However, genetically related VP2 proteins 3 and 7, or 5 and 8, (Fig. 2) in each of the cocktails did not increase nAbs titers against their related serotypes. No nAbs were detected against unrelated serotypes (Table 1). Further, nAb titers against each VP2 protein differed strongly after immunization with a cocktail or with single VP2 protein. Non-neutralizing Abs were raised by cocktails of VP2 proteins; i.e. Abs against serotype 4, 5 and 9

by the cocktail of 1, 3, 7, 8, and Abs against serotype 8 by the cocktail of 2, 4, 5, 6, 9 (Table 2). Perhaps, AHSV serotypes have common epitopes on VP2 but these differ in avidity or affinity for these Abs. As a result, binding to epitopes occurs and will immunostain AHSV infected monolayers but this binding will not neutralize AHSV. Currently used cocktails of live-attenuated vaccines (LAVs) induce a broader protection. Even LAV for serotype

VRT752271 5 and 9 are not included, and protection against AHSV-5 and -9 are achieved by serotype-related LAVs for serotype 8 and 6, respectively [36]. However, when using cocktails of LAVs it was also suggested that there are substantial differences in cross-reactivity between serotypes; e.g. cross-reactivity between AHSV-5 and -8 seems to be stronger than between AHSV-6 and -9 [37]. Importantly, undesirable events such as reversion to virulence and reassortment between LAVs or with field virus are highly Histone Demethylase inhibitor likely. Furthermore, LAVs induce an immune response against all viral proteins and are therefore not ‘DIVA’ (differentiating infected from vaccinated animals)

vaccines. In contrast, VP2 subunit vaccine induces Abs solely against VP2, and horses vaccinated with VP2 subunit vaccines should therefore be seronegative for VP7 antibodies. An AHSV infection results rapidly in seroconversion for VP7 antibody and VP7 is the target for several commercially available tests to detect AHSV infections. DIVA testing by these commercially available tests will be Megestrol Acetate very supportive in combination with vaccination with VP2 subunit vaccine. Thus, rapid control of AHS outbreaks as well as confirming the virus-free status of animals for international movements irrespective of the vaccination status can be achieved with the current available and extensively validated VP7 ELISA. In summary, we demonstrated that multi-serotype VP2 subunit vaccines for AHS are potentially feasible, as shown here by immunization of guinea pigs as an alternative animal model. The guinea pig model can be initially used for immunogenicity studies in order to reduce experiments in horses. The considerable difference in immunogenicity between VP2 proteins in guinea pigs has to be taken into account and should be investigated further prior to the formulation of single as well as cocktail VP2 subunit vaccines for African horse sickness.

In patients with primary infection, the median (min–max) of the number (/106 PBMC) of ASC (IgA + IgG + IgM) was 241 (175–613) for those specific to Salmonella Typhi, 85 (32–225) to Paratyphi A, 30 (24–133) to Paratyphi B and 8 (6–10) to Paratyphi C ( Fig. 3A). In the patient with the relapse, the numbers of ASC were 28, 14, 28 and 4/106 PBMC, respectively ( Fig. 3 B). In the patient with a Salmonella Paratyphi A infection, the respective numbers were 13, 23, 19 and 0/106 PBMC, with no response to Salmonella Egusi ( Fig. 3C). The

expressions of HR (mean ± SD) on Salmonella Typhi – and Salmonella PS-341 Paratyphi B-specific ASC in the vaccinees are shown in Fig. 4. Almost all of the ASC expressed the intestinal HR, α4β7-integrin (95 ± 5% to Salmonella Typhi and 97 ± 6% to Salmonella Paratyphi B), while the peripheral lymph node HR, l-selectin, and the cutaneous HR, CLA, were found on smaller proportions of them (27 ± 17% and 0.4 ± 1% to Salmonella Typhi and 49 ± 18% and 7 ± 8% to Salmonella Paratyphi B, respectively). The expressions of HR on pathogen-specific ASC in patients with enteric fever are shown in Fig. 4. Almost all ASC expressed α4β7-integrin (92 ± 7%), while l-selectin and CLA were expressed less frequently (50 ± 25% and 8 ± 10%), selleck chemical thus resembling the HR-profile of the Salmonella Typhi- and Paratyphi B-specific responses in vaccinees in this and previous studies [18] and [31]. There are no vaccines

