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“One of the major successes in the management of HIV-positive patients has been the PMTCT of HIV-1. With the widespread implementation of routine antenatal screening for HIV-1, transmission of HIV-1 from mother

to child is now a rare occurrence in the UK. Despite few recent RCTs regarding the use of ART in pregnancy or obstetric intervention, practice continues to evolve. This is largely informed by observational data, theoretical considerations and expert opinion. At the outset, the aim of the Writing Group was to make these guidelines as clinically relevant and as practical

as possible. The Writing selleck Group drew up a list of questions reflecting day-to-day practice and queries. It was acknowledged that the level of evidence for many of these topics was poor but recognized that there was a need to provide guidance. These guidelines have expanded on all areas relevant to the clinical care of HIV-positive pregnant women. The guidelines are intended to inform and aid healthcare workers in the management of pregnant women with HIV. They are not intended to be prescriptive or restrictive and it is recognized that situations will arise where the optimum management may deviate from these recommendations and new data will emerge to better inform practice. A particular E7080 in vivo focus has been obstetric management. An increasing number

of women are aiming for and achieving a vaginal delivery but the rate of emergency CSs has increased. It is hoped that the recommendations contained within these guidelines will enable a further increase in the proportion of vaginal deliveries and a reduction in the number of emergency CSs. Linked to this is the proposed starting gestation for women temporarily taking HAART in pregnancy, which has been brought forward depending on baseline VL. It is anticipated that this will result in a larger proportion of women achieving a VL <50 HIV RNA copies/mL by 36 weeks' gestation, thereby allowing them to plan for a vaginal Montelukast Sodium delivery. Additional guidance has been provided with regard to conception on HAART, the choice of specific drugs or drug classes and the management of women with HBV or HCV coinfection. For the first time these guidelines have addressed the issue of continuation of HAART post delivery in women with a baseline CD4 cell count >350 cells/μL. The paediatric section provides further guidance on infant PEP, drug dosing and safety. It is clear that there exists an urgent need for paediatric syrup preparations for a wider variety of ARV drugs because the current options, particularly in the case of maternal viral resistance, are limited.

All of these were abundantly produced by S. mycoparasitica on F. graminearum Selleckchem Galunisertib hyphae. Formation of these structures as well as haustorial penetration appeared 2 days later in F. graminearum than in F. avenaceum and F. oxysporum (Goh & Vujanovic, 2010). Soon after, S. mycoparasitica sporulated on F. avenaceum and F. oxysporum (Goh & Vujanovic, 2010), as well as on both F. graminearum chemotypes as presented in this study. Sporulation is an additional criterion for determining mycoparasite host ranges because melanosporaceous biotrophic mycoparasites were observed to undergo sporulation on specific Fusarium isolates only (Harveson & Kimbrough, 2001a, b). The germination test of S. mycoparasitica

ascospores in Fusarium filtrates showed that F. graminearum is one of the principal hosts of the mycoparasite, together with F. avenaceum and F. oxysporum. In contrast, F. proliferatum and F. sporotrichioides do not appear to be hosts. A few biotrophic,

mycoparasitic fungi (Gonatobotrys, Dicyma, Stephanoma, Melanospora and Piptocephalis) acquire certain nutrients (mycotrophein, biotin or aneurin) from their hosts for growth and generation of sexual reproductive organs (Hawker, 1938; Jeffries & Young, 1994; Rakvidhyasastra & Butler, 1973; Whaley & Barnett, 1963). During interactions with F. graminearum 3-ADON (but not with 15-ADON) and by an as yet unknown mechanism, S. mycoparasitica removed the pathogen red-colored compounds, possibly aurofusarin (Kim et al., Gefitinib 2005), and subsequently released crystal-like red-colored substances (Fig. 3). We hypothesize that S. mycoparasitica absorbs aurofusarin from attacked Fusarium cells through lysis of the pathogen membrane components, such as chitin by production of chitinase and chitosanases (Goh & Vujanovic, 2010; Manocha, 1987). This property of S. mycoparasitica could imply detoxification or neutralization of aurofusarin, a notable F. graminearum mycotoxin ALOX15 (Dvorska et al., 2001; Dvorska & Surai, 2004). Moreover, trichothecene mycotoxins

