-IDUs, with particularly marked increases in risk for liver-related deaths, and those from violence and non-AIDS infection. While liver-related deaths and deaths from direct effects of substance abuse appear to explain much of the excess mortality in IDUs, they are at increased risk for many other causes of death, which may relate to suboptimal management of HIV disease in these

individuals. Injecting drug use (IDU) is one of the most frequent routes of HIV transmission in selleck chemical many industrialized countries [1] and is responsible for up to one-third of HIV transmission globally, outside of sub-Saharan Africa [2]. Since the introduction of combination antiretroviral therapy (cART) in 1996, mortality rates related to HIV infection have significantly decreased [3–9]. Rates of morbidity and mortality subsequent to initiation of cART are higher in HIV-positive IDUs than in other HIV-positive persons [10–13], although some studies found only

limited evidence for this effect [6,14,15]. Several factors may contribute to the relatively poor response to treatment observed in HIV-positive patients who have a history of IDU. They have been shown to have decreased access to HIV care and treatment [16,17], more comorbid conditions associated with drug use and addiction [such as hepatitis C virus (HCV) coinfection], poorer adherence to treatment [18], and more adverse drug interactions [19,20]. They are also more likely to come from PD-0332991 concentration particular ethnic or racial groups that have historically been disadvantaged with respect

to health outcomes [21]. In some studies, immunological or virological responses to cART appeared to be lower in HIV-positive IDUs than in other patients [11,22]. However, it is important to distinguish between those who are and are not actively injecting Non-specific serine/threonine protein kinase drugs, as the former will have additional risks from overdose, accidents and violence. Given the high prevalence of IDU among HIV-positive individuals receiving cART, it is important to understand what factors affect disease progression and death in this group: for example, in order to design programmes to reduce disparities in health outcomes between IDUs and non-IDUs receiving cART. We examined determinants of disease progression and death among IDUs and non-IDUs initiating cART in participants in a large multinational collaboration of HIV treatment programmes, and compared causes of death in IDU and non-IDU populations. The Antiretroviral Therapy Cohort Collaboration (ART-CC) is a multinational collaboration of HIV cohort studies. The collaboration has been described in detail elsewhere [12,23,24]. In brief, it was established in 2001, updated in 2004, 2006 and 2008, and includes cohort studies from Canada, Europe and the USA.

Between January 2001 and April 2003, 169 HIV-1 infected patients started antiretroviral therapy. Two-thirds of patients were women (n=113). The median age was 35.0 years [interquartile range (IQR) 29.3–41.1]. Most patients were symptomatic for HIV (42% were at Androgen Receptor animal study Centers for Disease Control and Prevention stage B and 44% were at stage C). The median CD4 count was 135 cells/μL (IQR 67–218) and median HIV-1 viral load was 5.3 log10 RNA copies/mL (IQR 4.7–5.6). Patients received either zidovudine, lamivudine and nevirapine (n=85) or stavudine, lamivudine and nevirapine (n=84). Seventeen patients (10.1%) had positive HBsAg results; one other patient (0.6%) had an indeterminate result. In a sub-set of 109 patients, antibodies

to hepatitis B core (anti-HBc) learn more were found

in 89 patients (81.7%) and three other patients (2.8%) had indeterminate results. HBV DNA was detected in 14 of the 18 patients with positive or indeterminate HBsAg results [8.3% of the total study population, 95% confidence interval (CI) 4.6–13.5]. The positive predictive value of HBsAg was 76.5% (13 of 17 patients). The median HBV viral load in the 14 patients was 2.47 × 107 IU/mL (IQR 3680–1.59 × 108; range 270 to >2.2 × 108). The only patient with an indeterminate HBsAg result was found to be positive for anti-HBc and had an HBV viral load of 3680 IU/mL. Serology for HCV was positive in 28 patients (16.6%) and indeterminate in four other patients (2.4%). Twenty-one patients (12.4% of the total study population, 95% CI 7.9–18.4) were found with HCV RNA (all with positive HCV serology). Therefore, the positive predictive value of HCV serology was 75.0%. The median HCV viral load was 928 000 IU/mL (IQR 178 400–2.06 × 106; range 640–5.5 × 106). No patient was co-infected with HBV and HCV. Patients co-infected with HBV or HCV were comparable in most characteristics to those infected with HIV alone (Table 1). However, HCV co-infected patients were more likely to be older