against paratyphoid fever in clinical use. This study presents immunological evidence supporting studies that have previously reported the potential of Ty21a vaccine to protect against paratyphoid fever. There

are four studies evaluating the protective efficacy of either Ty21a or the old parenteral whole cell vaccine (no longer in use) against Salmonella Paratyphi A. Two of these report protection [3] and [18] and two of them do not [19] and [41]. In a study in travelers to Nepal, the majority of those immunized with a whole-cell parenteral vaccine and some MycoClean Mycoplasma Removal Kit with Ty21a, Schwartz et al. estimated an overall efficacy of 95% against Salmonella Typhi and 72–75% against Salmonella Paratyphi A [18]. Meltzer et al. evaluated imported cases of enteric fever in Israeli travelers to India in an observational study. Travellers were immunized with Ty21a until 2001 and after that with parenteral Vi-polysaccharide vaccine. The general attack rate by Salmonella Paratyphi A was 0.26 in 10,000 during Ty21a and 0.79 during Vi-vaccination. Thus, Ty21a was suggested to confer some protection against Salmonella Paratyphi A [3]. In contrast to these studies, in a large field trial in Plaju, Indonesia, Ty21a was not found to protect against paratyphoid A [19]. However, in that study three doses of Ty21a were administered at an interval of seven instead of two days between doses, leading also to a poor protective efficacy of only 42% against typhoid fever.

Additionally, the tribal participants understood how to work with the appropriate tribal IRB and research review boards, an essential component of publishing with Native American communities, and a process that is often poorly understood by outside academics. Several lessons were identified from the development of these workshops. First, there is a clear need for funders and community partners to plan evaluation and publication efforts together from the outset of the intervention work, and include the appropriate tribal leadership and tribal IRB approval boards in this planning. Extending the scope of the workshops

to address the full range of technical assistance needed in data analysis and writing is also recommended. In addition, presenting the workshops

less as one-directional trainings and more as partnerships between implementation High Content Screening experts and academics, each bringing skills that complement and contribute to the partnership, will likely produce the greatest results, as bi-directional Selleckchem Tyrosine Kinase Inhibitor Library learning, cultural humility, and relational accountability proved critical in translating the publication process into practice with these participants. Indeed, the tribal awardee who was able to complete their manuscript, gain appropriate tribal permissions to publish, and submit their manuscript for publication partnered with academic faculty members after the completion of the workshops and continued to utilize the participatory manuscript development process (Fig. 1). What began as a training developed into a true partnership based not on the continued provision of technical assistance but on a collaborative and co-learning process of translating a successful project of the CPPW initiative for publication in the scientific literature. most It is unlikely that this work would have been developed into a publishable manuscript were it not for these workshops and the partnerships that resulted from them. The resulting paper is the first of its kind to report on specific issues around smoking bans

and tribal casinos, providing a strong contribution to the scientific literature and addressing gaps in public health knowledge. The novel participatory manuscript development process outlined here is a pathway by which tribal community health practitioners can contribute their work to the published literature. The manuscripts created by the tribal awardees capture critical implementation knowledge that can guide other practitioners in employing environmental approaches to address obesity and smoking within Native American communities. Such a ‘roadmap’ for implementing environmental approaches does not exist within the current literature and must be informed by those directly implementing such approaches. The translation of research into practice, beyond just within Native American communities, depends on trustworthy, well-written reports, particularly written from a community perspective, which is what this effort facilitated.

In contrast to the Control and Glucantime groups, none of the dogs in the two vaccine treatment groups died of CVL during the first 6 months (Fig. 1). All 15 dogs in the Vaccine group showed initial improvement at this same evaluation point (Table 2; three additional dogs that died of other causes – cardiac infarction, canine distemper, and intoxication – were censored). Selleckchem ABT-199 Similarly, 80% (12 out of 15) of Glucantime dogs and 92% (12 out of 13) of Vaccine + Glucantime dogs showed initial improvement (Table 2). During this initial 6-month period, the survival

curves of the immunotherapy and the immuno-chemotherapy groups (Fig. 1) were significantly different from the Control group (P = 0.003 and P = 0.010 for immunotherapy and immuno-chemotherapy, respectively, by the logrank test), while curves for the chemotherapy alone and Control groups were not significantly different Selleckchem Antidiabetic Compound Library (P = 0.081). At the 36-month follow-up examination, 75% (9/12, exact 95% CI 43–95%) of dogs in the Vaccine group were considered cured. Similar, but slightly lower cure rates of 64% and 50% were observed for dogs in the Glucantime

