The conference discussed in detail the five aforementioned barriers to testing and other reasons for late presentation. The final results will be published and widely disseminated in

2010 and beyond. However, at present HIV in selleck chemicals Europe recommends: the initiation of audits to evaluate whether testing is being conducted in situations where there is an obvious indication (and if not, why not?); This article has been written as part of the HIV in Europe Initiative and special recognition is given to the HIV in Europe Steering Committee. Conflicts of interest: None. Sources of funding: The HIV in Europe Initiative has received unrestricted funding from Gilead Sciences, Merck,

Tibotec, Pfizer, Schering-Plough, Abbott, Boehringer Ingelheim, Bristol-Myers Squibb, NVP-BEZ235 GlaxoSmithKline and the Swedish Research Council. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Authors’ contributions: JVL drafted the initial manuscript in collaboration with DR. RJ, MW, AP, JH, JG, TC, AS and JDL have provided input into the development of the manuscript. All authors read and approved the final manuscript. “
“Data from observational cohorts may be influenced by population structure and loss to follow-up (LTFU). Quality of care may be associated with participation in cohort networks. We aimed to study the participation, characteristics and retention rates of immigrants in the Swiss HIV Cohort Study (SHCS). We compared enrolment over time (1996–1999, 2000–2003 and 2004–2008) and LTFU between individuals from different geographical regions. In 2008, we performed Staurosporine a cross-sectional survey to investigate the proportion of individuals not participating in the SHCS but who were in care at SHCS institutions. Predictors for LTFU were analysed using

Cox proportional hazard models, and those for nonparticipation using logistic regression. A total of 7840 individuals entered the SHCS during the observation period. The proportion of immigrants increased over time, especially the proportion of women from sub-Saharan Africa, which increased from 21 to 48% during the observation period. Overall LTFU was 3.76 [95% confidence interval (CI) 3.58–3.95]/100, with the highest hazard ratio in men from sub-Saharan Africa (2.82/100 patient-years; 95% CI 2.30–3.46/100), compared with men from northwestern countries. Other predictors for LTFU were age <30 years, lower education, injecting drug use, and higher baseline CD4 cell counts. Participants taking antiretroviral therapy had reduced LTFU. The survey showed that 84% of HIV-infected patients in care at SHCS institutions were enrolled in the cohort.

22 Benevolo G, Stacchini A, Spina M et al. Final results of a multicenter trial addressing role of CSF flow cytometric analysis in NHL patients at high risk for CNS dissemination. Blood 2012; 120: 3222–3228. 23 Sarker D, Thirlwell C, Nelson M et al. Leptomeningeal

disease in AIDS-related non-Hodgkin’s lymphoma. AIDS 2003; 17: 861–865. 24 Lister TA, Crowther D, Sutcliffe SB et al. Report of a committee convened to discuss the evaluation and staging of patients with Hodgkin’s disease: Cotswolds meeting. J Clin Oncol 1989; 7: 1630–1636. 25 Straus DJ, Huang J, Testa MA et al. Prognostic factors in the treatment of human immunodeficiency virus-associated non-Hodgkin’s lymphoma: analysis of AIDS check details Clinical Trials Group protocol

142–low-dose versus standard-dose m-BACOD plus granulocyte-macrophage colony-stimulating factor. National Institute of Allergy and Infectious Diseases. J Clin Oncol 1998; 16: 3601–3606. 26 Levine AM, Sullivan-Halley J, Pike MC et al. Human immunodeficiency virus-related lymphoma. Prognostic factors predictive of survival. Cancer 1991; 68: 2466–2472. 27 Kaplan LD, Lee JY, Ambinder RF et al. Rituximab does not improve clinical outcome in a randomized phase 3 trial of CHOP with or without rituximab in patients with HIV-associated non-Hodgkin lymphoma: AIDS-Malignancies Consortium Trial 010. Blood 2005; 106: 1538–1543. 28 Bower M, Gazzard B, Mandalia S et al. A prognostic index for systemic AIDS-related non-Hodgkin lymphoma BMS-354825 concentration treated in the era of highly active antiretroviral therapy. Ann Intern Med 2005;