and to have serum liver enzyme elevations. HBV co-infected patients had significant serum aspartate aminotransferase (AST) elevations Decitabine only. In multivariate analysis, HCV co-infection remained associated with greater age [≥45 years vs. <45 years, odds ratio (OR) 11.89, 95% CI 3.49–40.55, P<0.001] and abnormal serum alanine aminotransferase (ALT) level (≥1.25 × ULN vs. <1.25 × ULN, OR 7.81, 95% CI 1.54–39.66, P=0.01) but not with abnormal serum AST level (≥1.25 × ULN vs. <1.25 × ULN, OR 2.65, 95% CI 0.72–9.78, P=0.14). After adjustment for gender and serum ALT level, HBV co-infection was associated with abnormal serum AST level only (OR 4.33, 95% CI 1.32–14.17, P=0.02). In this study, we found high rates of active HBV and HCV co-infection in HIV-positive patients initiating antiretroviral therapy in Cameroon (8.3 and 12.4%, respectively). Most of these patients had high HBV or HCV viral load and moderate serum liver enzyme elevations.

However, this difference was not statistically significant (P = 0.15). Pulmonary mRNA expression of cytokines DNA Damage inhibitor and immune molecules in the lungs of the test mice was also analysed (Fig. 3). After 4 weeks, pulmonary mRNA expression

of IL-2 and IFN-ar1 was significantly higher in the test mice than in the control mice (P < 0.01). Pulmonary mRNA expression of IL-12a and IL-12rb1 tended to be higher in the test mice than in the control mice. However, such changes were not statistically significant (P = 0.074 and 0.068, respectively). TMC0356 is a new probiotic strain of L. gasseri that was originally isolated from the intestine of a healthy human adult (Hosoda et al., 1998). This bacterium has expressed strain-dependent immune regulatory effects such as apparent simulation

of IL-12 production from macrophages in cell line and animal studies (Morita et al., 2002; Harata et al., 2009; Kawase et al., 2009). In several recent animal and human studies, TMC0356 significantly improved allergic symptoms in patients with Japanese cedar pollinosis and in ovalbumin-immunized animals, protected host animals from influenza virus infection, and significantly suppressed the growth ALK phosphorylation of translated tumors (Kawase et al., 2006, 2007a, b, 2009; Harata et al., 2009; Wang et al., 2009). These health-promoting effects of TMC0356 are believed to be partly a result of a strain-dependent regulatory effect on cell-mediated immunity (CMI) of host animals characterized by elevated IFN-γ production and increased Th1-type immunity. Recently, some selected Lactobacillus and Bifidobacterium strains with properties that bolster CMI have been found to possess potent health-promoting effects against various age-associated physiological changes such as the development of osteoporosis (Kimoto-Nira et al., 2007, 2009). In light of these findings, Sulfite dehydrogenase we hypothesized that TMC0356 might positively alter the immunosenescence of aged host animals by stimulating their CMI, and consequently might improve the

natural defense of aged host animals against various infections. SAM is a well-known murine model of accelerated senescence. SAM consists of SAMP (prone) and SAMR (resistant) lines. SAMP lines are characterized by the accumulation of senile features as well as earlier onset and faster progress of age-related pathological phenotypes, such as amyloidosis, impaired immune responses, senile osteoporosis, and deficits in learning and memory (Hanada et al., 1991). Furthermore, age-related early loss of immune function has been clearly demonstrated in SAMP strains such as profound defects in the antibody response to a TD antigen, early onset of regression and a sharp decline in NK cell activity from the level in the control mice at 2 months of age (Hosokawa et al., 1987a, b). In the present study, splenic activation of NK cells of the control SAMP1 mice decreased with age from 20 to 24 weeks (between 4 and 8 weeks of oral administration of saline).