(7/11, exact 95% CI 31–89%) and Vaccine + Glucantime treatment groups (5/10, exact 95% CI 19–81%), respectively (Table 2). A response rate of the vaccine group was at least comparable, if not better than that observed in animals treated with Glucantime (64% cure) and contrasts with the poor outcome for dogs in the Control arm. The survival curves for the Vaccine alone and Vaccine + Glucantime groups are nearly identical for the first 24 months (Fig. 1), only diverging at the 36-month evaluation mark (not statistically significant, P = 0.487 by the logrank test). While chemotherapy alone showed a relatively rapid decline during the first 6 months after initiation of treatment, its course thereafter mimicked the declines observed for the other two treatment groups. Over the life of the study, aminophylline there were no significant differences in survival rates between the different treatment groups

(P > 0.30 for all pair-wise comparisons by the logrank test). Because of the apparent therapeutic efficacy of the Vaccine when administered alone and because no immunological analyses were performed as part of the Open Trial, a second trial was performed. Trial #2 was performed as a blinded study. Dog allocation into a study group was based on the enrollment order and followed a chart prepared before the start of the study. Mean values ± SD of each study group’s initial clinical scores were 6.4 ± 2.3 (range: 3–9, where a larger score means more severe clinical symptoms) for the Saline group, 6.4 ± 1.5 (range: 4–8) for the Adjuvant group, and 7.5 ± 2.1 (range: 5–12) for the Vaccine group. Thus, at study inclusion the Vaccine-group dogs had a higher mean CS (7.5 vs. 6.4) with a larger range (7 vs.

For subjects with multiple episodes, only the first episode was counted. Exact inference was used, and

follow-up time was accounted for in the calculations. The primary analysis of efficacy was based on the per-protocol subject population. For the per-protocol (PP) efficacy analyses, children with laboratory-confirmed wild type rotavirus disease earlier than 14 days post-dose 3 were considered to be non-evaluable. Also, subjects with at least one gastroenteritis episode that could not be classified as RVGE or non-RVGE with certainty due to incomplete data – and with Selleckchem LY2157299 no other episodes classified as RVGE – were considered non-evaluable. Intention-to-treat analyses were also performed. They encompassed all children who received at least one dose of vaccine or placebo, including protocol violators, and with a timeframe starting immediately following

Dose Src inhibitor 1 as the starting point for case evaluation. The 95% confidence intervals (CI) for the rate reduction (incidence in the placebo group minus the incidence in the vaccine group) were derived using the method of Miettinen and Nurminen [13]. Analysis of immunogenicity was also based on a per-protocol strategy; subjects with laboratory confirmed wild type rotavirus disease between vaccine doses were considered non-evaluable. Seroresponse rates and GMTs were calculated with corresponding 95% CIs based on binomial and normal distributions, respectively. A total of 1960 infants were enrolled in the trial at the Mali sites, of whom 979 received PRV and 981 received placebo; 1013 of the infants were males and the median age at the first dose was 48.0 days (Fig. 1). Table 1 indicates that the number and incidence of serious adverse events (SAEs) that occurred within 14 days of ingestion of each dose among subjects in the vaccine versus the placebo group were comparable. Overall, 5 subjects (0.5%) who received PRV and 6 subjects (0.6%) who received placebo reported a SAE; 4 subjects (1 in Astemizole the PRV group) dropped out of the

study due to a SAE. Among the subjects who received PRV, none of the SAEs was considered to be vaccine-related. A total of 8 deaths occurred within 14 days following any vaccination during the study; 3 deaths (0.3%) were in PRV recipients and 5 (0.5%) in placebo recipients. The most common SAE for both the PRV and the placebo groups was pneumonia, 0.2% and 0.3%, respectively. Two separate serological assays were utilized to address the immune responses elicited by PRV. Serum anti-rotavirus IgA antibodies were measured by EIA because these are useful for measuring immune responses to vaccine in young infants (IgA antibodies are not transferred transplacentally as IgG antibodies are); both the vaccine and placebo groups had a GMT of 1.6 at baseline (pD1) prior to receiving the first dose of vaccine. Table 2 shows that 82.

