This was a cross-sectional analysis in 322 HIV-uninfected and 534 HIV-infected men in the Multicenter AIDS Cohort Study. Main outcomes were coronary artery calcification presence, defined as a coronary artery calcium (CAC) score > 10 (CAC score was the geometric mean of the Agatston scores of two computed tomography replicates), and far wall common carotid intima-media thickness (IMT)/carotid lesion presence by B-mode ultrasound.

Compared with the HIV-uninfected men in our sample, HIV-infected men were younger, with lower body mass index (BMI) and more often Black. HIV-infected men had lower FT (age-adjusted FT 88.7 ng/dLvs. 101.7 ng/dL in HIV-uninfected men; P = 0.0004); however, FT was not associated with CAC, log carotid IMT, or the presence of carotid lesions. HIV status was not associated with CAC presence or log carotid IMT, but was associated with carotid lesion presence (adjusted odds ratio 1.69; 95% confidence interval 1.06, 2.71) in HIV-infected men compared with HIV-uninfected men.

Compared with HIV-uninfected men, HIV-infected men had lower FT, as well as more prevalent carotid lesions. In both groups, FT was not associated with CAC presence, log carotid IMT, or carotid lesion presence, suggesting that FT does not influence subclinical CVD in this population of men with and at risk for HIV infection.

A retrospective review of all HIV-1-infected patients who attended mass H1N1 vaccination between October 2009 and March 2010 at an Australian HIV clinic was carried out. Pre- and post-vaccination H1N1 antibody titres were measured. The main outcome measure was response to the vaccination, which was defined as an H1N1 antibody titre of ≥ 1:40 using a haemagglutination inhibition (HI) assay.

Baseline blood samples were collected from 199 patients, of whom 154 agreed to receive vaccination; of these, 126 had pre- and post-vaccination HI titres measured. Seventy-seven of 199 patients (38.7%) showed a baseline antibody titre of ≥ 1:40. Eighty-five (67.4%) showed a fourfold or greater increase in titre and 109 of 126 (86.5%) achieved an antibody titre of ≥ 1:40 after vaccination. The serum HI H1N1 antibody geometric mean titre (GMT) for the 126 paired samples was 39.32 ± 3.46 pre-vaccination and increased to 237.36 ± 3.94 [standard deviation (SD)] post-vaccination (P < 0.001). In a binary logistic regression analysis, HIV viral load and baseline HI antibody titre were significantly associated with post-vaccination increase in HI H1N1 antibody titre.

A high prevalence of HI H1N1 antibodies was found before vaccination in the cohort, consistent with previous exposure to H1N1 influenza virus. The response to vaccination was considered adequate, as more than two-thirds of patients achieved a fourfold or more increase in antibody titre after vaccination. The response to vaccination was significantly greater in those patients who were aviraemic for HIV, suggesting that antiretroviral therapy improves the humoral response, which is important in optimizing vaccine effectiveness.

Routinely collected data for all patients who initiated ART from 2005 to 2009 were analysed. Median baseline CD4 cell counts by year of ART initiation were compared using the Cuzick test for trend. Mortality and TB incidence rates in the first year of ART were computed. Hazard ratios (HRs) were calculated using multivariable Cox proportional hazards models.

First-line ART was initiated in 7659 patients; 64% were women, and the mean age was 37 years (standard deviation 9 years). Median baseline CD4 counts increased from 2005 to 2009 [82 cells/μL (interquartile range (IQR) 24, 153) to 148 cells/μL (IQR 61, 197), respectively; P < 0.001]. The mortality rate fell from 6.5/100 person-years at risk (PYAR) [95% confidence interval (CI) 5.5–7.6 PYAR] to 3.6/100 PYAR (95% CI 2.2–5.8 PYAR). TB incidence rates increased from 8.2/100 PYAR (95% CI 7.1–9.5 PYAR) to 15.6/100 PYAR (95% CI 12.4–19.7 PYAR). A later year of ART initiation was independently associated with decreased mortality (HR 0.91; 95% CI 0.83–1.00; P = 0.04).

Baseline CD4 cell counts have increased over time and are associated with decreased mortality. Additional reductions in mortality might be a result of a better standard of care and increased TB case finding. Further efforts to initiate ART earlier should be prioritized even in a setting of capped or reduced funding for ART programmes.