143: 265–273. 29 Kassam S, Bower M, Lee SM et al. A retrospective, multicenter analysis of treatment intensification for human immunodeficiency virus-positive patients with high-risk diffuse large B-cell lymphoma. Leuk Lymphoma 2013; 54:1921–1927. 30 A predictive model for aggressive non-Hodgkin’s lymphoma. The International Non-Hodgkin’s Lymphoma Prognostic Factors Project. N Engl J Med 1993; 329: 987–994. 31 Sehn CHIR-99021 LH, Berry B, Chhanabhai M et al. The revised International Prognostic Index (R-IPI) is a better predictor of outcome than the standard IPI for patients with diffuse large B-cell lymphoma treated with R-CHOP. Blood 2007; 109: 1857–1861. 32 Lim ST, Karim R, Tulpule A et al. Prognostic factors in HIV-related diffuse large-cell lymphoma: before versus after highly active antiretroviral therapy. J Clin Oncol 2005; 23: 8477–8482. 33 Kaplan LD, Straus DJ, Testa MA et al. Low-dose compared with standard-dose m-BACOD chemotherapy for non-Hodgkin’s lymphoma associated with human immunodeficiency virus infection. National Institute of Allergy and Infectious Diseases AIDS Clinical Trials Group. N Engl J Med 1997; 336: 1641–1648. 34 Mounier N, Spina M, Gabarre J et al. AIDS-related non-Hodgkin lymphoma: final analysis of 485 patients treated with risk-adapted intensive chemotherapy. Blood 2006; 107: 3832–3840. 35 Dunleavy K, Little RF, Pittaluga S et al.

The scale bar represents substitutions per site. NJ trees were constructed using mega 4.1 with 1000 bootstrap replications and Kimura 2-parameter as

a model Selleck Talazoparib of nucleotide substitution. All the termites from 14 populations representing two genera, and two families (seven Odontotermes horni, five Odontotermes spp. and two C. heimi colonies), screened initially for the presence of Wolbachia, using PCR assays with the wsp gene were found to be positive. At least one MLST gene was sequenced for all the 14 colonies (Table 1). Repeated failures to PCR amplify Wolbachia genes (MLST and 16S rRNA gene) resulted in incomplete profiles. Sequence typing was performed using the Wolbachia MLST database (http://pubmlst.org/Wolbachia/), which resulted in the assignment of full sequence type (ST) to four strains (Table 1). All of the alleles and allelic profiles characterized for the termite strains were new to the MLST database, except for B supergroup C. heimi Wolbachia (Table 1). Alleles were shared among some of the strains, showing their relatedness, but at the same time showing a distinct difference for other strains. The divergence among the strains accounted for 591 variable selleck inhibitor sites (VI) out of 2079 sites (28.43%), with a concatenated alignment of all five Wolbachia MLST genes (Table 2). The gene hcpA showed the highest

nucleotide divergence with 154 variable sites out of 444 (34.38%), followed by fbpA with 128 variable sites out of 429 (29.83%) (Table 2). The average Ka/Ks per gene was found to be ≪1 (the average Ka/Ks across genes is 0.0933), which indicated strain evolution mainly by synonymous substitutions. This is compatible with a scenario of a strong purifying selection. Recombination

events were not indicated in either single gene or concatenated MLST dataset alignments (P<0.05) by MaxChi analyses. Phylogenetic reconstructions for all genes by both Bayesian inference and neighbor-joining methods showed similar results, and therefore only Bayesian phylogenetic trees were included. Phylogenetic reconstructions based on the concatenated alignment Oxymatrine of hcpA, gatB, coxA, ftsZ and fbpA genes indicated a strong clustering of termite Wolbachia from this study with Wolbachia from bed bug Cimex lectularis and form a sister clade within F supergroup with different species of scorpion genus Opistophthalmus (Fig. 1). Two major clusters were observed for termite Wolbachia in the present study (MCT, W5, G29 and RA) (T1, T3, T21 and THYD) (Fig. 1). On the basis of single-gene analyses, all the strains consistently belonged to the same supergroup. All Odontotermes spp. harbored F supergroup Wolbachia, with the exception of a population from O. horni (T2). Two C. heimi colonies harbored two different supergroup Wolbachia. One of these (TERMITE3) belonged to supergroup F, whereas the other (TLR) belonged to supergroup B (Table 1, Fig. 2).

We can thus propose that antioxidative defense systems of D. vulgaris Hildenborough can overcome the negative effects of low-peroxide stress, and so after an initial increase in the transcriptional responses, the gene expression levels revert to basic levels after elimination of H2O2.

