Ltd, Tokyo, Japan) HAI assays were performed in V-bottomed 96-we

Ltd, Tokyo, Japan). HAI assays were performed in V-bottomed 96-well microtitre plates (Nunc Roskilde, Denmark), as previously described [8, 9]. Sera were subjected to 2-fold serial dilutions (from 1:8 to 1:16 384) in phosphate-buffered saline (PBS) prior to incubation with 4 HA units of the influenza A/California/7/09 (H1N1)

virus [provided by the WHO Influenza Collaborating Centre, National Institute for Medical Research (NIMR), London, UK]. Glutaraldehyde-fixed turkey red blood cells (0.4%) were added at room temperature and after 30 min a reading was taken[10, 11]. To minimize assay variation, sera from one positive and one negative healthy www.selleckchem.com/products/carfilzomib-pr-171.html subjects were used in each plate for plate validation, paired samples DAPT order were assessed in the same test, samples were repeated at least twice in independent experiments, plates were read twice in flat and tilted positions by two or three trained individuals and the geometric mean of the different readings was calculated. HAI titres were considered valid if two independent readings did not differ by more than one dilution. Results were expressed as the reciprocal of the highest dilution showing a positive HAI. Negative samples were assigned a titre of 1:4 for computational purposes and individual values were log-transformed to calculate the geometric mean antibody titres (GMTs). The MN assay was adapted from a previously described procedure [12]. Briefly,

decomplemented sera were serially diluted 2-fold (starting at 1:10) in flat-bottomed 96-well microtitre plates. Virus [2 × 104 tissue culture infective dose 50 (TCID50)/mL] was added and neutralization 17-DMAG (Alvespimycin) HCl allowed to proceed for 1 h at 37°C prior to the addition of Madin Darby Canine Kidney (MDCK) cells (5 × 105 cells/mL). Sixteen hours later, monolayers were scored for confluency, fixed and treated with a monoclonal antibody (MCA400, clone AA5H, AbD Serotec, Duesseldorf, Germany) against influenza A nucleoprotein. Staining was revealed by adding anti-immunoglobulin G (HRP-IgG; Dako, Glostrup, Denmark) followed by tetramethyl benzidine (TMB) substrate

(Invitrogen, Zug, Switzerland), prior to measuring the absorbance at 650 and 450 nm (for background subtraction). The average optical density (OD) values from five replicate wells containing virus and cells (V+C) and cells only (C) were used to calculate the 50% neutralizing endpoint. The endpoint titre was expressed as the reciprocal of the highest dilution of serum with an OD value less than X, where X = [(average of V+C wells) − (average of C wells)]/2 + (average of C wells). Assay variations were limited by several means: positive and negative control samples were included in one plate per run, samples were tested at least twice in independent experiments and plates were validated using stringent criteria. Negative samples were assigned a titre of 1/5 for computational purposes.

Agrobacterium tumefaciens C58C1 strains carrying the vector pBin-

Agrobacterium tumefaciens C58C1 strains carrying the vector pBin-Hyg-Tx, pBin::nopT1, and pBIN::nopT2 were infiltrated into N. tabacum cv. Xanthi and N. benthamiana leaves. NopT1 elicited localized cell death in both Nicotiana species (Fig. 4b). By contrast, leaves infiltrated with A. tumefaciens carrying pBin::nopT2 did

not show any visible symptoms (Fig. 4c). No visible symptoms of cell death were observed when Agrobacterium with an empty vector was infiltrated (Fig. 4a). In light of these results, further studies focused on the analysis of NopT1 function. To determine whether the putative catalytic triad (C/H/D) of NopT1 is required for the HR-like cell death in tobacco, we constructed substitutions at positions 100 (C100S), 213 (H213A), and 228 (D228A) with Ala (Fig. 2d). Ibrutinib Dasatinib clinical trial The coding regions of the site-directed mutants were subcloned into a binary Agrobacterium vector and tested for ability to elicit the HR in N. tabacum and N. benthamiana when overexpressed directly within the plant cells via the Agrobacterium-transient expression system. None of the mutants elicited cell death (Fig. 4e–g), whereas the wild-type NopT1 elicited a strong HR (Fig. 4b). We also

