This study

investigated the effect of trace iron conditions on the growth of these two species, as well as their response to iron sequestration by chelators. Metal analysis by ICP-MS revealed high residual concentrations (0.12 μM) of iron in the chemically defined medium used in spite of the absence of added iron and demonstrated the requirement for deferration and confirmatory trace Fe analysis. The iron contamination from other medium constituents could be successfully reduced to <0.02 μM in batch processes using an insoluble chelating resin. Cu concentrations were also significantly reduced in the extracted chemically defined medium, but significant recovery of growth could be Navitoclax mw achieved by supplementation of the extracted medium with Fe only. Both C. albicans and C. vini were found to require selleck chemicals approximately 0.5 μM added iron for complete unrestricted growth in the extracted chemically defined medium, but differed in their abilities to grow at reduced iron concentrations. The observed differences between C. albicans and C. vini were consistent with the different environments these

respective yeast species typically colonize or invade. Grape musts and wines, in which C. vini typically appears as a spoilage yeast, generally have high Fe concentrations of between 30 and 200 μM (Ough et al., 1982). The predominantly reducing environment and the low pH of grape musts and wines also favour the formation of the more soluble free ferrous species, and this Fe would be expected to have a higher bioavailability (Howard,

1999). In sharp contrast, the ecological niches that C. albicans can colonize or invade in relation to human pathogenesis are highly limiting for Fe (Weinberg, 1999). Desferrioxamine and deferiprone are two chelators used clinically Fenbendazole to relieve the Fe overload associated with certain human haematological disorders such as thalassaemia (Chaston & Richardson, 2003; Franchini, 2006). Desferrioxamine failed to inhibit both C. albicans and C. vini. Deferiprone did not inhibit C. vini while leading to a slightly increased lag phase in C. albicans. However, the observed differences between C. albicans and C. vini persisted in their growth response in the presence of lactoferrin. Lactoferrin is a major component of the mammalian innate immune system (Actor et al., 2009) and one of the vertebrate host defence Fe chelators, which is present in mucosal secretions (Gonzalez-Chavez et al., 2009). Lactoferrin, at the physiologically relevant concentration of 0.25 mg mL−1 and at pH 4.5, and thus, representative of the vaginal environment (Novak et al., 2007), only led to a transient inhibition of C. albicans, but inhibited the growth of C. vini over the incubation period. The results are in agreement with the lack of observed pathogenicity of C. vini and its greater susceptibility to iron restriction, while the pathogenicity of C.

However, in the absence of NspS, this effect is less pronounced. Conversely, the large reduction seen in biofilm formation in the nspS mutant with high NspC levels suggests that NspC is not required for the effect of NspS on biofilm formation.

The fact that biofilm formation is maximal when both pathways are intact may imply a direct or an indirect interaction between these two pathways that enhance the effect of the other. One possible interaction could Tanespimycin research buy involve an autocrine-type signaling mechanism where a modified form of norspermidine is secreted by V. cholerae; this molecule is detected by NspS and activates the NspS signaling pathway. Polyamines can be modified by acetylation and exported to maintain polyamine homeostasis in cells (Igarashi & Kashiwagi, 2010). This process has not been studied in V. cholerae; however, an ortholog of the speG gene encoding spermidine acetyltransferase is found check details in the V. cholerae genome. It is possible that this protein is capable of acetylating norspermidine; acetylated norspermidine could then potentially interact

with NspS. Alternatively, norspermidine signaling and norspermidine biosynthesis pathways can act independently of each other and provide additive inputs into regulation of V. cholerae O139 biofilm formation. The distinction between these two possibilities will require more in-depth studies of these pathways. We thank Dr Sue Bauldry, Serena Heinz, Krista Kennerly, and the students in the immunology class of Spring 2009 at Appalachian State University for the production of the anti-NspC antibody, Dr Sue Edwards for the goat anti-rabbit antibody, Drs Mary Connell, Mark Venable, Ted Zerucha at Appalachian State University, Dr Paula Watnick at Harvard Medical School and Dr Tony Michael at UT Southwestern Medical Center for helpful discussions, and Dr Howie Neufeld at Appalachian State University for help with statistical analysis. Funding for this work was provided by the following sources: Appalachian State University Department of Biology, University Research Interleukin-2 receptor Council (2008–2009 grant to E.K.), Office of Student Research (grants

to M.W.M., Z.M.P. and S.S.P.), Graduate Student Association (grants to M.W.M. and Z.M.P.), and Sigma-Xi grants-in-aid of research (grant to M.W.M.). This project was also supported in part by the Grant Number AI096358 from the National Institute of Allergy and Infectious Diseases to E.K. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institute of Allergy and Infectious Diseases or The National Institutes of Health. Z.M.P. and S.S.P. have contributed equally to this work. “
“Streptomyces coelicolor, with its 8 667 507-bp linear chromosome, is the genetically most studied Streptomyces species and is an excellent model for studying antibiotic production and cell differentiation. Here, we report construction of S.