may play an important role in the aggressiveness of F. graminearum towards plant hosts (Doohan et al., 1999). In this study, S. mycoparasitica demonstrated a capacity to markedly reduce the amount of Tri5 gene fragments in both 3-ADON and 15-ADON strains (P=0.05). Mycoparasitic biodegradation of mycotoxins is often related to production of lactonase enzymes involved in mycotoxin hydrolysis. Gliocladium roseum, a mycoparasite, showed detoxification of zearalenone mycotoxin through hydrolysis of fungitoxic zearalenone by these catalysts, followed by a spontaneous decarboxylation (Utermark & Karlovsky, 2007). A previous study highlighted degeneration of the cytoplasm of F. avenaceum and F. oxysporum hyphal cells challenged with S. mycoparasitica (Goh & Vujanovic, 2010). In this study, linear growth of both F. graminearum chemotypes was significantly decreased in the presence of S. mycoparasitica (Fig. 4), with similar cytoplasmic breakdown.

All patients were required to have a suppressed viral load, defined as a viral load ≤500 copies/mL, at baseline. Patients were excluded if there was no viral load meas-urement in the 6 months after Navitoclax cost baseline. Virological failure was

defined as a viral load >500 copies/mL measured at least 4 months after baseline. Patient follow-up was measured from baseline to date of virological failure or date of last viral load measurement. Poisson regression analysis was used to identify viral load response prior to baseline associated with virological failure after starting new ARVs. Potential explanatory variables included age, gender, year of starting cART, ARV exposure status at cART initiation (ARV-naïve or ARV-experienced), risk group, ethnicity, region of Europe, baseline

CD4 cell count, CD4 nadir, peak viral load, previous AIDS diagnosis, time on cART, current selleck treatment regimen, number of previous treatment regimens, time spent on cART prior to baseline, number of ARVs to which the patient was previously exposed and the reason reported for starting the new ARV. In addition to the traditional explanatory variables investigated above, variables that summarized the history of viral suppression after cART initiation prior to baseline were investigated. The variables used to summarize the history of viral suppression after cART initiation were as follows. 1 Months to initial suppression (HIV RNA ≤500 copies/mL) after starting cART. Viral suppression was

defined as a measurement of HIV RNA ≤500 copies/mL. Viral rebound was defined as a viral load >500 copies/mL measured after a period of suppression prior to the regimen change. For variable 5, any period of time when the patient was off cART and the first 4 months after starting a new cART regimen were excluded. Thus, only periods during which the patient was on cART and should have been virally suppressed were included. Any variable that was significant at the 10% level in the univariate model was then included in a multivariate model. The sensitivity analysis considered confirmed virological failure after baseline (i.e. two consecutive viral load measurements above 500 copies/mL) and, in the subgroup of patients who had viral load measured using an assay with a lower limit Oxalosuccinic acid of detection of 50 copies/mL, virological failure after baseline defined as a viral load above 50 copies/mL. Analyses were also repeated taking account of HIV drug resistance at baseline in the subset of patients with resistance data, using genotypic sensitivity scores (GSS) calculated using the rega algorithm, version 7.1 [29]. A total of 1827 patients (67%) were included in the analysis. Table 1 describes the characteristics of the patients included in the analysis. Eight hundred and seventy-eight patients (48%) were treatment naïve at cART initiation.

All patients were required to have a suppressed viral load, defined as a viral load ≤500 copies/mL, at baseline. Patients were excluded if there was no viral load meas-urement in the 6 months after Roxadustat supplier baseline. Virological failure was

defined as a viral load >500 copies/mL measured at least 4 months after baseline. Patient follow-up was measured from baseline to date of virological failure or date of last viral load measurement. Poisson regression analysis was used to identify viral load response prior to baseline associated with virological failure after starting new ARVs. Potential explanatory variables included age, gender, year of starting cART, ARV exposure status at cART initiation (ARV-naïve or ARV-experienced), risk group, ethnicity, region of Europe, baseline