However, this difference was not statistically significant (P = 0.15). Pulmonary mRNA expression of cytokines BIBF 1120 ic50 and immune molecules in the lungs of the test mice was also analysed (Fig. 3). After 4 weeks, pulmonary mRNA expression

of IL-2 and IFN-ar1 was significantly higher in the test mice than in the control mice (P < 0.01). Pulmonary mRNA expression of IL-12a and IL-12rb1 tended to be higher in the test mice than in the control mice. However, such changes were not statistically significant (P = 0.074 and 0.068, respectively). TMC0356 is a new probiotic strain of L. gasseri that was originally isolated from the intestine of a healthy human adult (Hosoda et al., 1998). This bacterium has expressed strain-dependent immune regulatory effects such as apparent simulation

of IL-12 production from macrophages in cell line and animal studies (Morita et al., 2002; Harata et al., 2009; Kawase et al., 2009). In several recent animal and human studies, TMC0356 significantly improved allergic symptoms in patients with Japanese cedar pollinosis and in ovalbumin-immunized animals, protected host animals from influenza virus infection, and significantly suppressed the growth MEK inhibitor of translated tumors (Kawase et al., 2006, 2007a, b, 2009; Harata et al., 2009; Wang et al., 2009). These health-promoting effects of TMC0356 are believed to be partly a result of a strain-dependent regulatory effect on cell-mediated immunity (CMI) of host animals characterized by elevated IFN-γ production and increased Th1-type immunity. Recently, some selected Lactobacillus and Bifidobacterium strains with properties that bolster CMI have been found to possess potent health-promoting effects against various age-associated physiological changes such as the development of osteoporosis (Kimoto-Nira et al., 2007, 2009). In light of these findings, selleck inhibitor we hypothesized that TMC0356 might positively alter the immunosenescence of aged host animals by stimulating their CMI, and consequently might improve the

natural defense of aged host animals against various infections. SAM is a well-known murine model of accelerated senescence. SAM consists of SAMP (prone) and SAMR (resistant) lines. SAMP lines are characterized by the accumulation of senile features as well as earlier onset and faster progress of age-related pathological phenotypes, such as amyloidosis, impaired immune responses, senile osteoporosis, and deficits in learning and memory (Hanada et al., 1991). Furthermore, age-related early loss of immune function has been clearly demonstrated in SAMP strains such as profound defects in the antibody response to a TD antigen, early onset of regression and a sharp decline in NK cell activity from the level in the control mice at 2 months of age (Hosokawa et al., 1987a, b). In the present study, splenic activation of NK cells of the control SAMP1 mice decreased with age from 20 to 24 weeks (between 4 and 8 weeks of oral administration of saline).

We analysed patient-reported

use of medicines before and after abolition of the prescription charge, noting changes in the number of items prescribed, number of non-prescription medicines purchased and participants not collecting all prescribed items (primary non-adherence). Daporinad concentration Methods  A sample of community pharmacists across Wales (n = 249) issued questionnaires to customers at the point of dispensing who were not exempt from the prescription charge. A second questionnaire was delivered by post to those who returned the first questionnaire (n = 1027) and expressed a willingness to participate further. Paired t-tests were applied to responses from those completing both questionnaires (n = 593). Further analyses were carried DZNeP clinical trial out according to gender, age and reported levels of household income. Key findings  There was a statistically significant (P = 0.03) rise in the number of items prescribed, and a statistically

significant fall (P = 0.02) in the number of non-prescription medicines purchased. Primary non-adherence was also found to fall between pre- and post-abolition periods. Those most affected in terms of increase in number of prescribed items prescribed were the older age group (45–59 years), and those with household income of between £15 600 and £36 400. The most affected in the fall in number of medicines purchased were males, those in the lower age group (25–34 ioxilan years) and those with a higher

household income (>£36 400). Conclusions  Although the rise in number of items prescribed and fall in number of medicines purchased was generally anticipated, there appeared to be little or no effect for those on the lowest incomes. “
“This study aims to pilot a community pharmacy chronic obstructive pulmonary disease (COPD) case finding service in England, estimating costs and effects. Patients potentially at risk of COPD were screened with validated tools. Smoking cessation was offered to all smokers identified as potentially having undiagnosed COPD. Cost and effects of the service were estimated. Twenty-one community pharmacies screened 238 patients over 9 months. One hundred thirty-five patients were identified with potentially undiagnosed COPD; 88 were smokers. Smoking cessation initiation provided a project gain of 38.62 life years, 19.92 quality-adjusted life years and a cost saving of £392.67 per patient screened. COPD case finding by community pharmacists potentially provides cost-savings and improves quality of life. “
“To explore pharmacists’ perceptions of the skin conditions they encounter, sources of postgraduate dermatological training and views of their role in the management of patients with skin problems. A self-completion questionnaire was sent to a random sample of 3500 community pharmacists in England and Wales.