RC and phenotypic resistance testing were performed at baseline and week 12 on plasma samples from patients randomized to undergo a 12-week ARV drug-free period (ARDFP) or initiate immediate salvage therapy (no-ARDFP group) in the Options in Management with Antiretrovirals (OPTIMA) trial. Dichotomous and incremental phenotypic susceptibility scores (dPSSs and iPSSs, respectively) were calculated. The predictive value of RC and PSS for ARV therapy response and/or ARDFP was evaluated using multivariate regression analysis and Pearson correlations.

In 146 no-ARDFP subjects, baseline RC (50.8%) did not change at week 12 and was not correlated with CD4 cell count or viral load changes at week 12 (P = 0.33 and P = 0.79, respectively) or at week 24 (P = 0.96 and P = 0.14, respectively). dPSS predicted virological but not CD4 cell count response to ARV therapy at weeks 12, 24 and 48 (P = 0.002, P < 0.001 and P = 0.005, respectively). RC was significantly correlated with dPSS and iPSS at baseline, but did not increase their predictive value. In the 137 ARDFP patients, RC increased significantly (from 52.4 to 85.8%), but did not predict CD4 cell count and viral load changes during ARDFP (P = 0.92 and P = 0.26, respectively). RC after ARDFP did not predict subsequent CD4 cell count and viral load changes 12 weeks following ARV treatment reinitiation (P = 0.90 and P = 0.29, respectively).

We found no additional predictive value of replication capacity for virological or immunological responses (above what PSS provides) in patients undergoing salvage ARV treatment.

A total of 56 virologically suppressed patients were randomly assigned either to receive VPA plus HAART for 16 weeks followed by HAART alone for 32 weeks (arm 1; n = 27) or to receive HAART alone for 16 weeks and then VPA plus HAART for 32 weeks (arm 2; n = 29). VPA was administered at a dose of 500 mg twice a day (bid) and was adjusted to the therapeutic range. A quantitative culture assay was used to assess HIV reservoirs in CD4 T cells at baseline and at weeks 16 and 48.

No significant reductions in the frequency of CD4 T cells harbouring replication-competent HIV after 16 and 32 weeks of VPA therapy were observed. In arm 1, median (range) values of IU per log₁₀ billion (IUPB) cells were 2.55 (range 1.20–4.20), 1.80 (range 1.0–4.70) and 2.70 (range 1.0–3.90; P = 0.87) for baseline, week 16 and week 48, respectively. In arm 2, median values of IUPB were 2.55 (range 1.20–4.65), 1.64 (range 1.0–3.94) and 2.51 (range 1.0–4.48; P = 0.50) for baseline, week 16 and week 48, respectively.

Our study demonstrates that adding VPA to stable HAART does not reduce the latent HIV reservoir in virally suppressed patients.

Gingival keratinocyte organotypic (raft) cultures were established. The raft cultures were treated with a range of zidovudine concentrations. Haematoxylin and eosin staining was performed to examine the effect of zidovudine on gingival epithelium growth and stratification. Raft cultures were immunohistochemically analysed to determine the effect of this drug on the expression of key differentiation and proliferation markers, including cytokeratins and proliferating cell nuclear antigen (PCNA).

Zidovudine dramatically changed the proliferation and differentiation state of gingival tissues both when it was present throughout the growth period of the tissue and when it was added to established tissue at day 8. Zidovudine treatment increased the expression of cytokeratin 10, PCNA and cyclin A. Conversely, cytokeratin 5, involucrin and cytokeratin 6 expression was decreased. The tissue exhibited characteristics of increased proliferation in the suprabasal layers as well as an increased fragility and an inability to heal itself.

Zidovudine treatment, even when applied at low concentrations for short periods of time, deregulated the cell cycle/proliferation and differentiation pathways, resulting in abnormal epithelial repair and proliferation. Our system could potentially be developed as a model for studying the effects of HIV and highly active antiretroviral therapy in vitro.

Analyses using case reports and follow-up data from the national HIV database held at the Health Protection Agency were performed.