Rhinitis was defined as nasal discharge or congestion. Cough could be dry Ixazomib clinical trial or productive. Signs of skin infection included redness, swelling, tenderness, and/or pus-like drainage. Arthralgia was defined as inflammatory or non-inflammatory

joint pain. Abdominal pain could be acute or recurrent. An episode of a symptomatic infection was defined as an aforementioned symptom at one or more consecutive days. Data were collected before departure to gain information about baseline symptoms, and for 2 weeks after return to encompass incubation periods of the most (acute) travel-related infectious diseases. In the Results section, the term “travel-related” refers to the period of travel itself and the 2 weeks thereafter. According to Selleckchem Protease Inhibitor Library the Dutch national guidelines on travel advice, of the pairs included, only the immunocompromised travelers were prescribed ciprofloxacin (500 mg 2 times a day, for 5 days in case of ISA and for 3 days in case of IBD), to be used as immediate self-treatment after the first passage of loose or watery stools.7 Controls were advised to see a doctor in case of diarrhea with fever, blood in stools, or diarrhea persisting for 3 days or more.7 Power analysis showed that 70 pairs were needed to prove a diarrhea outcome ratio of 2 or more, with α = 0.05and power = 80%. This study was

approved by a medical ethics committee. All participants gave their informed consent. A random effects Poisson regression model was used to estimate incidence rates (IRs) and accompanying incidence rate ratios

(IRR). IR was defined as the number of symptom onsets divided by the sum of symptom-free days for all individuals during a specific time period. A random effects logistic regression model was used to estimate the number of symptomatic days and accompanying odds ratios (ORs). The number of symptomatic days reflects an individual’s probability to have a symptom on an arbitrary day. It was calculated to compare the disease burden between the immunocompromised travelers and their controls. The random effects model takes into account two levels of correlation: (1) immunocompromised Histone demethylase travelers and their travel companions had more or less the same exposure, and thus are not independent; (2) for IRs, there may be repeated episodes of a symptom within an individual; for numbers of symptomatic days, presence of symptoms over the days within an individual are correlated. ISA pairs and IBD pairs were analyzed separately. For estimation of the parameters, a Bayesian approach was used, starting with non-informative priors. Posterior distributions were obtained by Markov Chain Monte Carlo methods, using the WinBUGS program.16,17 Three chains were generated, based on different sets of starting values. Parameter estimates are the medians of the posterior distributions. The range from the 2.5% to the 97.5% quantile is used to quantify the uncertainty in the parameter estimates.

13 ST131 were detected in the ESBL-producing isolates using a PCR for the pabB allele, recently described by Clermont and colleagues.14 MLST was performed on those isolates that tested positive for ST131 using seven conserved housekeeping genes (adk, fumC, gyrB, icd, mdh, purA, and recA). A detailed Antidiabetic Compound Library protocol

of the MLST procedure, including allelic type and ST assignment methods, is available at MLST databases at the ERI, University College Cork web site (http://mlst.ucc.ie/mlst/dbs/Ecoli). The ESBL-positive isolates were assigned to one of the four main E coli phylogenetic groups (A, B1, B2, and D) by the use of a multiplex PCR-based method.15 The analysis was performed using Stata 9.2 (StataCorp, College Station, TX, USA). Samples submitted from travelers and non-travelers were treated as independent samples and grouped for analysis. Proportions were compared using Fisher’s exact test and continuous data using the Student’s t-test. For all comparisons a p-value <0.05 was deemed to represent statistical significance. A total of 226 Doxorubicin samples were included; 207 (92%) of samples were submitted from community-based collection sites

and 19 (8%) were submitted from emergency departments. The mean age (±SD) was 37.5 ± 22.5 years and 126 (57%) were females. Among the 113 foreign travelers, 21 traveled to Asia, 18 traveled within North America (17 Mexico and 1 USA), 18 to Caribbean/Central America, 17 to Africa, 12 to India, 10 to Europe, 8 to South America, 6 to the Middle East, and 3 to Australia/New Zealand. Among the 226 stool samples, 191 (85%) were negative, 31 (14%) were positive for ESBL-producing E coli. A number of factors were compared