examined whether the site-directed mutants retained enzymatic activity. As shown in Fig 2b, all site-directed mutants had lost the NopT1 processing in E. coli, although not completely and their in vitro enzymatic activity ID-8 was significantly reduced in comparison with wild-type protein (Fig. 3c). These results corroborate further the prediction that that NopT1 is a cysteine protease and requires an intact catalytic triad for both enzymatic and HR-eliciting activity. Previous studies have shown

that all YopT/AvrPphB family members identified so far contain an embedded consensus site for eukaryotic fatty acylation which may be exposed following autoproteolytic processing of these effectors (Puri et al., 1997; Nimchuk et al., 2000; Dowen et al., 2009). Similarly, NopT1 possesses putative sites (Fig. 1b) for both N-myristoylation (G50) and S-palmitoylation (C52 and C53) that lack experimental validation. To investigate whether these acylations play a role in cell death elicitation by NopT1, we made deletion and site-directed mutants affecting either one or both sites. Initially, we made a deletion mutant, Δ50N, in which an ATG codon was introduced just before the A51 codon by replacing the glycine (G) residue at position 50 by a methionine (M) residue. Transient expression via agroinfiltration of this mutant displayed identical necrotic phenotype to that elicited by the full-length protein, in terms of both timing and intensity of the necrotic response (Fig. 4d). Although myristoylation of NopT1 has not been demonstrated biochemically, it is tempting to speculate that an intact myristoylation motif may not be required for HR elicitation by NopT1 at least in plants tested.

05 or less) Increased detection of CCR5 over CXCR4 was seen in C

05 or less). Increased detection of CCR5 over CXCR4 was seen in CD14 cells (P < 0.05). No significant differences in CCR5 or CXCR4 expression selleck chemical were found in samples from asymptomatic women with or without chlamydial infection. Co-receptor expression confirms the potential for CD1a Langerhans cells, monocytes/macrophages and T-helper cells in the cervix as primary targets for HIV infection. Previously observed selective

transmission of CCR5-tropic isolates cannot be accounted for by a lack of CXCR4-expressing CD4 cervical immune cells. We were unable to identify any specific impact of chlamydial infection on co-receptor expression in this study. “
“The aim of the study was to determine whether the incidence of first-line treatment discontinuations and their causes changed according to the time of starting highly active antiretroviral therapy (HAART) in an Italian cohort. We included in the study patients from the Italian COhort Naïve Antiretrovirals (ICoNA) who MAPK inhibitor initiated HAART when naïve to antiretroviral therapy (ART). The endpoints were discontinuation within the first year of ≥1 drug in the first

HAART regimen for any reason, intolerance/toxicity, poor adherence, immunovirological/clinical failure and simplification. We investigated whether the time of starting HAART (stratified as ‘early’, 1997–1999; ‘intermediate’, 2000–2002; ‘recent’, 2003–2007) was associated with the probability of reaching the endpoints by a survival analysis. Overall, the 1-year probability of discontinuation of ≥1 drug in the first regimen was 36.1%. The main causes of discontinuation were intolerance/toxicity (696 of 1189 patients; 58.5%) and poor adherence (285 of 1189 patients; 24%). The hazards for all-reason change were comparable according