Fifteen per cent (2066 of 13 891) of UK-born adults diagnosed in England, Wales and Northern Ireland between 2002 and 2010 acquired HIV infection abroad. Thailand (534), the USA (117) and South Africa (108) were the countries most commonly reported. As compared with UK-born adults acquiring HIV infection in the UK, those acquiring HIV infection abroad were significantly (P < 0.01) more likely to have acquired it heterosexually (70% vs. 22%, respectively), to be of older age at diagnosis (median 42 years vs. 36 years, respectively), and to have reported sex with a commercial sex worker (5.6% vs. 1%, respectively). Among men infected in Thailand, 11% reported sex with a commercial sex worker.

A substantial number of UK-born adults are acquiring HIV infection in countries with generalized HIV epidemics, and in common holiday destinations. Of particular concern is the high proportion of men infected reporting sex with a commercial sex worker. We recommend HIV prevention and testing efforts be extended to include travellers abroad, and that sexual health advice be provided routinely in travel health consultations and in occupational health travel advice packs, particularly to those travelling to high HIV prevalence areas and destinations for sex tourism. Safer sex messages should include an awareness of the potential detrimental health and social impacts of the sex industry.

Patients presenting to two busy NPEP sites who reported a source partner of unknown HIV status were routinely asked if their source could be traced. If the exposed person indicated that their source partner was traceable they were asked to contact them and discuss the possibility of having an HIV test.

No sources were enrolled and the study was terminated.

We hypothesize that there are a number of differences between Australia and Switzerland that make source tracing unfeasible in Australia.

A systematic search of MEDLINE using the search terms “HIV” and “MRSA” identified references published during the HAART era (January 1996 to January 2011). Relevant articles on MRSA in the general population were also reviewed for comparison.

The most common type of MRSA infection among HIV-infected persons is SSTI caused by USA300, Panton-Valentine leukocidin (PVL)-positive strains. HIV-infected persons have an increased risk for both initial MRSA infections and recurrent infections compared with the general population. Risk factors for MRSA infections in this population include immunosuppression, comorbid conditions and certain lifestyle behaviours such as high-risk sexual behaviours and illicit drug use. Further research is needed on the optimal treatment and prevention strategies for MRSA infections among HIV-infected persons.

HIV-infected persons have a propensity for MRSA SSTI and a high rate of recurrent disease. The reasons for the elevated rates of MRSA infections among HIV-infected persons appear to be multifactorial, but may be mitigated with optimized HIV control and reductions in associated risk factors.

We conducted a retrospective analysis of data from the completed AIDS Clinical Trials Group (ACTG) A5029 study using multi-state Markov models. Two sets of high-risk HPV types from 2003 and 2009 publications were considered.

There was some evidence that VL > 400 HIV-1 RNA copies/mL was marginally associated with a higher rate of HPV detection [P = 0.068; hazard ratio (HR) = 4.67], using the older set of high-risk HPV types. Such an association was not identified using the latest set of HPV types (P = 0.343; HR = 2.64). CD4 count >350 cells/μL was significantly associated with more rapid HPV clearance with both sets of HPV types (P = 0.001, HR = 3.93; P = 0.018, HR = 2.65). There was no evidence that HPV affects VL or CD4 cell count in any of the analyses.

High-risk HPV types vary among studies and can affect the results of analyses. Use of HAART to improve CD4 cell count may have an impact on the control of HPV infection. The decrease in VL may also have an effect, although to a lesser degree.

The design of the study was cross-sectional. Serum anti-HEV IgG was determined by enzyme immunoassay in 238 HIV-infected patients consecutively attending our out-patient clinic between April and May 2011. In HEV-seropositive patients, HEV RNA was analysed by nested reverse transcriptase–polymerase chain reaction (RT-PCR). Associations between anti-HEV and liver cirrhosis, route of HIV infection, hepatitis B virus (HBV) and hepatitis C virus (HCV) serological markers, age, sex and alanine aminotransferase (ALT) levels were examined by univariate and multivariate analysis.

One hundred and forty patients (59%) had chronic liver disease (99% were HBV- and/or HCV-coinfected). Liver cirrhosis was detected in 44 individuals (19%). Two hundred and twelve patients (89%) were on antiretroviral treatment; the median CD4 T-cell count was 483 cells/μL [interquartile range (IQR) 313–662 cells/μL] and the HIV viral load was < 25 HIV-1 RNA copies/mL. Overall, 22 patients (9%) were anti-HEV positive. Liver cirrhosis was the only factor independently associated with the presence of anti-HEV, which was documented in 23% of patients with cirrhosis and 6% of patients without cirrhosis (P = 0.002; odds ratio 5.77). HEV RNA was detected in three seropositive patients (14%), two of whom had liver cirrhosis.