among travelers and non-travelers and are Monoiodotyrosine shown in Table 1. Notably, travelers were 5.2 (95% CI 2.1–31.1) times more likely than non-travelers to have an ESBL-producing E coli cultured from their stool (Table 1). Among the 31 isolates, 27 (87%) were non-susceptible (ie, intermediate or resistant) to SXT, 23 (74%) to AMC, 12 (39%) to TZP, 26 (84%) to CIP, 21 (68%) to TOB, 18 (58%) to GEN, and 2 (6%) to AMK. No resistance was detected to ERT or MER. We used the latest CLSI breakpoints for ERT (0.25 µg/mL) and MER (1 µg/mL). Among the 113 foreign travelers, the location of travel was associated with the likelihood of positivity of stool for ESBL-producing E coli as shown in Table 2. The highest rates of ESBL positivity were associated with travel to Africa or the Indian subcontinent (p = 0.001). All the E coli isolates were positive for blaCTX−M genes: 22 produced CTX-M-15, 8 produced CTX-M-14, and 1 produced CTX-M-8. Some of the CTX-M-producing isolates also produced TEM-1 (ie, those with CTX-M-14 and -15) and OXA-1 (only those with CTX-M-15) β-lactamases. No other types of ESBLs were present.

In 2014, a systematic review and meta-analysis of observational cohorts reported birth outcomes among women exposed to efavirenz during the first trimester [57]. The primary endpoint was a birth defect of any kind with secondary outcomes

including rates of spontaneous abortions, termination of pregnancy, stillbirths and preterm delivery. Twenty-three studies met the inclusion criteria. The analysis found no increased risk of overall birth defects among 2026 women exposed to efavirenz during EPZ015666 molecular weight first trimester (n = 44, 1.63% 95% CI 0.78–2.48%) compared with exposure to other antiretroviral drugs. Only one neural tube defect was observed with first-trimester efavirenz exposure, giving a prevalence of 0.05% (95% CI < 0.01–0.28%). Furthermore, the prevalence of overall birth defects with first-trimester efavirenz exposure was similar to the ranges reported in the general population. This meta-analysis includes published data up to 30th June 2013 including data from the APR and the

IeDEA and ANRS databases [57]. Two publications have reported higher rates of congenital birth defects associated with efavirenz, Sirolimus mouse Brogly et al. (15.6%) [58] and Knapp et al. (12.8%) [59]. The Writing Group considers these rates to be inflated. Recruitment occurred prenatally but also up to 12 months of age, which could confer recruitment bias. Although the overall study numbers were large, the number of efavirenz exposures used as the denominator in the final analyses Adenylyl cyclase of first-trimester exposure was small, 32 and 47, respectively. There was no difference in the anomaly rate found with no exposure versus any exposure in T1/T2/T3. In addition, no pattern of anomalies specific to efavirenz was described by these studies: patent foramen ovale (n = 1); gastroschisis (n = 1); polydactyly

(n = 1); spina bifida cystica (n = 1); plagiocephaly (n = 1); Arnold Chiari malformation (n = 1) and talipes (n = 1). The reporting of two cases of congenital malformation was duplicated in the two studies. The paper by the NISDI Perinatal Study Group [60], which was used as a comparator by Knapp et al. to support their findings, reported similar overall congenital anomaly rates of 6.16% and also accepted reports up to 6 months of age. Adjustment of the congenital anomaly rate by the authors to those noted within 7 days, as reported by the APR (2.7%) and the non-HIV background rate (2.8%), gives a similar rate of 2.4% and is consistent with reported rates in the UK (3.1% for first trimester and 2.75% for second/third trimester-only ARV exposure) [61]. Thus, it remains the recommendation of the Writing Group, based on current evidence, that efavirenz can be used in pregnancy without additional precautions and considerations over and above those of other antiretroviral therapies.