to calendar period [2000–2002, adjusted relative hazard (ARH) 0.82, 95% confidence interval (CI) 0.69–0.98; 2003–2007, ARH 0.94, 95% CI 0.76–1.16, vs. 1997–1999; global P-value=0.08]. Patients who started HAART during the ‘recent’ period were less likely to change their initial regimen because of intolerance/toxicity (ARH 0.67, 95% CI 0.51–0.89 vs. ‘early’ period). Patients who started in the ‘intermediate’ and ‘recent’ periods had a higher risk of discontinuation because of simplification (ARH 15.26, 95% CI 3.21–72.45, and ARH 37.97, 95% CI 7.56–190.64, Avelestat (AZD9668) vs. ‘early’ period, respectively). It seems important to evaluate reason-specific trends in the incidence of discontinuation in order to better understand the determinants of changes over time. The incidence of discontinuation because of intolerance/toxicity has declined over time while simplification strategies have become more frequent in recent years. Intolerance/toxicity remains the major cause of drug discontinuation. Optimization of the initial highly active antiretroviral therapy (HAART) in terms of both virological potency and tolerability is crucial for the prognosis of HIV-infected patients starting HAART [1–3].

8 M−1 cm−1) One unit of peroxidase activity is defined as the am

8 M−1 cm−1). One unit of peroxidase activity is defined as the amount of enzyme required to oxidize 1 μmol of ABTS per 1 min. SOD activity in the cell-free extracts was determined spectrophotometrically at 25 °C using the xanthine oxidase–cytochrome c method (McCord & Fridovich, 1969). The assay mixture in deionized water (1 mL of reaction volume) contained 50 mM potassium phosphate buffer (pH 7.8), 0.1 mM EDTA disodium salt, 10 μM cytochrome c (Sigma), 50 μM E7080 in vitro xanthine (Sigma) and 1.7 mU xanthine oxidase (Sigma). The reduction of cytochrome c by the superoxide anion radical, generated from O2 during the oxidation of xanthine in the xanthine oxidase reaction, was recorded by an increase in the absorption

at 550 nm for 5 min. One unit of SOD activity is defined as the amount of enzyme required to inhibit the linear rate of reduction of cytochrome c by 50%. Protein concentrations were determined using the Protein Assay click here Kit (Bio-Rad Laboratories). For total RNA isolation, cell pellets were rinsed three times with 10 mM Tris-HCl (pH 8.0) RNase-free buffer and finally resuspended in 200 μL of 10 mM Tris-HCl, 1 mM EDTA (pH 8.0) RNase-free buffer. Total RNA was isolated using the High Pure RNA Isolation

Kit (Roche Diagnostics) according to the manufacturer’s instructions with an extra DNase I digestion step in order to eliminate contaminating DNA. Extracted RNA (10 μg) was reverse transcribed using a random hexamer primer, dNTPs and Superscript II (Invitrogen) as described previously (Fournier Tangeritin et al., 2006). cDNA was purified on a microcon YM-30 centrifugal filter unit (Millipore) and stored at −20 °C. qRT-PCR was performed using the LightCycler® FastStart DNA MasterPLUS SYBR Green I Kit (Roche Diagnostics). cDNA was mixed with 0.5 μM of each primer and 2 μL of Master Mix in a 10 μL final volume. The pairs of oligonucleotide primers used to quantify the selected genes expression levels are shown in Supporting Information, Table S1. Real-time PCR runs were carried out on a LightCycler® Real-Time PCR System (Roche Diagnostics), with one cycle at 95 °C for

8 min, followed by up to 45 cycles at 95 °C for 12 s, 60 °C for 10 s and 72 °C for 20 s. For each couple of primers, real-time PCRs were run in triplicate on each cDNA. relative expression software tool (rest) was used to calculate the relative expression of each gene under each condition (Pfaffl et al., 2002). The coefficients of variation of the determined crossing points for each set of replicates were lower than 0.46%. The 16S RNA gene was used as a reference for normalization. The influence of H2O2 on exponentially growing cells in a lactate/sulfate medium is shown in Fig. 1. While the addition of 0.05 mM H2O2 did not significantly perturb D. vulgaris Hildenborough growth, higher concentrations of H2O2 treatment induced both a lower growth rate and a lower final cell density. When 0.