Our findings show a high prevalence of anti-HEV in HIV-infected patients, strongly associated with liver cirrhosis. Chronic HEV infection was detected in a significant number of HEV-seropositive patients. Further research is needed to ascertain whether cirrhosis is a predisposing factor for HEV infection and to assess the role of chronic HEV infection in the pathogeneses of cirrhosis in this population.

A retrospective chart review of all patients with a discharge diagnosis of HIV or AIDS was performed. Only patients actively managed by the hospital out-patient HIV clinic at the time of discharge were included in the final analysis. We compared the ART initially prescribed during hospitalization with the clinic records. Medication errors were separated by type and the prescriber's area of specialty was noted.

From 1 January 2009 to 31 December 2009, 90 admissions in 62 patients were included in the final analysis. In 47 of those admissions, the patient had an initial regimen considered to be incorrectly prescribed; in 17 of these 47 admissions, the patient was not prescribed any ART, and in the remainder the errors were related to drug omissions, incorrect frequency/dose, and prescription of the wrong drug. The majority of admissions were by an internal medicine or non-infectious disease (ID) specialist. Average time to ART initiation was comparable among all prescribers. No statistically significant correlation was found between the number of admissions per patient or the prescriber's area of specialty and the percentage of incorrect regimens ordered.

Hospital HIV medication management still remains an area of focus because of the complexity of regimens, poor medication reconciliation and limited non-HIV/ID specialist knowledge.

We conducted a systematic review of literature published in either English or Chinese to collate available HIV testing data among MSM in China. Linear regression and Spearman's rank correlation were used to study factors associated with HIV testing rates.

Fifty-five eligible articles were identified in this review. The proportion of MSM who had ever been tested for HIV has significantly increased, from 10.8% in 2002 to 51.2% in 2009. In comparison, reported rates of HIV testing in the past 12 months have also significantly increased, from 11.0% in 2003 to 43.7% in 2009.

Chinese MSM have relatively low HIV testing rates compared with MSM in other settings. It is important to continue to promote HIV testing among MSM in China.

An open-label, parallel-group, noninferiority, randomized (2:1 NVP XR:NVP IR) study was performed. Adult HIV-1-infected patients receiving NVP IR plus a fixed-dose nucleoside reverse transcriptase inhibitor (NRTI) combination of lamivudine (3TC)/abacavir (ABC), tenofovir (TDF)/emtricitabine (FTC) or 3TC/zidovudine (ZDV) with undetectable viral load (VL) were enrolled in the study. The primary endpoint was continued virological suppression with VL < 50 HIV-1 RNA copies/mL up to week 24 (calculated using a time to loss of virological response algorithm). Cochran's statistic (background regimen adjusted) was used to test noninferiority. Adverse events (AEs) were recorded.

Among 443 randomized patients, continued virological suppression was observed in 93.6% (276 of 295) of NVP XR- and 92.6% (137 of 148) of NVP IR-treated patients, an observed difference of 1% [95% confidence interval (CI) −4.3, 6.0] at 24 weeks of follow-up. Noninferiority (adjusted margin of −10%) of NVP XR to NVP IR was robust and further supported by SNAPSHOT analysis. Division of Acquired Immunodeficiency Syndrome (DAIDS) grade 3 and 4 events were similar for the NVP XR and NVP IR groups (3.7 vs. 4.1%, respectively), although overall AEs were higher in the NVP XR group (75.6 vs. 60.1% for the NVP-IR group).

NVP XR administered once daily resulted in continued virological suppression at week 24 that was noninferior to that provided by NVP IR, with similar rates of moderate and severe AEs. The higher frequency of overall AEs with NVP XR may be a consequence of the open-label design.

A retrospective case note review of pregnant women with perinatal/early acquired HIV infection, conceiving before 1 September 2009 and attending participating centres in the UK and Ireland, was carried out.