Data are presented as the estimated mean ± standard error of the mean. An analysis of variance (anova) was used to test for differences between the treatments. To test for differences in proportions between the treatments, a χ2 test was used. The proportion

of patients experiencing loss of virological response over 48 weeks was compared between study arms using Kaplan–Meier estimates and tested using the log rank statistic [as used by the US Food and Drug Administration (FDA)]. The time to loss of virological response (TLOVR) is an ITT analysis that defines response as two consecutive on-treatment measurements of HIV RNA of<50 copies/mL, achieved and maintained to week 48 without intervening discontinuation and virological rebound (two consecutive on-treatment measurements of plasma HIV RNA≥50 copies/mL or last measured plasma HIV RNA≥50 copies/mL). No OSI-744 mouse Bonferroni corrections of the α-error spending were used. For all statistical tests, statistical significance was assumed below a two-sided α level of 0.05. Statistical analyses were performed using sas version 9.1 (SAS Institute

Inc., Cary, NC, USA). This study is registered at ClinicalTrials.gov (number NCT00389402). A total of 123 HIV-1-infected, treatment-naïve patients were randomized in this study, of whom 32 were originally randomized in the SSAR 2004/0002 trial find protocol and 91 were newly randomized. Patients’ dispositions and baseline characteristics are shown in Figure 1 and Table 1. Patients were comparable between arms mafosfamide with respect to baseline demographic and HIV-disease characteristics. Insufficient baseline samples remained for centralized retesting of lipids for five SSAR 2004/0002 study participants (SQV/r arm, n=3; ATV/r arm, n=2). Thus, 113 patients (SQV/r arm, n=54; ATV/r arm, n=59) were included in the primary analysis. Absolute changes in lipids are shown in Table 2 and changes in TC in Figure 2. During 24 weeks of follow-up, TC increased significantly by +9.0 ± 2.7% in the SQV/r arm and +5.6 ± 2.3% in the ATV/r arm (difference 3.4

± 3.6%; P=0.3). HDL cholesterol increased significantly in both arms, +16.1 ± 3.8% in the SQV/r arm and +12.2 ± 3.4% in the ATV/r arm (difference 3.9 ± 5.1%; P=0.5). The TC/HDL cholesterol ratio did not change significantly in either arm. ApoA1 increased significantly in both arms, +6.0 ± 2.2% in the SQV/r arm and +6.1 ± 16.2% in the ATV/r arm (difference 0.1 ± 3.1%; P=1.0). Comparable changes in lipids were seen during further follow-up. The concentration of TC stabilized after 24 weeks, with a total increase of+8.0 ± 2.8% in the SQV/r arm and+7.2 ± 2.5% in the ATV/r arm after 48 weeks (difference 0.8 ± 3.6%; P=0.8). A significant further increase in HDL cholesterol was observed in both arms, by +26.4 ± 5.8% in the SQV/r arm and+14.8 ± 3.2% in the ATV/r arm over the whole 48 weeks (difference 11.6 ± 6.4%; P=0.07).

, 2012). Ammonium, nitrite, and nitrate were extracted from the soil with 2 M KCl and measured using a SAN++ Continuous Flow Analyzer (Skalar Analytical, The Netherlands). Total nitrogen, soil organic matter, Mn2+, and Mn4+ were measured according to standard methods (Bao, 2000). Soil pH was determined at a soil/water ratio of 1 : 2.5. All analyses were performed in triplicate on each sample. The in situ measurement of oxygen concentration was achieved by OXY Meter S/N 4164 with stainless electrode sensor (Unisense, Denmark) (Gundersen et al., 1998). Statistical analyses were performed using program spss for Windows. DNA in soil and sediment samples were extracted

from 0.25 g SB431542 in vivo samples using the Powersoil DNA isolation kits (Mobio). DNA from enriched anammox biomass was extracted according to the method described previously (Schmid et al., Selleckchem PD-1/PD-L1 inhibitor 2008). For the specific PCR amplification of the anammox hzsB gene,