Because high-peroxide stresses are too deleterious for the cells, the corresponding genes (most of them encoding Fe-containing proteins) are downregulated to limit free-metal-induced damages and increase survival. Rubrerythrins encoding genes (rbr1 and rbr2) were the most upregulated members of the PerR regulon at the transcript level under low-peroxide stress (0.1 mM H2O2, 30 min). Previously, they have been identified as important enzymes for oxygen Selleckchem CB-839 Bortezomib and other oxidative stresses (Fournier et al., 2003). Interestingly, the sor gene was also strongly upregulated under such peroxide

stress conditions, whereas no significant upregulation of this candidate was observed during 0.1% O2 exposure (Mukhopadhyay et al., 2007). Therefore, NADH-dependent H2O2 peroxidases (rubrerythrins, nigerythrin), together with thiol peroxidase and SOR, might play a major role in the H2O2 stress response. Transcript analysis revealed that gene expression reverted to the same level as in untreated cells and even lower for a time period longer than 30 min (0.1 mM H2O2 stress), which can explain the continuing decrease in peroxidase-specific activity during the 60–240 min of exposure. H2O2 quantification revealed that H2O2 was rapidly consumed over time and no remaining H2O2 could be detected after 90 min when either 0.1 or 0.3 mM was added. It should

be noted that oxidized compounds (for instance, polysulfide) could be formed due to the chemical reaction between H2O2 and hydrogen sulfide produced by D. vulgaris cells. It should be also noted that the presence of H2S is the physiologic situation for these cells in their biotopes, and the addition of H2O2 (as ROS formed under temporary oxic conditions) to H2S-producing cells can be considered as quite normal. Even if those we cannot exclude that a part of H2O2 was chemically reduced by the end-product of the sulfate reduction, our data suggest that the observed H2O2 consumption corresponds to a cell-mediated reaction. Most probably, H2O2 stresses include direct effects from H2O2 itself and indirect effects from H2O2-derived reactive chemical species together with increased redox potential. The data show that addition of either 0.1 or 0.3 mM H2O2 to a mid-exponential culture results in a rapid consumption of the H2O2 in a cell-mediated reaction. However, exposure to 0.3 mM H2O2 appears to be much more toxic to the cells as all tested genes were strongly downregulated even when H2O2 was no longer detectable in the culture. This phenomenon provides evidence for the high stress state of the cells, which is not the case when they are exposed to a lower concentration of H2O2 (0.1 mM). In the presence of 0.

“
“Extraintestinal pathogenic Escherichia coli (ExPEC) is an important pathogen that can cause systemic infections in a broad spectrum of mammals and birds. To date, commercial vaccines selleck monoclonal humanized antibody against ExPEC infections in pigs are rare and antibiotic resistance has become a serious clinical problem. Identification of protective

antigens is helpful for developing potentially effective vaccines. In this study, two outer membrane porins, OmpC and OmpF, of porcine ExPEC were cloned and expressed to investigate their immunogenicity. Intraperitoneal immunization of mice with the purified recombinant proteins OmpC and OmpF stimulated strong immunoglobulin G (IgG) antibody responses. Both IgG1 and IgG2a subclasses were induced, with a predominance of IgG1 production. After challenge with 2.5 × 107 CFU (5 × LD50) of the highly virulent ExPEC strain PCN033, 62.5% and 87.5% protection was observed in mice immunized with OmpC and OmpF, respectively. In addition,

both anti-OmpC and anti-OmpF sera can mediate complement-dependent opsonophagocytosis. Phylogenetic analysis showed that the ompC gene was ubiquitously present in all E. coli strains, whereas the ompF gene was mutated in certain strains. Furthermore, the selection analysis indicated that gene ompC may be subject to strong immune pressure. Our results demonstrated that OmpC is a promising vaccine target against ExPEC infections in swine. Pathogenic Escherichia coli is an important zoonotic etiological agent that can infect a broad spectrum of mammals and birds. Pathogenic E. coli Torin 1 manufacturer can be divided into two classes: intestinal and extraintestinal pathogenic E. coli (ExPEC) strains (Russo & Johnson, 2000). ExPEC strains possess certain specific virulence traits that enable them to invade