Among 252 women with perinatal/early acquired infection aged 12 years and older under follow-up in 21 centres, 42 pregnancies were reported in 30 women (19 women with a single pregnancy, 10 women with two pregnancies, and one woman with three pregnancies). Fifteen women (50%) had previous AIDS-defining diagnoses. The median age at first reported pregnancy was 18 years (range 14–22 years). Of the 42 pregnancies, 34 (81%) were reportedly unplanned, 31 (74%) involved regular partners, and in 21 (50%) of the 42 pregnancies the partners were reported to be unaware of maternal HIV status. Fifteen of the 42 pregnancies (36%) were electively terminated, six of the 42 (14%) resulted in first-trimester miscarriages and 21 of the 42 (50%) resulted in live births. Maternal viral load was detectable close to delivery in seven of 21 pregnancies (33%). Four infants required neonatal intensive care, three of whom were delivered preterm. One infant is HIV infected, there are ongoing concerns about the development of three of 21 infants (14%), and two of 21 (10%) have been fostered.

Despite access to ongoing sexual health and contraceptive services, unplanned pregnancies are occurring in young women growing up with HIV. Pregnancy care and prevention of onward transmission require complex case management for this emerging population.

Five Portuguese hospitals provided data on HIV-2-infected patients from 1984 to the end of 2007. Data concerning demographic characteristics and clinical variables were extracted. Patients were stratified according to date of diagnosis in approximately 5-year categories.

The sample included 442 patients, accounting for 37% of all HIV-2 infections notified in Portugal during that period. HIV-2-infected patients showed clearly different characteristics according to the period of diagnosis. Until 2000, the majority of HIV-2-infected patients were Portuguese-born males living in the north of the country. From 2000 to 2007, most of the patients diagnosed with HIV-2 infection had a West African origin, were predominantly female and were living in the capital, Lisbon. The average age at diagnosis and loss to follow-up significantly increased over time.

HIV-2 infection has been documented in Portugal since the early 1980s and its epidemiology appears to reflect changes in population movement. These include the movements of soldiers and repatriates from African territories during the independence wars and, later, migration and mobility from high-endemicity areas. The findings of this study stress the importance of promoting migrant-sensitive health care.

The International Maternal Pediatric and Adolescent AIDS Clinical Trials (IMPAACT), formerly Pediatric AIDS Clinical Trials Group (PACTG), study P1026s is a prospective pharmacokinetic study of HIV-infected pregnant women taking antiretrovirals for clinical indications, including a cohort taking emtricitabine 200 mg once daily. Intensive steady-state 24-hour emtricitabine pharmacokinetic profiles were performed during the third trimester and 6–12 weeks postpartum, and on maternal and umbilical cord blood samples collected at delivery. Emtricitabine was measured by liquid chromatography–mass spectrometry with a quantification limit of 0.0118 mg/L. The target emtricitabine area under the concentration versus time curve, from time 0 to 24 hours post dose (AUC_0-24), was ≥7 mg h/L (≤30% reduction from the typical AUC of 10 mg h/L in nonpregnant historical controls). Third-trimester and postpartum pharmacokinetics were compared within subjects.

Twenty-six women had pharmacokinetics assessed during the third trimester (median 35 weeks of gestation) and 22 postpartum (median 8 weeks postpartum). Mean [90% confidence interval (CI)] emtricitabine pharmacokinetic parameters during the third trimester vs. postpartum were, respectively: AUC: 8.0 (7.1–8.9) vs. 9.7 (8.6–10.9) mg h/L (P = 0.072); apparent clearance (CL/F): 25.0 (22.6–28.3) vs. 20.6 (18.4–23.2) L/h (P = 0.025); 24 hour post dose concentration (C₂₄): 0.058 (0.037–0.063) vs. 0.085 (0.070–0.010) mg/L (P = 0.006). The mean cord:maternal ratio was 1.2 (90% CI 1.0–1.5). The viral load was <400 HIV-1 RNA copies/mL in 24 of 26 women in the third trimester, in 24 of 26 at delivery, and in 15 of 19 postpartum. Within-subject comparisons demonstrated significantly higher CL/F and significantly lower C₂₄ during pregnancy; however, the C₂₄ was well above the inhibitory concentration 50%, or drug concentration that suppresses viral replication by half (IC₅₀) in all subjects.

While we found higher emtricitabine CL/F and lower C₂₄ and AUC during pregnancy compared with postpartum, these changes were not sufficiently large to warrant dose adjustment during pregnancy. Umbilical cord blood concentrations were similar to maternal concentrations.