CD4 cell count, CD4 nadir, peak viral load, previous AIDS diagnosis, time on cART, current PI3K inhibitors ic50 treatment regimen, number of previous treatment regimens, time spent on cART prior to baseline, number of ARVs to which the patient was previously exposed and the reason reported for starting the new ARV. In addition to the traditional explanatory variables investigated above, variables that summarized the history of viral suppression after cART initiation prior to baseline were investigated. The variables used to summarize the history of viral suppression after cART initiation were as follows. 1 Months to initial suppression (HIV RNA ≤500 copies/mL) after starting cART. Viral suppression was

defined as a measurement of HIV RNA ≤500 copies/mL. Viral rebound was defined as a viral load >500 copies/mL measured after a period of suppression prior to the regimen change. For variable 5, any period of time when the patient was off cART and the first 4 months after starting a new cART regimen were excluded. Thus, only periods during which the patient was on cART and should have been virally suppressed were included. Any variable that was significant at the 10% level in the univariate model was then included in a multivariate model. The sensitivity analysis considered confirmed virological failure after baseline (i.e. two consecutive viral load measurements above 500 copies/mL) and, in the subgroup of patients who had viral load measured using an assay with a lower limit oxyclozanide of detection of 50 copies/mL, virological failure after baseline defined as a viral load above 50 copies/mL. Analyses were also repeated taking account of HIV drug resistance at baseline in the subset of patients with resistance data, using genotypic sensitivity scores (GSS) calculated using the rega algorithm, version 7.1 [29]. A total of 1827 patients (67%) were included in the analysis. Table 1 describes the characteristics of the patients included in the analysis. Eight hundred and seventy-eight patients (48%) were treatment naïve at cART initiation.

Additional concerns regarding continuous ART are the induction of drug resistance, high costs, and treatment fatigue in patients. Structured treatment interruption (STI) strategies have therefore been explored in patients with viral replication suppressed under ART [3-6]. Overall, results were disappointing, with a significant

Selleck Target Selective Inhibitor Library proportion of patients showing rapid increases in viral load, declining CD4 T-cell counts, and an increased risk for disease progression [4, 7]. However, a subgroup of patients are able to suppress HIV replication for prolonged periods of time after STI [8]. A marker identifying such patients would be of great practical value and might renew interest in STI. Several studies have identified genetic factors influencing the pretreatment set-point viral load and time to progression to AIDS in untreated patients: the first locus identified was human leucocyte antigen (HLA)-B [9]. The natural killer (NK) cell receptor pair killer cell immunoglobulin-like receptor 3DL1 (KIR3DL1)/KIR3DS1 followed [10]. More recently, whole-genome association studies provided the information that two single nucleotide polymorphisms, found in or close to the HLA complex, both correlate with HIV viral load in untreated individuals [11]. The

first (rs9264942) is located 35 kbp upstream of HLA-C (HLA-C −35 C/T) and governs the level of surface expression of HLA-C [12]. The second (rs2395029) AZD4547 purchase lies in the HLA complex P5 (HCP5) and is in strong linkage disequilibrium with HLA B*5701, the HLA-B allele associated with the strongest protection from disease progression. Interestingly, all of

these polymorphisms are potentially associated with the function of NK cells, a subgroup of lymphocytes important in defence against viral infection: KIR3DL1 is an inhibitory receptor binding HLA-B antigens that carry the Bw4 epitope [13]. HLA-C is the ligand for the NK cell receptors KIR2DL1, KIR2DL2, KIR2DL3 and KIR2DS1 [14]. KIR–HLA interactions are important during NK cell development, as only NK cells carrying inhibitory KIR and their HLA ligands acquire full functional competence [15]. As antiviral effects of NK cells have been shown to operate most effectively in states of low viral load [16], we hypothesized that these polymorphisms may have a role in predicting Selleck Dolutegravir which patients are able to maintain suppressed viral load after STI. We therefore studied the association of these polymorphisms with the evolution of viral load after STI in 130 Swiss HIV Cohort Study patients. Patients were recruited from Swiss HIV Cohort Study participants of the Strategies for Management of Anti-Retroviral Therapy (SMART), Swiss Spanish Treatment Interruption Trial (SSITT)/2nd SSITT, and STACCATO (A Trial of CD4 Guided Treatment Interruption, Compared to Continuous Treatment, for HIV Infection) trials [3-6].