8%

transmission rate among women with CD4 cell counts >200 cells/μL is similar to that of the zidovudine monotherapy arm of ACTG 076 (8.3%), intrapartum intravenous zidovudine was not associated with lower rates of transmission [246]. One rationale for intrapartum intravenous zidovudine in ACTG 076 was that labour would be associated with poor absorption of oral therapy. While not strictly comparable, the well-recognized rapid absorption of single-dose nevirapine during labour suggests that the impact of labour on absorption may be overestimated. Pharmacokinetic data from an RCT of oral zidovudine monotherapy vs. placebo indicate that adequate (therapeutic) zidovudine concentrations are achieved in cord blood with oral Selleckchem DAPT dosing. Although the concentrations are lower than have been reported with intravenous infusion, transmission was not associated with zidovudine cord blood concentration [247]. Intravenous zidovudine has historically

been considered for women whose plasma VL has not been completely suppressed at the time of delivery. There is no evidence that the intravenous administration of zidovudine alters the rate of placental transfer but higher maternal plasma levels will be reflected in the cord blood concentrations. Intravenous zidovudine (as part of an intervention package; see Section 5: Use of antiretroviral therapy in pregnancy) has also been recommended for women who present in labour, having not received ART. However, data from the New York State HIV diagnostic service (1995–1997) suggest that intrapartum intravenous zidovudine alone does not Selleckchem ABT199 significantly reduce transmission (10%; 95% CI 3.3–21.8%),

as, provided neonatal prophylaxis is commenced within 48 h of delivery (this being the only intervention accessed), the latter has similar efficacy (9.3%; 95% CI 4.1–17.5%) [138]. From the French data there is no evidence that intrapartum intravenous zidovudine further reduces the risk of MTCT in women on HAART unless maternal HIV VL is >10 000 copies/mL [23]. However, individual circumstances vary, and intravenous intrapartum zidovudine may be considered as one of a number Cyclin-dependent kinase 3 of maternal intrapartum ART options for women with VLs > 50 HIV RNA copies/mL who present in labour, or with ROMs or who are admitted for planned CS provided this does not delay other interventions. The evidence for the efficacy of intravenous zidovudine in the HAART era is generally poor. However, data from the French cohort support this practice for women on HAART with a VL >10 000 HIV RNA copies/mL. One could extrapolate that it may be of potential benefit in women presenting untreated in labour with an unknown current VL although this is not supported by the New York State data. Therefore in this setting, the Writing Group recommends the immediate administration of oral agents (see Section 5: Use of antiretroviral therapy in pregnancy) with intravenous zidovudine as an option.

8%

transmission rate among women with CD4 cell counts >200 cells/μL is similar to that of the zidovudine monotherapy arm of ACTG 076 (8.3%), intrapartum intravenous zidovudine was not associated with lower rates of transmission [246]. One rationale for intrapartum intravenous zidovudine in ACTG 076 was that labour would be associated with poor absorption of oral therapy. While not strictly comparable, the well-recognized rapid absorption of single-dose nevirapine during labour suggests that the impact of labour on absorption may be overestimated. Pharmacokinetic data from an RCT of oral zidovudine monotherapy vs. placebo indicate that adequate (therapeutic) zidovudine concentrations are achieved in cord blood with oral Selleck 17-AAG dosing. Although the concentrations are lower than have been reported with intravenous infusion, transmission was not associated with zidovudine cord blood concentration [247]. Intravenous zidovudine has historically

been considered for women whose plasma VL has not been completely suppressed at the time of delivery. There is no evidence that the intravenous administration of zidovudine alters the rate of placental transfer but higher maternal plasma levels will be reflected in the cord blood concentrations. Intravenous zidovudine (as part of an intervention package; see Section 5: Use of antiretroviral therapy in pregnancy) has also been recommended for women who present in labour, having not received ART. However, data from the New York State HIV diagnostic service (1995–1997) suggest that intrapartum intravenous zidovudine alone does not EPZ-6438 significantly reduce transmission (10%; 95% CI 3.3–21.8%),

as, provided neonatal prophylaxis is commenced within 48 h of delivery (this being the only intervention accessed), the latter has similar efficacy (9.3%; 95% CI 4.1–17.5%) [138]. From the French data there is no evidence that intrapartum intravenous zidovudine further reduces the risk of MTCT in women on HAART unless maternal HIV VL is >10 000 copies/mL [23]. However, individual circumstances vary, and intravenous intrapartum zidovudine may be considered as one of a number RANTES of maternal intrapartum ART options for women with VLs > 50 HIV RNA copies/mL who present in labour, or with ROMs or who are admitted for planned CS provided this does not delay other interventions. The evidence for the efficacy of intravenous zidovudine in the HAART era is generally poor. However, data from the French cohort support this practice for women on HAART with a VL >10 000 HIV RNA copies/mL. One could extrapolate that it may be of potential benefit in women presenting untreated in labour with an unknown current VL although this is not supported by the New York State data. Therefore in this setting, the Writing Group recommends the immediate administration of oral agents (see Section 5: Use of antiretroviral therapy in pregnancy) with intravenous zidovudine as an option.