The GMT levels corresponding to the G1 and P1A[8] serotypes at PD3 were about 4-fold and 3-fold lower, respectively, in the African subjects who received PRV than that observed to these serotypes in similar studies conducted in other regions [6], [18], [20], [21], [22] and [23]. The GMTs for serotypes G2, G3, and G4 for the African infants who received PRV were generally similar (varying from 1-fold, i.e. no decrease [G2] to 1.5-fold [G4])

when compared to the GMTs for the corresponding rotavirus serotypes among subjects who received PRV in the other studies. In addition, for serotypes G1 http://www.selleckchem.com/products/Pazopanib-Hydrochloride.html and P1A[8], the ≥3-fold SNA response rates in African subjects were approximately 50 and 40 percentage points, respectively, lower than those exhibited by subjects in the US, EU, Taiwan, Korea, and Latin America [6], [18], [19], [20], [21], [22] and [23]. For serotypes G2, G3, and G4, the SNA response rates were approximately 30, 25, and 30 percentage points, respectively, lower than those exhibited by subjects in other regions [6], [19], [20], [21], [22] and [23]. Thirdly, in a previous multicenter, open labeled clinical study conducted with 735 randomized subjects

in SCH772984 in vitro Mexico, Brazil, Costa Rica and Guatemala, the immune responses to PRV when administered concomitantly (the same day) with OPV were evaluated [18]. The study showed that (i) concomitant administration of PRV with OPV was well tolerated within the 14 day period following vaccination; (ii) the immunogenicity of OPV was not affected; and (iii) although PRV was immunogenic when administered

concomitantly with OPV (concomitant group), the immunogenicity of PRV, as measured by serum anti-rotavirus IgA GMT, was decreased by 46% when compared to that when PRV was administered 2 weeks prior to OPV (staggered group). However, the sero-response rate, defined by the proportion of subjects with ≥3-fold Linifanib (ABT-869) increases in serum anti-rotavirus IgA titres, was only slightly lower (∼93%), but non-inferior to that in the staggered-use group (∼97%) [18]. Similar results were obtained when SNA responses against the 5 human rotavirus serotypes (G1, G2, G3, G4, and P1A[8]) contained in PRV were evaluated. For serotypes G1 and P1A, the GMT and sero-response rate in the concomitant-use group was lower, but non-inferior, to that in the staggered-use group. For G2, G3, and G4, the GMTs and sero-response rates were generally comparable between groups [18]. Taken together, these findings showed that concomitant use of the PRV and OPV does not interfere with immune responses to OPV but may reduce the level of some immune responses to PRV [18].

In this form chlamydiae are refractory to killing by azithromycin [40] and this may allow for in vivo persistence of the pathogen. In humans, immune responses to resolve C. trachomatis genital tract infections apparently develop over months to years. In uncomplicated, productive chlamydial genital infections, a myriad of host immune responses are elicited

that include innate and adaptive immune mechanisms acting to clear infection and to resist re-infection [41] (summarized in Fig. 1(b) and reviewed in [42]). Chlamydia can, however, also grow inside macrophages and selleck screening library dendritic cells (DCs) to produce persistently infected cells (reviewed in [43]). In both productively and persistently infected chlamydial host cells inflammatory cytokines are released that may induce and sustain tissue damage and host inflammatory responses [44], [45] and [46]. Chlamydial infections induce both innate and adaptive cascades but it is acknowledged that the key effectors for

both protection and pathology pathways are IFN-g and interleukin 17. While high levels of IFN-g are chlamydicidal, low levels can actually result in persistence and this may lead to worse pathology. This highlights the critical nature of the correct balance between mechanisms of protection (as will be required for effective vaccines) versus triggering adverse GDC-0449 price pathology. During active primary infections in women, serum and genital mucosal IgA and IgG antibodies to chlamydial EBs and specific chlamydial proteins including heat-shock (HSP) and plasmid proteins, are usually detected [47]. In patients with current genital infections, the predominant serum responses are maintained for at least 6 months and are mainly IgG1 and IgG3 antibodies [48]. Local IgA antibodies correlate with reduced shedding of the chlamydial organism from the genital tract [49]. However, high titres of local IgA antibodies do not correlate with resolution