5% uranyl acetate in methanol at −90°C in a Leica AFS freeze-substitution unit, infiltrated at −45°C with Lowicryl HM-20 resin (Lowi, Waldkraiburg, CDK inhibitor Germany) and polymerized with UV light. After etching with saturated sodium ethanolate solution for 3 s, ultra-thin sections on nickel grids were treated successively with 1% human serum albumin (Wako, Osaka, Japan) with 0.1% Tween 20 in Tris-buffered saline (HTBST; pH 7.5) for 1 h, primary antibodies to GluA subunits (15 μg/ml for each) in HTBST overnight, and colloidal gold (10 nm)-conjugated antirabbit IgG (1:100; British Bio Cell International, Cardiff, UK) in HTBST for 2 h. Finally, grids were stained with uranyl acetate for 15 min.

Electron micrographs were taken with an H7100 electron microscope (Hitachi, Tokyo, Japan). For quantitative analysis, the number of metal particles and the length of synaptic membrane were measured on electron micrographs, using IPLab software (Scanalytics, Fairfax, VA, ATR inhibitor USA). Procedures for FISH have been reported previously (Yamasaki et al., 2010). Briefly, fresh frozen sections were hybridized with mixtures of digoxigenin (DIG)- or fluorescein-labeled cRNA probes for mouse γ-7 (nucleotide residues 181–828, AF361349.1) and 67-kDa glutamic acid decarboxylase

(GAD67; 1036–2015, NCBI Reference Sequence NM_008077) or GLAST (1571–2473, AF330257.1). Supporting Fig. S2A–C shows overall patterns of FISH labeling, which were consistent with those of in situ hybridization using radiolabeled probes (Shibata et al., 1996; Fukaya et al., 2005; Uchigashima et al., 2007). DIG and fluorescein were detected using the two-step method: the first detection with peroxidase-conjugated antifluorescein antibody (Roche Diagnostics, 1:500) for 1 h and the FITC-TSA plus amplification kit (PerkinElmer), and the second detection with

peroxidase-conjugated anti-DIG antibody (Roche Diagnostics, 1:500) for 1 h and the Cy3-TSA plus over amplification kit (PerkinElmer). Residual activities of peroxidase introduced in the first detection were inactivated by incubation of sections with 0.6% H2O2 for 30 min. TOTO3 (Invitrogen) was used for fluorescent nuclear counterstaining. Animals were anesthetized with carbon dioxide and parasagittal cerebellar slices (250 μm thickness) were prepared from mice aged postnatal day (P)24 to P95 as described previously (Edwards et al., 1989; Hashimoto & Kano, 2003). Whole-cell recordings were made from visually identified Purkinje cell somata using an upright microscope (BX50WI; Olympus, Tokyo, Japan). Ionic currents were recorded with an Axopatch 1D (Molecular Devises, Sunnyvale, CA, USA) patch-clamp amplifier. Resistances of patch pipettes were 2–3 MΩ when filled with an intracellular solution composed of (in mm): CsCl, 60; Cs D-gluconate, 10; TEA-Cl, 20; BAPTA, 20; MgCl2, 4; ATP, 4; and HEPES, 30 (pH 7.3, adjusted with CsOH). The pipette access resistance was compensated by 70–80%. The holding potential was corrected for liquid-junction potential.

The results show that the transient component of the Franssen stimulus, with a shorter first spike latency and higher discharge rate than the sustained tone, encodes the perception of sound location. Furthermore, the persistent erroneous perception of the sustained stimulus location is due to continued excitation of the same neurons, first activated by the transient, by the sustained stimulus without location information. These results demonstrate

for the first time, on a trial-by-trial selleck chemical basis, a correlation between perception of an auditory spatial illusion and a subcortical physiological substrate. “
“Hippocampal CA1 pyramidal cells, which receive γ-aminobutyric acid (GABA)ergic input from at least 18 types of presynaptic neuron, express 14 subunits of the pentameric GABAA receptor. The relative contribution