Efavirenz plasma concentrations were obtained for 66 HIV-infected Ugandans initiating efavirenz- based regimens, with blood samples collected at eight time-points over 24 h on day 1 of treatment, and at a further eight time-points on day 14. Noncompartmental analysis was used to describe the pharmacokinetics of efavirenz.

The mean steady-state minimum plasma concentration (C_min) of efavirenz was 2.9 μg/mL, the mean area under the curve (AUC) was 278.5 h μg/mL, and mean efavirenz clearance was 7.4 L/h. Although overall mean clearance did not change over the 2 weeks, 41.9% of participants showed an average 95.8% increase in clearance. On day 14, the maximum concentration (C_max) of efavirenz was >4 μg/mL in 96.6% of participants, while C_min was <1 μg/mL in only 4.5%. Overall, 69% of participants experienced adverse central nervous system (CNS) symptoms attributable to efavirenz during the 2-week period, and 95% of these participants were found to have efavirenz plasma concentrations >4 μg/mL, although only half maintained a high concentration until at least 8 h after dosing.

The findings of this study show that HIV-infected patients on efavirenz may exhibit autoinduction to various extents, and this needs to be taken into consideration in the clinical management of individual patients. Efavirenz CNS toxicity during the initial phase of treatment may be related to C_max, regardless of the sampling time.

Plasma samples of HIV-1 treatment-naïve patients diagnosed between 2001 and 2009 at the Tel Aviv Medical Center were screened for DRMs.

Samples obtained from patients following the HIV diagnosis were analysed retrospectively. Genotyping was carried out using the Trugene HIV-1 genotype kit (Siemens, Berkeley, CA, USA). Phylogenetic relationships among viral sequences were estimated using the maximum likelihood method.

Thirty-eight of the 266 analysed sequences (14.3%) had DRMs, all occurring exclusively in the group of men who have sex with men (MSM). The rate of DRMs has constantly risen, reaching a peak of 21.9% in 2009. Notably, protease inhibitor (PI) DRMs became the most frequent DRMs in 2009. Phylogenetic analysis showed a tight cluster comprising 13 of 14 viruses harbouring the L90M major PI resistance mutation, suggesting a single infection source.

There was an unexpectedly high rate of the major L90MPI resistance mutation in the MSM group. The clustered transmission of this mutation might be related to a high-risk sexual behaviour. Added to nonnucleoside reverse transcriptase inhibitor and nucleoside reverse transcriptase inhibitor resistance mutations, such a PI mutation may limit future therapeutic options for this particular patient population.

Antiretroviral therapy (ART)-naïve individuals aged ≥18 years who initiated triple combination ART between January 2000 and June 2006 in British Columbia, Canada were enrolled in the study. We compared genotypic sensitivity scores (GSSs) derived from the development of resistance mutations between participants who initiated ART with ritonavir-boosted protease inhibitors (PIs) with those who initiated ART with NNRTIs, and determined the effects of these mutations on remaining active drugs.

A total of 1666 participants initiated ART, 818 (49.1%) with NNRTI-based regimens and 848 (50.9%) with boosted PI-based regimens. Among participants who developed resistance mutations, those who initiated NNRTI-based regimens had a lower median GSS than those on boosted PI-based regimens (9.8 vs. 11.0, respectively; P<0.001). Participants on boosted PI-based regimens [adjusted odds ratio (AOR) 3.68; 95% confidence interval (CI) 2.25, 6.01], those with ≥95% adherence to highly active antiretroviral therapy (HAART) (AOR 1.84; 95% CI 1.16, 2.92) and those with baseline CD4 count >200 cells/μL (AOR 3.44; 95% CI 1.73, 6.84) were more likely to have the maximum number of drug options.

The use of NNRTI-based first-line ART regimens may limit the options for second-line treatment when the number of available drugs is limited.

We included RCTs published in 2003–2010 that assessed the 48-week immunological and virological efficacy of adding new antiretroviral drugs vs. placebo to optimized background therapy (OBT) in treatment-experienced subjects. These drugs included maraviroc, vicriviroc, enfuvirtide, raltegravir, etravirine, tipranavir and darunavir. We collected baseline descriptive characteristics, CD4 cell count changes and virological suppression proportions (percentage with HIV RNA <50 HIV-1 RNA copies/mL).