The activity was measured by decreasing the A340 nm based on the

The activity was measured by decreasing the A340 nm based on the transformation of vanillin to vanillic acid. Influence on latent absorbance by the production of NAD(P)H was adjusted by molar extinction coefficients. Calculations were based on molar extinction coefficients

of vanillin (10.6 × 103; pH 7) and NAD(P)H (6.30 × 103) at 340 nm. The reaction mixture comprised 100 mM KPB, 5 mM NAD(P)+, and 0.25 mM vanillin at the final concentration. The other method investigated the enzyme’s substrate specificity and the effect of pH or temperature on it. AC220 Enzyme activity was determined by quantification of corresponding oxidized products from aromatic aldehydes by HPLC as described above. The reaction mixture (1.0 mL) comprised 100 mM appropriate buffer, 5 mM NAD(P)+, 2.5 mM substrates, and 0.23 and

0.26 U of purified VDH from Micrococcus sp. TA1 and B. cepacia TM1, respectively. The reaction mixture was incubated for 20 min at an appropriate temperature, after which the reaction was stopped by adding 0.2 mL of Lapatinib manufacturer 0.5 N HCl. The acid produced was quantified by HPLC. One unit of enzyme activity was defined as the amount of enzyme that catalyzes the transformation of 1 μmol of vanillin to vanillic acid. The enzyme from Micrococcus sp. TA1 that catalyzes the dehydrogenation of vanillin was purified from cells as follows: after cultivation on 2 g L−1 vanillin as a carbon source with each liquid medium as described in Materials and methods, cells were harvested by centrifugation (10 000 g, 10 min, 4 °C). The pellet was resuspended in 50 mM KPB (pH 7.5) and the suspension was treated 5-Fluoracil purchase with an ultrasonicator (201 M sonicator; Kubota, Tokyo, Japan) at 9 KHz and 170 W for 15 min; the utmost care was taken to maintain the temperature below 5 °C. The lysate was then centrifuged at 16 000 g for 20 min. The resulting supernatant was used as the cell extract. The cell extract dialyzed against 10 mM Tris-HCl buffer (pH 8.5) was applied to a 100 mL DEAE-Sepharose FF column (GE Healthcare Bio-Science, Buckinghamshire, UK). The enzyme was eluted with a

linear gradient of increasing NaCl concentration (0–0.5 M, total volume 1.5 L). The fractions with VDH activity were pooled. NaCl (2 M) was added with gentle stirring to the pooled fraction, and this solution was applied to a 30-mL butyl-Sepharose column (GE Healthcare Bio-Science). The enzyme was eluted using a gradient of decreasing NaCl concentration (2–0 M, total volume 600 mL). The active fractions were dialyzed against 10 mM Tris-HCl buffer (pH 8.5). The dialyzed enzyme solution was applied to a 1-mL Resource Q column (GE Healthcare Bio-Science). The enzyme was eluted with a linear gradient of increasing NaCl concentration (0–0.5 M, total volume 100 mL). The enzyme from B. cepacia TM1 was purified from the cell extract as follows: the cell extract of B.

The effects of maternal care on developing DA pathways and reward

The effects of maternal care on developing DA pathways and reward-directed behavior of female offspring that we have observed may play a critical role in the behavioral transmission of maternal LG from mother to daughter, and account for individual differences in the mesolimbic DA system. “
“In rat brain, the detection and integration of chemosensory and neural signals are achieved, inter alia, by the median preoptic

nucleus (MnPO) during a disturbance of the hydromineral balance. This is allowed through Selleck GSK3235025 the presence of the sodium (Na+) sensor neurons. Interestingly, enkephalins and mu-opioid receptors (μ-ORs) are known for their role in ingestive behaviors and have previously been shown to regulate the excitability of MnPO neurons following a single Na+ depletion. However, little is known about the role of these μ-ORs in the response enhancement following repeated Na+ challenge. Therefore, we used whole-cell recordings in acute brain slices to determine neuronal plasticity in the electrical properties of the MnPO Na+ sensor-specific