and colonize extraintestinal sites and cause a wide range of infections, such as urinary tract infections, meningitis, pneumonia, osteomyelitis, and surgical site infections (Orskov & Orskov, 1985). Recent reports show that ExPEC has been isolated frequently from clinical samples in the pig industry in China (Tan et al., 2012). However, to date, the Calpain damage caused by ExPEC infections in swine has not been paid sufficient attention. The two common approaches for prevention and therapy of bacterial diseases are vaccination and antibiotic therapy. Our recent study has demonstrated that antibiotic resistance is ubiquitously present in the porcine ExPEC strains isolated in China; 95.2% of which carried resistance to at least five antibiotics, and 60.3% were resistant to > 10 antimicrobials (Tang et al., 2011). Therefore, antibiotic treatment against ExPEC infections in pigs is limited. In addition, Tan et al. (2012) have reported that ExPEC infections are epidemic in China and have become a potential public health threat. It is desirable to find potential vaccine candidates to prevent this serious swine disease.

The estimated half-life of σS changed from 0.7 min in pgsA+ (JU01) cells to 8.5 min in pgsA3 (JU02) cells (Fig. 3). This result indicates that degradation of σS in the mutant cells is indeed retarded, and this is likely due to the presumably reduced content of ClpXP protease, although the involvement of other factor(s) in the degradation cannot be completely ruled out. In order to further assess the contribution of clpPX repression to the extended half-life TSA HDAC datasheet of σS in pgsA3 cells, we examined the effect of the introduction

of a clpPX plasmid (pHR718-clpPX). The highly increased content (7.9-fold over wild type) of σS in the pgsA3 cells (strain ST002) decreased to almost the level found in ST001 (pgsA+) cells after the introduction of the clpPX plasmid (Fig. 2c). This result reconfirms the conclusion that the pgsA3 mutation represses the expression of clpPX (as shown in Fig. 2a and b) GSK J4 mw and may also indicate that other factors participating in the regulation of the activity of ClpXP protease

(Hengge-Aronis, 2002) are not involved in, or contribute less to, the long half-life of σS. These other conceivably involved factors include Rsd, which is believed to affect σS association with core RNA polymerase by a putative action as anti-σD (Jishage & Ishihama, 1999), and Crl, which is assumed to act by modulating the association with the RNA polymerase core (Pratt & Silhavy, 1998); however, neither rsd nor crl expression is reduced in the pgsA mutant cells as evidenced by microarray analysis (Nagahama et al., 2007). The activity of σS in the mutant cells is therefore not

affected by these regulatory factors. The repression of clpPX may Teicoplanin thus very well be the main defect in the ClpXP degradation pathway of σS in cells with acidic phospholipid deficiency. We have arrived at the conclusion that the slower degradation of σS in the mutant cells contributes considerably to the accumulation of σS and that this is caused by the repression of clpPX. However, how does the acidic phospholipid deficiency trigger the repression of clpPX in pgsA3 mutant cells? It is known that the expression of the clpPX operon involves promoters under the control of σE, σH, and σD (Li et al., 2000; Phodius et al., 2006; Regulon DB ver. 6.4, http://regulondb.ccg.unam.mx/index.jsp). The expression of rpoE, which codes for σE, is negatively regulated by the Cpx two-component signal transduction system (De Wulf et al., 2002). The expression of rpoH, which codes for σH, is controlled by σE in addition to σD. The Cpx system is activated in mutant cells lacking the zwitterionic phospholipid phosphatidylethanolamine, the third major phospholipid in E. coli membranes (Mileykovskaya & Dowhan, 1997). We observed a significant activation (8.

parahaemolyticus and 46 non-V. parahaemolyticus bacterial strains templates. The iron-regulated virulence regulatory protein IrgB associated with iron utilization may have profound influences, besides iron acquisition, on the pathogenesis of V. parahaemolyticus (Wong et al., 1996). Therefore, the identification of the irgB gene in V. parahaemolyticus will not only provide a species-specific target for diagnostic application but may also lead to a

better understanding of the genetic mechanisms of its survival in its niche environments as well as its pathogenicity. The detection of tdh and trh genes in V. parahaemolyticus is necessary to determine the real risk posed to human health by the presence of this microorganism. The species-specific irgB gene can be used