, 1999), formaldehyde dehydrogenase (1 mM in Pseudomonas putida C-83; Ando et al., 1979) and formate dehydrogenase (in Methylosinus trichosporium OB3bT; Jollie & Lipscomb, 1991). Detoxification of the mercuric ion in Bacteria proceeds via a FAD-containing, NAD(P)H-dependent

mercuric reductase (EC 1.16.1.1), catalysing the reaction: The elemental mercury formed is volatile and nonenzymatically Verteporfin molecular weight removed from the cell. Mercuric reductase has been characterized in a number of organisms and is encoded by merA, found in an operon with other genes of mercuric ion detoxification (Ravel et al., 2000). Purified cytochrome c oxidase (aa3 type, EC 1.9.3.1) from Acidithiobacillus ferrooxidans MON-1 catalyses reduced check details cytochrome c-dependent reduction of the mercuric ion (Sugio et al., 2010): The merA gene is predicted in the M. capsulatus (Bath) genome (AAU92601), with a predicted mass 59.3 kDa, similar to that of MerA from A. ferrooxidans, P. putida and Escherichia coli (Booth & Williams, 1984, Sahlman et al., 1984; Rinderle et al., 1983). Other genes of the

mer mercury detoxification system are also predicted. Subunits I–III of an aa3-type cytochrome c oxidase are predicted in the M. capsulatus (Bath) genome (AAU92994, AAU92995, AAU92991, respectively) with 78% identity at protein level of subunit I (AAU92994) to that in A. ferrooxidans ATCC 23270T (ACK79083). Although the biochemistry and genetics of mercury (II) detoxification are well studied, the physiological processes that fuel the process in vivo are not. Here we present strong evidence for the reduction of the mercuric ion to by M. capsulatus (Bath) and the physiological changes in methane oxidation in response to mercury (II). Methylococcus capsulatus (Bath) was obtained from the University of Warwick Culture Collection and maintained as previously described on nitrate mineral salts (NMS) medium (Whittenbury et al., 1970) solidified with 1.5% Oxoid No. 1 agar with methane as sole source of carbon and energy. [14C]-methane (specific

activity 54 mCi mmol−1) was obtained from Amersham Radiochemicals and was diluted in [99% 12C, 1% 13C]-methane (Air Liquid Ltd) in 38-mL serum tubes (Bellco) sealed with blue butyl rubber vaccine stoppers to give working stocks, which were displaced with mercury into gas-tight syringes for SPTLC1 use. All reagents were analytical grade from Sigma-Aldrich. Formaldehyde solutions were prepared by thermal depolymerization of paraformaldehyde (Boden et al., 2010). Nicotinamides were washed with ether before use (Boden et al., 2010). Liquid scintillation cocktails were from Perkin-Elmer. Mercuric chloride was 99.999% pure and obtained from Sigma-Aldrich. Methane of 99.5% chemical purity from Air Liquid Ltd was used throughout. Biomass was determined as previously described (Boden et al., 2010), with calibration curves constructed using cell suspensions of known optical density at 440 nm (OD440 nm) dried to constant weight.

, 1992). A feedback regulatory loop exists among AbrB, SigH, and Spo0A. During the early and mid-exponential phase of growth, the transition state regulator AbrB directly represses the synthesis of the sigma factor SigH. When activated by phosphorylation, Spo0A directly represses abrB transcription, thus relieving AbrB-mediated repression of spo0H and leading to SigH-dependent

transcription of spo0A (Strauch et al., 1990). The level and activity of Spo0A are progressively increased with time. It is generally believed that genes that play auxiliary roles in development, such as cannibalism and biofilm formation, are turned on by lower levels of activated Spo0A at an earlier stage, whereas genes that play a direct role in sporulation are turned on by higher levels of activated Spo0A at a later stage (Fujita & Losick, 2005; Fujita et al., 2005). In this report, Vincristine concentration we present the first genetic evidence that Spo0A is involved in controlling PHB accumulation and expression of genes for PHB biosynthesis in B. thuringiensis. Our findings have uncovered a new role for Spo0A in the regulation of stationary-phase-associated processes. The bacterial strains and plasmids used in this study are listed in Table 1. The oligonucleotides are listed in Supporting Information, Table S1. Escherichia coli and B. thuringiensis cells were grown in Luria–Bertani (LB) medium