click here neuronal population following multiple Na+ depletions. Our results show that the population of Na+ sensor neurons was represented by 80% of MnPO neurons after a single Na+ depletion and was reduced after three Na+ depletions. Interestingly, the subpopulation of Na+ sensors responding to D-Ala2,N-MePhe4,Gly-ol-enkephalin (DAMGO), a specific μ-OR agonist, represented 11% of MnPO neurons after a single Na+ depletion and the population doubled after three Na+ depletions. Moreover, Na+ sensor neurons displayed modifications in the discharge pattern distribution and shape of

calcium action potentials after three Na+ depletions but these changes did not occur in Na+ sensors responding to DAMGO. Thus, the reinforced μ-OR functionality in Na+ sensors might take place to control the neuronal hyperexcitability and this plasticity in opioid-sensitive and Na+ detection MnPO networks might sustain Cyclin-dependent kinase 3 the enhanced salt ingestion induced by repeated exposure to Na+ depletion. “
“Pavlovian cues [conditioned stimulus (CS+)] often trigger intense motivation to pursue and consume related reward [unconditioned stimulus (UCS)]. But cues do not always trigger the same intensity of motivation. Encountering a reward cue can be more tempting on some occasions than on others. What makes the same cue trigger more intense motivation to pursue reward on a particular encounter? The answer may be the level of incentive salience (‘wanting’) that is dynamically generated by mesocorticolimbic brain systems, influenced especially by dopamine and opioid neurotransmission in the nucleus accumbens (NAc) at that moment.

Among the trombiculid chiggers including the scrub

Among the trombiculid chiggers including the scrub Vorinostat in vitro typhus-transmitting Leptotrombidium species, only the larvae are human and animal ectoparasites. The larger chigger nymphs and adults are free-living and feed on small insects and their eggs. All trombiculid

larvae exhibit a unique method of feeding on hosts and transmitting salivary secretions, which may contain O tsutsugamushi, the causative agent of scrub typhus, in endemic regions. Larvae pierce the skin with sharp mouthparts and infuse tissue-dissolving saliva to fill a pool of lymph, other body fluids, and dissolved epithelial cells to aspirate from (Figure 1). The repeated injection of saliva into bite wounds incites a host reaction forming a straw-like hollow tube, the hypostome (stylostome), which extends downwards firmly anchoring the mite into the host’s skin. 1 All of the non-infectious chigger larvae can cause scrub itch or trombidiosis with the American chigger mite, Eutrombicula alfreddugesi, being the most common culprit in the United States; the European autumn harvest mite, Neotrombicula autumnalis, the most common culprit in Europe; and the Asian chigger, Eutrombicula sarcina, the most common culprit in Asia (Table 1). Initially painless, chigger bites will cluster where clothing is tight against the skin, especially on the genitalia, thighs,

buttocks, IDH mutation flanks, waists, and ankles. find more Localized itching and discomfort ensue when the larvae withdraw their mouthparts and depart after feeding for 3 to 6 hours for most non-infectious chiggers. Although some trombiculid larvae remain attached to and feeding on human hosts for up to a month, the larval vectors of scrub typhus feed

for 2 to 10 days before dropping to the ground engorged, and ready to mature into free-ranging nymphs. Forcibly removing feeding chiggers often decapitates larvae leaving mouthparts embedded to cause further inflammation. 1 Several untested strategies for removing feeding, engorged chiggers intact have included painting chigger bite sites with colloidion, clear fingernail polish, or Liquid Skin, then drying the sites with a hair dryer and peeling the coated and dried chiggers off the skin intact. Localized intense itching will often be followed by prurigo, an eruption of intensely pruritic erythematous papules by 10 to 12 hours, followed by crusting and healing by 24 to 48 hours. 1 Treatment of mild infestations is supportive with soap and water cleansing, warm water soaks, and topical local anesthetics and antihistamines. Prurigo should be treated specifically with topical corticosteroids, with oral corticosteroids indicated for severe cases. Impetigo and other secondary infections are potential complications that would necessitate antibiotic treatment. Tetanus prophylaxis is recommended, if indicated.