as a tool to identify accurately V. parahaemolyticus species by PCR methods, and toxin genes may inform the pathogenic properties of pathogens. ICG-001 cost Thus, we developed a multiplex PCR assay targeting species-specific marker irgB and toxin genes tdh and trh to detect total and virulent strains of V. parahaemolyticus, which has the potential to reduce V. parahaemolyticus-associated illness in humans. In conclusion, our results demonstrated the successful application of comparative genomics to mine specific markers used in PCR methods for accurate detection and identification of V. parahaemolyticus. The irgB gene was validated as a new V. parahaemolyticus-specific marker. A multiplex PCR assay targeting irgB, APO866 tdh and trh genes was successfully developed to detect total and virulent strains of V. parahaemolyticus, which has a potential to be applied in food industries, diagnostics and taxonomic studies. Using this comparative genomics method, it is conceivable the specific targets could be identified for the detection of any bacterium for which Cytidine deaminase a genome sequence is available. This work was jointly supported by the grant No. 2009BAK43B31 from the Ministry of Science and Technology of China, the grant Nos. 08391911000, 08142200700 and 08DZ0504200 from Science & Technology Commission of Shanghai Municipality. Table S1. List of 23 CDSs with the lowest e-value ≥0.1 from

Vibrio parahaemolyticus. Please note: Wiley-Blackwell is not responsible for the content or functionality of any supporting materials supplied by the authors. Any queries (other than missing material) should be directed to the corresponding author for the article. “
“Progress in molecular biology and the advent of rapid and accurate molecular techniques have contributed to precise and rapid detection and differentiation of microbial pathogens. Identification of the Botryosphaeriaceae species based on morphology has been problematic over time. In this study, we used rep-PCR technique as a molecular tool for typing and differentiation of the Botryosphaeriaceae species, well-known and cosmopolitan fungal pathogens on woody plants.

The consideration of specific aggravating circumstances or points of mitigation in determining impairment of fitness to practise were compared with their subsequent consideration when determining the severity of sanction. Additionally, the proportion of cases that highlighted aggravating circumstances deemed Epacadostat by the GPhC as serious enough to warrant the sanction of erasure were monitored to determine if they were more likely to give rise to this sanction. Fifty-one cases heard by the GPhC between 1 October 2011 and 30 September 2012 met with the inclusion criteria. Pearson’s χ2 test

was used to detect a variation from the expected distribution of data. Of

the four aggravating/mitigating circumstances considered, all but one was more likely to be heard when determining sanction having first been factored in to the consideration of impairment. There was a statistically significant correlation between both risk of harm and dishonesty as aggravating factors and the sanction erasure from the Medical Register. The GPhC do, in general, consider relevant factors at all stages of their deliberations into practitioner misconduct, as required by the determinations in the cases of Cohen, Zygmunt, and Azzam, and subsequently consider their ISG regarding dishonesty as an aggravating circumstance in

determining which sanction to apply. “
“Objective  This study aimed to investigate Thiazovivin cost inpatients’ and outpatients’ need for information about medication, to what extent those needs were addressed and patient attitudes regarding pharmaceutical services. Method  Self-administered questionnaires were distributed to a sample of outpatients and inpatients in a UK district general hospital. Themes included satisfaction with information given about medication, potential confusion over medication prescribed by the general practitioner and by the hospital, access to a member of the pharmacy team and preferences on how information on medication should be given. Key findings  ZD1839 supplier Ninety-one outpatient and 126 inpatient questionnaires were available for analysis. All outpatients who responded acknowledged that they were told how long they might need to wait for their medicines to be dispensed, although approximately one-fifth felt they had to wait a long time. Nearly three-quarters of outpatients felt there was an opportunity to ask medication-related questions of the pharmacy team. Nearly three-quarters of inpatients reported they were encouraged to bring into any hospital any medication they were taking at home. Twenty-eight per cent of 95 inpatients reported that some of their existing medication was stopped while in hospital.