of any subunit to synaptic and extrasynaptic receptors influences the dynamics of GABA and drug actions. Synaptic receptors mediate phasic GABA-evoked conductance and extrasynaptic receptors contribute to a tonic conductance. We used freeze-fracture replica-immunogold labelling, a sensitive quantitative immunocytochemical find more method, to detect synaptic and extrasynaptic pools of the alpha1, alpha2 and beta3 subunits. Antibodies to the cytoplasmic loop of the subunits showed immunogold particles concentrated on distinct clusters of intramembrane particles (IMPs) on the cytoplasmic face of the plasma membrane on the somata, dendrites and axon initial segments, with an abrupt decrease in labelling at the edge of the IMP cluster. Neuroligin-2, a GABAergic synapse-specific adhesion molecule, co-labels all beta3 subunit-rich IMP clusters, therefore we considered them synapses. Beta adrenergic receptor kinase Double-labelling for two subunits showed that virtually all somatic synapses contain the alpha1, alpha2 and beta3 subunits. The extrasynaptic plasma membrane of the somata, dendrites and dendritic spines showed low-density immunolabelling.

Synaptic labelling densities on somata for the alpha1, alpha2 and beta3 subunits were 78–132, 94 and 79 times higher than on the extrasynaptic membranes, respectively. As GABAergic synapses occupy 0.72% of the soma surface, the fraction of synaptic labelling was 33–48 (alpha1), 40 (alpha2) and 36 (beta3)% of the total somatic surface immunolabelling. Assuming similar antibody access to all receptors, about 60% of these subunits are in extrasynaptic receptors. “
“Disorders implicating the basal ganglia are often characterized by postural deficits, but little is known about the role of the basal ganglia in posture control. Using wireless multi-electrode recording, we measured single unit activity from GABAergic and dopaminergic neurons in the substantia nigra as unrestrained mice stood on an elevated platform while introducing continuous postural disturbances in the roll plane.

This work was partially financed by grants from the Fondo de Investigacion Sanitaria (07/0976, 08/1032, 08/1195, 08/1715 and 10/2635); Fondos Europeos para el Desarrollo Regional (FEDER); Fundación para la Investigación y Prevención del Sida en España (FIPSE 06/36572, 06/36610 and 36-0998-10); Ministerio de Ciencia e Innovación (SAF2008-02278); Programa de suport als Grups de Recerca AGAUR (2009 SGR 284, 959, 1061 and 1257); Red de Investigación en Sida (RIS, RD06/006/0022 and RD06/0006/1004); learn more and the Instituto de Salud Carlos

III, Ministerio de Sanidad y Consumo, Spain. XE is supported by a fellowship from the JdlC programme and grant JDCI20071020. CIBERdem and CIBERobn are ISCIII projects. The comments and critiques of the anonymous reviewers helped us to improve the manuscript and are greatly appreciated. “
“Antiretroviral therapy

(ART) medication prescribing errors in hospitalized patients still remain common. This study aimed to examine the initial prescribing of antiretroviral drug regimens for HIV clinic patients admitted Alpelisib to an urban academic teaching hospital. 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 Fludarabine solubility dmso 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. Highly active antiretroviral therapy (HAART) has significantly altered the natural progression of HIV infection and AIDS [1-3]. The appropriate usage and monitoring of these medications in recent years have led to dramatic improvements in the patients’ qualify of life.

This has also been observed in patients treated with nucleos(t)ide therapy (lamivudine, adefovir or tenofovir) with reduced rates of eAg seroconversion in patients with a baseline HBV DNA >7 log10 IU/mL

[102]. During therapy, HBV DNA testing is used to decide whether to continue or stop interferon treatment (see ‘Therapy’, section 4.3 below) [101]. This also applies to nucleos(t)ide therapy where primary nonresponse is defined as a <1 log10 IU/mL drop in HBV DNA level from baseline at 3 months, and response is defined as an undetectable HBV DNA by real-time polymerase chain reaction (PCR) assay within 48 weeks of therapy. Partial virological response is defined as a >1 log10 IU/mL drop in HBV DNA but detectable HBV DNA by real-time PCR assay [101,102]. In HIV-uninfected patients, a partial virological response should lead to a decision about modifying therapy at 24 weeks of therapy for lamivudine and telbivudine (which have BYL719 a low barrier to resistance) and at 48 weeks for entecavir, adefovir and tenofovir (which have a high barrier to resistance) [102]. How this should be applied in coinfected patients is uncertain. Virological breakthrough on treatment, defined as a confirmed increase of >1 log10 IU/mL above nadir HBV DNA level on therapy, means either nonadherence or resistance [102]. The lower limit of detection of the assays used to monitor HBV DNA should be 10–15 IU/mL and this level should also be the aim of treatment