of infection, but can act as markers of prior chlamydial infections. The major role antibodies appear Thalidomide to play in clearance of infection is in the enhancement of Th1 activation with CD4+ T cells secreting IFN-g correlating primarily with the resolution of infections. Of note however, is the fact that CD4+ T cell immunity is slow to develop and therefore infections frequently are repeated and chronic. Chronic infections are characterized by genital tract inflammation and infiltration of innate immune cells along with inflammatory mediators to the genital mucosa [for a summary of chemokines and cytokines produced during chlamydial infections see [50]. High levels of IFN-g are found in the cervix and fallopian tubes in women with C. trachomatis genital tract infections [51]. IFN-g delays the developmental cycle of Chlamydia which may result in persistent and in-apparent infections that might contribute to promoting inflammatory damage of the genital tract [52].

2). Interestingly, fV3526 + Alhydrogel™ administered IM showed significantly lower neutralizing titers compared to IM administered fV3526, fV3526 + CpG + Alhydrogel™ and fV3526 + CpG (p < 0.05). The neutralizing titers induced by C84 were only significantly higher AC220 datasheet than SC administered

fV3526 formulations containing CpG (p < 0.05) and IM administered fV3526 + Alhydrogel™ on Day 49. No differences in ELISA or neutralizing antibody GMT were found between mice vaccinated with the same formulation administered IM versus SC except mice receiving fV3526 + CpG. Mice vaccinated IM with fV3526 + CpG had significantly higher ELISA and neutralizing antibody GMT on Day 49 compared to mice vaccinated SC with the same formulation (p < 0.05) ( Fig. 1 and Fig. 2). Anti-VEEV antibodies were below detectable levels in all sham-vaccinated mice. The immunogenicity and protective efficacy of SC vaccination with fV3526 formulations against challenge on Day 56 with VEEV TrD administered by the SC or aerosol route was evaluated. All mice receiving fV3526 formulations survived SC VEEV TrD challenge (Table 4). Further, no clinical signs of disease, including changes in body weight, were observed following SC challenge, demonstrating vaccination with the fV3526 formulations protected mice not only against death but also from development of overt

signs RAD001 chemical structure of illness. In this study, vaccination with C84 protected 80% of mice from SC challenge with VEEV TrD. The only C84 vaccinated of mice that showed clinical

signs of disease were those that ultimately succumbed to challenge. In sham-vaccinated mice, decreased body weight and mild signs of illness were first observed on Day 2 and 3 post-SC challenge, respectively. All sham-vaccinated mice succumbed to disease between Day 5 and 7 post-challenge. Although SC vaccination induced a high level of protection against SC challenge, SC vaccination did not protect all mice against an aerosol challenge (Table 4). High percentages of surviving mice were observed in groups of mice vaccinated with fV3526 + Alhydrogel™ and fV3526 + CpG + Alhydrogel™ where 8 of 9 and 7 of 10 mice, respectively, survived following aerosol challenge. In contrast, ≤40% of mice administered fV3526, fV3526/Viprovex® and fV3526 + CpG survived aerosol challenge when vaccinated SC at the tested dosages. SC vaccination with C84 at 4 μg/dose protected 70% of mice from death. The mean time to death was only significantly different from sham-vaccinated mice when the fV3526 was formulated with CpG + Alhydrogel™ (p < 0.05). Regardless of vaccine formulation, mice in all groups displayed mild clinical signs of disease (decreased grooming) and decreased body weight within 2 days post-challenge that resolved in surviving mice between Day 8 and 15 post-challenge, with mice vaccinated with fV3526 + CpG+ Alhydrogel™ showing resolution of symptoms first (Day 8) followed by mice vaccinated with fV3526 on Day 10.

P. phoenicea Linn. (Sterculiaceae), commonly known in Hindi as Dopa-hariya, is an annual erect herb. The capsules are mucilaginous and used for treatment of diseases of bowels. The water of boiled leaves of plant has been reported to be used traditionally for treatment of inflammatory glands, cough and cold; roots have been reported to be astringent, mildly thermogenic, constipating and febrifuge, and are useful in fever, diarrhea, burning sensation, psychopathy and vitiated conditions of vata and pitta. 4 A review ABT-199 datasheet of the literature did not throw any light on the scientifically

established biological activity of the plant. Thus P. phoenicea have been presently tested to assess the in-vitro antioxidant activity and to establish the hypoglycemic use with specificity to pancreatic α-amylase. 2,2-Diphenyl-1-picrylhydrazyl (DPPH), quercetin, methanol, chloroform, ethanol, acetone, hexane, n-butanol, sodium phosphate buffer, 3,5 dinitrosalicylic acid, α-amylase, potato starch, acarbose etc. The leaves P. phoenicea were collected from the local areas of