newly designed primer pair of hzsB_396F and hzsB_742R was applied based on our new findings in anammox molecular mechanism (Kartal et al., 2011; Harhangi et al., 2012). The pmoA gene of n-damo bacteria was amplified using a nested approach (first-step primer pair A189_b-cmo682, followed by primer pair cmo182-cmo568) according to Luesken et al. (2011c). The 16S rRNA gene of n-damo was amplified using a nested approach (first-step primer pair 202F-1545R, followed by primer pair qP1F-qP2R) according to Juretschko et al. (1998) and Ettwig et al. (2009). The sequences of primers and thermal profiles were shown in Table 1. PCRs

were performed with the PerfeCTa SYBR Green FastMix (Quanta). 10 min at 95 °C, followed by 35 cycles of 60 s at 95 °C, 60 s at 59 °C and 45 sat 72 °C (PCR) 3 min at 95 °C, followed by 40 cycles of 30 s at 95 °C, 30 s at 59 °C and 30 sat 72 °C (qPCR) 10 min at 95 °C, followed by30 cycles of 60 s at 95 °C, 60 s at 63 °C and 45 sat 72 °C (PCR, qP1F – qP2R) 3 min at 95 °C, followed oxyclozanide by 40 cycles of 30 s at 95 °C, 30 s at 63 °C and 30 sat 72 °C (qPCR, qP1F – qP1R) PCR amplified fragments were cloned using the pGEM-T Easy cloning kit (Promega) according to the manufacturer’s instructions. Plasmid DNA was isolated with the GeneJET Plasmid Miniprep kit (Fermentas, Lithuania). Plasmids were digested with EcoRI enzyme, and the digestion products were examined for an insert with expected size by agarose (1%) gel electrophoresis. Selected clones were sequenced using primer of M13f targeting vector sequences adjacent to the multiple cloning sites. Phylogenetic analysis was performed using mega 5.0 software (Tamura et al., 2011) by neighbor-joining (NJ) with the Jukes-Cantor correction. Diversity indices, including Chaol, Shannon, and Simpson, were generated by DOTUR for each clone library (Schloss & Handelsman, 2005). Quantitative PCR was performed on a Bio-Rad iQ5 real-time PCR instrument (Bio-Rad) with a SYBR Green qPCR kit (Quanta).

This vulnerability is reflected in high rates of HIV infection in many western African settings [1–5]. Several interventions have been carried out in this population, particularly in low- and middle-income

PD0332991 research buy countries, to reduce the incidence of sexually transmitted infections (STIs) and HIV infection. These interventions include free condoms distribution, communication for behavioural change, free and regular STI screening and treatment and, more recently, voluntary counselling and testing (VCT) [6]. Antiretroviral therapy (ART) roll-out has been a driving force for the expansion of programmes such as VCT, which is seen as more ethically acceptable in view of the increased availability of treatment. VCT constitutes an opportunity for both INCB018424 mouse primary prevention (i.e. preventing HIV-negative

people from contracting the infection) and secondary prevention (i.e. avoiding the progression of the disease in infected people by providing early health care and psychosocial support), as it encompasses counselling before and after HIV testing. Several studies conducted in resource-limited settings have demonstrated that VCT may be effective at preventing HIV infection and other STIs in some populations, including FSWs, serodiscordant couples and pregnant women [7–13]. Moreover, in a predominantly heterosexual transmission context, a VCT programme targeting high-prevalence groups with high numbers of partners such as FSWs can be very efficient in reducing the spread of HIV to the general population displaying a lower prevalence [14]. However, despite the widespread availability of VCT and the fact that it is free of charge in many low- and middle-income countries, low uptake of the intervention has been reported [15,16]. In 2000, the Joint United Nations Program on HIV/AIDS (UNAIDS) emphasized the need to increase understanding of the requirements, acceptability and consequences of VCT, particularly in vulnerable populations [17]. The MRIP concept of acceptability of VCT encompasses not only acceptance of the HIV test, but also the interest that it generates

by way of returning for test results and disclosure of serostatus [18]. Determinants of VCT acceptability that have been reported include knowledge about the disease, perceived risk of infection, availability of treatment, and fear of violence and stigma [19–22]. Some studies have shown that testing among women can result in stigma and sexual and physical violence even if positive life events related to VCT in this population are more prevalent [22–24]. Few studies have described the acceptability of VCT among FSWs, particularly in a sub-Saharan African context of poverty and potential gender-based violence [25–27]. We present here a study of an intervention aimed at FSWs in Conakry, the capital of Guinea. While procuring and soliciting are illegal in Guinea, sex work itself is neither forbidden nor permitted from a legal point of view.