[103]. Measurement of HBV DNA every 6–12 months is sufficient if the patient is not on HBV therapy [104]. 4.2.2.2 Measuring HBV serology during and after therapy. selleck kinase inhibitor The ideal outcome of treatment is HBe seroconversion in patients who are HBeAg positive and HBs seroconversion (very rare) in all patients [102]. Once HBV DNA is undetectable, HBeAg and eAb in HBeAg-positive patients and HBsAg in all patients should be tested every 12–24 weeks to pick up seroconversion. It should be noted that there

is no HBV DNA level at which seroconversion from HBeAg positive to negative is completely predictable [105]. Spontaneous or treatment-induced seroconversion from HBsAg positive to negative PIK3C2G is associated with ongoing undetectable HBV DNA but, in patients who convert from HBeAg positive to negative, HBV DNA may still be detectable at low levels [102,106]. 4.2.2.3 HBV resistance testing. Resistance testing is becoming more widely available and may be considered as a baseline pretreatment, especially if there is a history of previous exposure to anti-HBV drugs, as a means to inform treatment decisions in those with nonresponse to treatment or with virological breakthrough. A line probe assay for the detection of hepatitis B wild-type virus and a drug-induced mutation using direct sequencing can identify specific resistance mutations [107,108]. Direct sequencing of the HBV polymerase gene can detect variants that are present in 10–20% of the virus population [109].

The average incubation period for dengue infection is 5 days, followed by an infectious period of viremia lasting for an average of 4.5 days.4,5 There is no licensed dengue vaccine and the only means of prevention is through avoidance of bites from the mosquito vector. The principal dengue vectors, Aedes aegypti and Aedes albopictus mosquitoes, are common throughout the tropics and subtropics. Roughly, one third of the world’s population lives

in dengue-endemic areas in over 100 countries, with an estimated 50 to 100 million dengue cases occurring worldwide annually.6 Over the past two decades, dengue epidemics with cases of DHF have been occurring with increasing frequency around the globe.7,8 Although the vast majority of dengue click here infections occur among residents of dengue-endemic areas, dengue is being increasingly diagnosed among travelers to these destinations.9 Recent findings from the GeoSentinel Surveillance Network9,10 indicate that dengue is the

most commonly reported cause of acute febrile illness in travelers returning from the Caribbean, South America, south central Asia, and southeast Asia. Moreover, dengue was found to be the second most common cause of febrile this website illness (after malaria) in travelers returning from sub-Saharan Africa and Central America.9 In the United States, this upward trend will likely continue with the increasing rates of international travel in recent years,11 and the increasing number of new US immigrants from endemic countries12 who are likely to visit friends and relatives in their countries of origin.13,14 Concern over the risk of reintroduction of dengue virus into the United States has been recently expressed.15Ae. aegypti mosquitoes

exist in a few states in the southeastern United States.16 However, Ae. albopictus mosquitoes exist in 26 states throughout the southeastern United States and Hawaii.17 The presence of competent vectors in the continental United States and Hawaii, along with the O-methylated flavonoid increasing global incidence of dengue and travel to dengue-endemic areas, underscores the need for vigilance regarding possible importation of dengue virus via travel-associated cases. The Division of Vector-Borne Infectious Diseases at the US Centers for Disease Control and Prevention (CDC) conducts dengue surveillance in collaboration with the Puerto Rico Department of Health. This laboratory-based Passive Dengue Surveillance System (PDSS) collects serum samples and epidemiologic information from suspected dengue cases reported by healthcare providers from Puerto Rico, the US Virgin Islands, and the 50 US states and the District of Columbia. This analysis uses PDSS surveillance data to describe the epidemiology of travel-associated dengue among travelers from the United States during the period of 1996 to 2005.