Kanpur, in the month of September, 2011. The plants were identified by taxonomist & voucher specimens were preserved at the herbarium section of departmental museum of C.S.J.M. University, Kanpur for future reference. The air dried powder of P. phoenicea leaves (100 g) was extracted EGFR inhibitor by maceration in 70% methanol at room temperature for 24 h and filtered off. The marc was re-percolated again (process repeated four times) for exhaustive extraction. The combined hydroalcoholic extracts (HME) were concentrated under reduced pressure at a temperature not exceeding 35 °C and the residual water was removed by lyophilization. The concentrate was subjected to fractionation with hexane (HXF), chloroform (ClF), ethyl acetate (ETF), n-butanol (BUF) and water (AQF). All the fractions were subjected to activity studies. To obtain polysaccharide fraction (PSF); leaf powder was extracted twice with two volumes of deionized

water under constant stirring for 3 h in a 60 °C water bath. The mixture was filtered and the filtrate was precipitated by the addition of ethanol to a final concentration of 75% (v/v) and the precipitates were collected by centrifugation, washed with acetone, dissolved in deionized water and finally lyophilized. 5 Brown Phosphoprotein phosphatase crude water soluble polysaccharides were obtained. Briefly, a 0.1 mM solution of DPPH in 100% methanol was prepared. To 1 ml of this solution was added 4 ml of sample solution in 40% methanol at different concentrations (1–100 μg/ml). The mixture was shaken vigorously and incubated for 30 min in the dark at room temperature until stable absorption values were obtained. The reduction of the DPPH radical was measured by continuously monitoring the decrease in absorption at 517 nm. In the control, 40% methanol was substituted for samples.6 Lower absorbances of the reaction mixture indicated higher free radical scavenging activity.

Activation of CD4+ T helper lymphocytes was inferred indirectly both by the IgG subclass response as well as by the production of cytokines by NS1-stimulated splenocytes (IFN-γ for a Th1-biased Navitoclax mouse pattern and IL5 for a Th2-biased response). Although IgG subclass response does not seem to be a particularly relevant parameter regarding DENV protection, INF-γ is known to interfere with viral replication and positively correlates with development of protective immunity [16] and [53]. In these two

aspects both FA and LTG33D showed similar behavior after s.c. administration to mice with a more balanced Th1/Th2 immune response pattern regarding animals immunized with NS1 and alum. It is conceivable that the partial protective immunity induced in mice immunized with FA or LTG33D Sorafenib purchase vaccine formulations is closely related to the circulating NS1-specific antibodies, in accordance to previous observations [12], [13], [20] and [21]. More proper evaluation of the protective role of anti-NS1 T cell responses, particularly those involving activation of cytotoxic responses,

will require the development of protein-based vaccines with improved effect on the induction of CD8+ T cell-dependent responses or the testing of more complex vaccine regimens, such as those involving priming with NS1-encoding DNA vaccines. The safety of the vaccine formulation is a major issue for those working on the development of anti-dengue vaccines. Although protein-based subunit vaccines tend to be safer than vaccines based on live attenuated

or recombinant viruses [3], incorporation of an adjuvant 4-Aminobutyrate aminotransferase required for induction of better immune response may result in undesirable side effects, including strong inflammatory reactions. In addition, previous studies showed that NS1-specific antibodies generated during DENV infection may cross-react with different host proteins including proteins exposed on the surface of platelets and endothelial cells [22], [23], [24] and [54]. In our experimental conditions, no hepatic damage, exacerbated inflammatory reactions and, more relevantly, altered hematological parameters have been detected in mice immunized with NS1 admixed with LTG33D. These results further confirm that LTG33D represents an effective and safe vaccine adjuvant, particularly following administrative via parenteral routes. Further experiments should address the question of deleterious effects induced in vaccinated mice following challenge with other DENV types. Collectively the present results demonstrated that anti-DENV vaccines based on purified recombinant NS1 protein adjuvanted with a non-toxic LT derivative represent a new and promising alternative for the development of acellular-based dengue vaccines.