We identified 10 studies which included a total of 6401 patients. New drugs were associated with increased virological suppression (pooled odds ratio 2.97) and larger CD4 count increases (pooled nonstandardized difference 39 cells/μL) compared with placebo. OBT genotypic sensitivity scores (GSSs) were also associated with larger differences in virological suppression (P<0.001 for GSS=0,≤1 and ≤2) and CD4 cell count increase (GSS=0, P<0.001; GSS ≤1, P=0.002; GSS ≤2, P=0.015) between the two groups. CCR5 inhibitors were not associated with significant gains in CD4 cell counts (P=0.22) compared with other new drugs.

Our study confirmed the overall immunological and virological efficacy of new antiretroviral drugs in treatment-experienced patients, compared with placebo. The main predictive factor for efficacy was the number of fully active drugs. CCR5 inhibitors did not increase CD4 cell count to a greater extent than other new drugs.

Acceptance of the test and return for test results at baseline and consequences of testing 1 year later were described. The perceived risk of HIV infection and perceived benefits and barriers to testing were examined using quantitative and qualitative methods.

All 421 FSW participants agreed to undergo VCT and most participants (92%) returned for their results. The main reason cited for VCT acceptance was the wish to know their HIV status. However, some managers of FSW worksites urged FSWs to be tested, curtailing FSWs' free decision-making. One year later, status disclosure was common (90% of the 198 individuals who knew their results among those who participated in the follow-up part of the study). Positive consequences of testing were far more frequently reported than negative consequences (98% vs. 2%, respectively). Negative life events included banishment from the worksite (one case) and verbal abuse (two cases).

Acceptability of VCT appears high in the FSW population in Conakry as a consequence of both perceptions of high individual risk and social pressures.

We evaluated HIV-infected patients aged ≥ 18 years, who initiated HAART in the Home-Based AIDS Care (HBAC) project in Tororo, Uganda, between May 2003 and February 2008 and were diagnosed with KS at baseline or during follow-up. We examined independent risk factors for having either prevalent or incident KS and risk factors for death among patients with KS.

Of 1121 study subjects, 17 (1.5%) were diagnosed with prevalent KS and 18 (1.6%) with incident KS over a median of 56.1 months of follow-up. KS was associated with male sex [adjusted odds ratio (AOR) 2.41; 95% confidence interval (CI) 1.20–4.86] and baseline CD4 cell count < 50 cells/μL (AOR 3.25; 95% CI 1.03–10.3). Eleven (65%) of 17 patients with prevalent KS and 13 (72%) of 18 patients with incident KS experienced complete regression (P = 0.137). Eighteen (64%) of 28 patients who remained on NNRTI-based HAART experienced regression of their KS and six (86%) of seven patients who were switched to protease inhibitor-containing HAART regimens had regression of their KS (P = 0.23). Mortality among those with KS was significantly associated with visceral disease (hazard ratio 19.22; 95% CI 2.42–152).

Prevalent or incident KS was associated with 30% mortality. The resolution of KS lesions among individuals who initiated HAART with NNRTI-based regimens was similar to that found in studies using only protease inhibitor-based HAART.

Since 2005, information on the initial CD4 cell count has been requested on all people newly diagnosed with HIV infection through antibody testing in New Zealand. Excluded in this analysis were those previously diagnosed overseas or for an immigration medical.

A CD4 cell count was provided for 606 (80.3%) of the 755 newly diagnosed adults. Overall, 50.0% were ‘late presenters’ and 32.0% had ‘advanced HIV disease’. Compared with men who have sex with men (MSM), people heterosexually infected were more likely to present late. ‘Late presentation’ and presentation with ‘advanced HIV disease’ were significantly more common among older MSM. Māori and Pacific MSM were more likely to present with ‘advanced HIV disease’. Compared with European MSM, the age-adjusted relative risks for Māori and Pacific MSM were 2.1 [95% confidence interval (CI) 1.4–3.2] and 2.5 (95% CI 1.2–5.0), respectively.

The high proportion of people presenting late reflects inadequate levels of HIV testing. The lower proportion of late presentations among MSM compared with those heterosexually infected may be explained by a higher proportion of recent locally acquired infections together with different testing patterns.