(Sambrook & Russell, 2001) at 37 °C. Antibiotics were used at the following concentrations (μg mL−1): ampicillin, find more 100 (for E. coli); chloramphenicol, 8; erythromycin, 2; kanamycin, 50; and tetracycline, 25 (for B. thuringiensis). To construct plasmids pENA1, pENA2, pENA3, pENA4, pENA5, and pENA6 for gene disruption, DNA fragments carrying an internal region close to the N-terminus

of the phaC, sigB, sigH, spo0A, spo0F, or sigF genes were amplified by PCR using the primer pairs described in Table S1. After digestion with HindIII and BamHI, these DNA fragments were individually ligated into the thermosensitive plasmid pRN5101 (Fedhila et al., 2002). To construct plasmid pENA7 for deletion of the chromosomal abrB gene and replacement PFKL with the kanamycin resistance gene (kan), a 0.33-kb DNA fragment containing a region located upstream of the abrB gene was amplified by PCR and digested with BamHI and EcoRI. After cloning of this DNA fragment into plasmid pDG780 (Guerout-Fleury et al., 1995), the resulting plasmid was restricted with BamHI and SalI to obtain a 1.8-kb DNA fragment carrying the kan gene. A 0.34-kb DNA fragment containing a region located downstream of the abrB gene was also amplified by PCR and digested with SalI and EcoRI. These two DNA fragments were then ligated together into BamHI- and EcoRI-digested plasmid pMAD (Arnaud et al., 2004). To construct plasmid pENA8 for overproduction of Spo0A in B.

EBV DNA levels were measured in whole blood and plasma in both arms using real-time polymerase chain reaction (PCR), up to 48 weeks after baseline (BL). Four lymphomas occurred, a median of 61 weeks [range 40−94 weeks] after randomization at a median CD4 cell count of 396 cells/μL (IQR 234–536 cells/μL). In the IL-2 arm, two patients developed EBV-positive Hodgkin’s lymphoma, and one developed EBV-negative Burkitt-type lymphoma. One patient in the control

group developed EBV-positive non-Hodgkin’s lymphoma. CD25 was negative in all cases. Among the 41 of 55 (control arm) and 44 of 58 (IL-2 arm) patients with detectable EBV DNA in whole blood at both BL and week 48, the median change in EBV DNA between BL and week Alectinib mw 48 was +0.04 log10 copies/ml in both arms (P = 0.7). In plasma, EBV was detected at least once in 22 of 52 controls and 21 of 54 IL-2-treated patients (P = 0.8). IL-2 therapy had no significant effect ABT888 on EBV replication over 48 weeks in these ART-naïve patients. The occurrence of lymphomas did not seem to be associated with IL-2 therapy. “
“Vaccination of HIV-infected patients against the influenza A/H1N1 subtype was proposed as a mandatory precautionary measure during the 2009 pandemic. The immediate cardiovascular effects of the novel vaccine have been largely unexplored. We investigated the impact of vaccination on indices of endothelial function in a cohort of HIV-infected patients. We included

24 HIV-infected patients in a study with a randomized, sham procedure-controlled design. A monovalent, adjuvanted vaccine against influenza A/H1N1 was used in the vaccine Interleukin-2 receptor arm (n=16); patients in the control group (n=8) were subjected to a sham procedure. Endothelial function, as assessed by flow-mediated dilatation (FMD), and inflammatory

markers were assessed prior to and 8 and 48 h post vaccination. FMD deteriorated following vaccination (baseline, 6.5 ± 1.1%; 8 h, 1.1 ± 1.5%; 48 h, 2.0 ± 1.4%; P=0.04). The white blood cell count increased at 8 h and remained elevated at 48 h. Soluble intercellular adhesion molecule-1 levels decreased after vaccination; the maximum decrease was noted at 48 h. Conversely, the sham procedure did not induce changes in endothelial function or inflammatory markers, apart from a reduction in the white blood cell count at 48 h. Acute systemic inflammation induced by vaccination against the influenza A/H1N1 virus resulted in a deterioration in endothelial function in HIV-infected patients, and this effect was sustained for at least 48 h. Our findings may have important implications in view of the high cardiovascular risk that HIV infection carries. The effect of the novel vaccine on endothelial function should be weighed against the immunological protection that it confers. In 2009, the medical community witnessed the world-wide spread of a novel strain of the influenza A virus, the H1N1 subtype, which reached pandemic levels.