Among the trombiculid chiggers including the scrub

Among the trombiculid chiggers including the scrub click here typhus-transmitting Leptotrombidium species, only the larvae are human and animal ectoparasites. The larger chigger nymphs and adults are free-living and feed on small insects and their eggs. All trombiculid

larvae exhibit a unique method of feeding on hosts and transmitting salivary secretions, which may contain O tsutsugamushi, the causative agent of scrub typhus, in endemic regions. Larvae pierce the skin with sharp mouthparts and infuse tissue-dissolving saliva to fill a pool of lymph, other body fluids, and dissolved epithelial cells to aspirate from (Figure 1). The repeated injection of saliva into bite wounds incites a host reaction forming a straw-like hollow tube, the hypostome (stylostome), which extends downwards firmly anchoring the mite into the host’s skin. 1 All of the non-infectious chigger larvae can cause scrub itch or trombidiosis with the American chigger mite, Eutrombicula alfreddugesi, being the most common culprit in the United States; the European autumn harvest mite, Neotrombicula autumnalis, the most common culprit in Europe; and the Asian chigger, Eutrombicula sarcina, the most common culprit in Asia (Table 1). Initially painless, chigger bites will cluster where clothing is tight against the skin, especially on the genitalia, thighs,

buttocks, Docetaxel flanks, waists, and ankles. SPTLC1 Localized itching and discomfort ensue when the larvae withdraw their mouthparts and depart after feeding for 3 to 6 hours for most non-infectious chiggers. Although some trombiculid larvae remain attached to and feeding on human hosts for up to a month, the larval vectors of scrub typhus feed

for 2 to 10 days before dropping to the ground engorged, and ready to mature into free-ranging nymphs. Forcibly removing feeding chiggers often decapitates larvae leaving mouthparts embedded to cause further inflammation. 1 Several untested strategies for removing feeding, engorged chiggers intact have included painting chigger bite sites with colloidion, clear fingernail polish, or Liquid Skin, then drying the sites with a hair dryer and peeling the coated and dried chiggers off the skin intact. Localized intense itching will often be followed by prurigo, an eruption of intensely pruritic erythematous papules by 10 to 12 hours, followed by crusting and healing by 24 to 48 hours. 1 Treatment of mild infestations is supportive with soap and water cleansing, warm water soaks, and topical local anesthetics and antihistamines. Prurigo should be treated specifically with topical corticosteroids, with oral corticosteroids indicated for severe cases. Impetigo and other secondary infections are potential complications that would necessitate antibiotic treatment. Tetanus prophylaxis is recommended, if indicated.

Such exposures frequently place patients in skin contact with inf

Such exposures frequently place patients in skin contact with infested hay, straw, or furniture during peak mite-feeding and breeding seasons in the spring and summer. Straw itch mite dermatitis is characterized by pruritic, maculopapulovesicular eruptions on the limbs and trunk, which resolve rapidly with topical corticosteroid therapy. 17,20 In 2000, Bellido-Blasco and colleagues 21 investigated three separate outbreaks of dermatitis afflicting over

Selleck Epigenetic inhibitor 100 patients caused by the European straw itch mite (P ventricosus) in Castellon, Spain. In 2006, Del Giudice and colleagues 22 described a similar outbreak, also suggestive of arthropod bite-induced dermatitis in southeastern France. The dermatitis was characterized by solitary to multiple, highly erythematous pruritic macules, some of which were accompanied by contiguous, linear erythematous macular tracts that resembled “comet tails” (Figure 2). 22 In a 2007 outbreak investigation of an additional 42 cases of dermatitis with comet tail signs in the same region, Del Giudice and colleagues identified P ventricosus mites as causative agents and described