Demographic and clinical characteristics, sexual behaviours, CD4 cell count and plasma HIV-1 RNA loads were measured at enrolment and longitudinally over 12 months of follow-up. The study included 70 cases who seroconverted during study follow-up and 167 matched controls who remained persistently serodiscordant. The incidence of HIV infection among the initially seronegative partners was 6.52 per 100 person-years. Persistently discordant patients were more likely to have initiated highly active

antiretroviral therapy (HAART) than patients in seroconverting relationships (62.9%vs. 42.9%) (P=0.001). Patients in seroconverting relationships had significantly higher plasma viral loads (PVLs) than patients in discordant relationships

see more at enrolment, at 6 months and at 12 months (P<0.05). Patients in seroconverting relationships were less likely to use condoms with their primary partners than patients in discordant relationships (P<0.05). Patients in relationships that seroconverted between 6 and 12 months were diagnosed more often with genital Herpes simplex than patients in discordant click here relationships (P=0.001). In the univariate and multivariate logistic regression, the following variables were associated with seroconversion: PVL >100 000 [odds ratio (OR): 1.82; 95% confidence interval (CI): 1.1–2.8], non-disclosure of HIV status (OR: 5.5; 95% CI: 4.3–6.2) and not using condoms (OR: 2.8; 95% CI: 2.4–3.6). Couples-based intervention models are crucial in Y-27632 2HCl preventing HIV transmission to seronegative spouses. Providing early treatment for sexually transmitted infections, HAART and enhancing condom use and disclosure could potentially decrease the risk of HIV transmission within Indian married couples. An increasing focus of HIV preventive strategies has been to move away from solely reducing the risk-taking behaviours of HIV-uninfected individuals to focusing on HIV-infected individuals who may continue to practice HIV risk-taking

behaviours [1]. Studies from the developed and developing world have documented that a sizeable number of HIV-infected individuals continue to engage in unprotected sexual intercourse with HIV-serodiscordant partners [2–6]. Unprotected intercourse may be more common among HIV-infected individuals in steady or regular relationships than in casual or non-regular sexual encounters [7]. Additionally, high plasma HIV-1 RNA levels and sexually transmitted infections (STIs) may put the HIV-uninfected partner at continued risk of infection [8–16]. These findings suggest that there are multiple biological and behavioural risk factors for HIV transmission among individuals in serodiscordant relationships where the HIV status of the partner is known. In traditional societies, the use of preventive measures by HIV-uninfected partners may be further hampered by social stigma, reproductive issues and gender inequality [17]. In India, it is estimated that 2.

Good prognostic markers can be unreliable surrogates even if the association between clinical outcome and marker changes is the same for all drugs, as the relative importance of other mechanisms of their action, including adverse events, may vary among drugs [14]. In fact, the major meta-analysis assessing the surrogacy of 24-week changes in CD4 cell count and plasma viral load for disease progression to 2 years

[15] found that these markers were imperfect surrogate endpoints, explaining some but overall relatively little clinical risk. These findings were supported by detailed analyses of the Delta trial [16], and a 47% reduction in risk of AIDS/death despite only moderate impact on HIV RNA in the first trial

of ritonavir-containing combination AZD8055 price therapy [17,18]. A recent review examining the magnitude of the effect of changes in CD4 cell learn more count, HIV RNA and progression to AIDS or death also noted that, within short-term clinical trials, it was not possible to estimate the proportion of the effect of treatment on clinical outcomes associated with such surrogate endpoints [19]. Of note, NORA in fact found reverse relationships between abacavir vs. nevirapine and clinical vs. laboratory markers, rather than a relationship with laboratory markers and no relationship with clinical outcome as noted for lopinavir/ritonavir vs. efavirenz (both with zidovudine/lamivudine) in a recent ART Cohort Collaboration analysis [11]. Nevertheless,

antiretroviral drugs are licensed primarily on the basis of their effect on HIV RNA, not assuming that this is a true surrogate for clinical outcome, but as a pragmatic decision as switch to second-line ART Tryptophan synthase occurs long before clinical disease progression in resource-rich settings. There are several possible reasons why participants receiving abacavir-containing combination ART might have done better clinically. The significantly greater toxicity of nevirapine could indirectly have led to more clinical events, for example because of lower adherence (although this might have been expected to have had greater impacts on viral load and CD4 cell counts). Against this, we found no evidence of poorer adherence with nevirapine, there was no clear relationship between toxicity and cause of death (reviewed by an independent committee blinded to treatment allocation), and there was only a weak nonsignificant trend towards more ART modifications in the nevirapine group. NORA was designed as a blinded safety study: given the potential for abacavir hypersensitivity reactions, all participants were very closely monitored and it is extremely unlikely that important toxicity was missed. More abacavir substitutions with clinically superior drugs could have been made because of poorer immunological/virological responses.