the epidemiology and outcomes of P ventricosus infestations in homes and humans. Most residences of case-patients with P ventricosus dermatitis were infested with live furniture beetles, Anobium punctatum, which this website do not bite or infest humans. Adult P ventricosus mites, common ectoparasites of furniture beetles, were present in stereomicroscopic examination of wood dust beneath beetle-infested furniture. Confocal laser scanning microscopy (CLSM) of a central

microvesicle in a maculopapular lesion on an experimentally infested co-investigator demonstrated an ovoid foreign body consistent with a P ventricosus mite Amino acid (Figure 2). Both naturally occurring and experimental infestations caused the characteristic maculopapular rash of P ventricosus dermatitis, again associated with comet signs (Figure 2). 23 Although oral prednisone (0.5 mg/kg) rapidly relieved pruritus, P ventricosus dermatitis would persist or recur in case-patients until beetle-infested furniture was removed from households or patients permanently vacated their infested residences, often in resort regions. 23 In 2004, a close relative of the North American straw itch mite, P tritici, the oak leaf gall mite (Pyemotes herfsi), which preferentially feeds on insect larvae in oak trees, caused an outbreak of plant insect mite dermatitis in the United States. 24 Over 300 residents of Pittsburg, Kansas, sought immediate medical attention for an intensely pruritic, erythematous maculopapular rash clustering on the face, neck, and limbs (Figure 3). 24 All lesions healed within days following topical treatment with antihistamines and corticosteroids.

Clinical diagnosis is often difficult, as infectious exanthematou

Clinical diagnosis is often difficult, as infectious exanthematous diseases such as measles, rubella, click here human parvovirus B19, dengue, human herpes virus (HHV)-6, roseola infantum, and scarlet fever have overlapping clinical symptoms. In Brazil, from 1994 to 1998, 327 patients presenting with pathologies characterized by variable combinations of exanthema, cough, conjunctivitis, coryza, and fever were studied. A laboratory-confirmed diagnosis was achieved in 71.3% of cases: 33% were diagnosed with dengue fever, 20% with rubella, 9.2% with human parvovirus B19, 6.7% with measles,

and 2.1% with HHV-6.[4] These results underline the important proportion of cosmopolitan febrile exanthemas. In France, Hochedez and colleagues screened 62 returning travelers presenting with fever and exanthema for exotic (if returning from endemic areas) and cosmopolitan infections. They found a specific etiology in over 90% of the patients. The three main diagnoses were chikungunya, dengue, and African tick bite fever, followed by infectious mononucleosis, human immunodeficiency virus-1 primary infection, cytomegalovirus primary infection, CDK inhibition measles, rubella, chicken pox, streptococcal infections, primary toxoplasmosis, acute schistosomiasis, and adverse drug reactions.[1]

Travelers presenting with febrile exanthema should therefore be screened not only for arboviral infections according to the area visited but also for more common infections. The diagnosis of dengue fever is based on the detection of NS1 Ag, antibodies (IgM and IgG) or reverse transcription (RT)-PCR (virus isolation is used less often). For early diagnosis (onset < 5 days), detection of NS1 Ag may

be used, but its moderate sensitivity requires the presence of both NS1 Ag and IgM for a definite diagnosis.[5] IgM are positive 4 to 5 days after disease onset and remain so for up to 3 to 6 months. IgG appear approximately 7–10 days after onset and are detectable thereafter for life. RT-PCR detection of viral RNA is a very reliable technique for patients presenting within 5 to 7 days of the onset of symptoms, but this method is more expensive, nonstandardized, and only a few centers in France use it unless routinely.[6] Consequently, serological tests are commonly used to establish or confirm a diagnosis of dengue. Currently available commercial rapid tests offer good sensitivity, but they lack specificity, which may lead to false-positive results as in our index case. Overall, possible explanations for false-positive results include cross-reactive flavivirus-specific antibodies, nonspecific binding of antibodies secreted in the course of various infections such as mononucleosis or hepatitis, and rheumatoid factor.[7] Cross-reactivity with measles antibodies is not commonly assumed by biologists and, to our knowledge, has only been reported once in Belgium.