In countries that have adopted rotavirus vaccine in their childhood immunisation programmes,

evidence of impact has been striking [10]. Importantly, evidence of reduction of diarrhoea deaths following routine rotavirus vaccination has recently been published from Mexico [11]. Finally, a recent study of Rotarix from Mexico and Brazil has documented that the benefit of routine rotavirus vaccination (reduction NSC 683864 ic50 in childhood diarrhoea hospitalisations and deaths) far outweighs a small, short term risk of intussusception that may be associated with use of this live, oral vaccine [12]. In 2009, following review of vaccine performance in Africa and resource-poor settings in Latin America, a global recommendation for rotavirus vaccine use was issued [13]. This recommendation was in part SB431542 in vitro informed by the results of a phase III, placebo-controlled clinical trial of RIX4414 undertaken in Malawi and South Africa [14]. In this study, vaccination with RIX4414 significantly reduced severe rotavirus gastroenteritis episodes in the first year of life in both settings, although efficacy was lower in Malawi (49.4% [95% CI 19.2–68.3]) compared

with South Africa (76.9% [56.0–88.4]). Notable findings in Malawi included a high incidence of severe rotavirus disease, a wide diversity of circulating rotavirus strains and a high exposure to natural rotavirus infection early in infancy [14]. This manuscript reports on vaccine performance and circulating rotavirus strains in Malawian children for an extended period of up to 24 months of age. A phase III, double-blind, randomized, placebo-controlled multicentre study was undertaken in South Africa and Malawi as previously reported [14]. In Malawi, children were enrolled

in four health centres in Blantyre, the largest city in the Southern region of the country. Healthy infants were randomized at their first Expanded Program on Immunisation (EPI) clinic visit into three groups. One group received three doses of placebo at 6, 10, and 14 weeks of age and a second group received three doses of RIX4414 at the same age. The third group received placebo at 6 weeks and RIX4414 found at 10 and 14 weeks. The study was designed to reflect, as far as possible, the conditions under which rotavirus vaccine would be administered under “real-life” conditions in a typical African infant population. Thus, all EPI vaccines including oral poliovirus vaccine (OPV) were co-administered; HIV-infected or -exposed infants were included; and no restriction on breastfeeding around the time of vaccination was imposed. Enrolment was conducted between October 2006 and July 2007. Subjects were initially followed-up until 12 months of age [14].

Finally, the reaction was finished as described above. Lysate of heart tissue was obtained from post mortem normal human myocardium, separated by 10% SDS–PAGE and blotted onto nitrocellulose membranes as described [29] and [30]. The blots were divided into strips and blocked with Tris buffered saline containing 5% of skim milk. The strips were sequentially treated with a pool of immunized and non-immunized (controls) transgenic mice sera, followed by a treatment with anti-mouse IgG alkaline phosphatase and revealed in the presence of NBT-BCIP solution

(Invitrogen, USA). Positive control: mouse anti-porcine myosin serum. Negative control: pre-immune mouse serum. After 12 months, immunized mice and controls were sacrificed and the heart, liver, spleen, brain, KRX-0401 kidney and articulations were collected. The tissues were immediately fixed in PBS containing 10% formaldehyde,

paraffin-processed, and histological sections were evaluated after staining with hematoxylin and eosin (H&E). StreptInCor was able to induce a robust immune response in all HLA class II transgenic mice studied 28 days after immunization. DQ6 and DQ8 Regorafenib order transgenic mice presented the highest titers of total IgG (>1:12,800) (Fig. 1). We observed variable IgG production among the DR4 transgenic mice (>1:800 and 1:12,800) (Fig. 1). Among the IgG isotypes, IgG1 and IgG2b were induced in all the transgenic mice and IgG3 was only produced in the DQ8 transgenic mice (Fig. 1). Control animals receiving only aluminum hydroxide did not present any reactivity to StreptInCor (data not shown). To verify whether the immune response against StreptInCor was specific, we analyzed the reactivity of the immunized transgenic mice recognize the immunogenic vaccine epitope in the heterologous M1 recombinant (rM1) protein. Our results showed that all DR2, DR4, and DQ8

mice and 3 out of 6 DQ6 mice were reactive against rM1 protein (Fig. 2). It is interesting to note that the levels of anti-IgG antibodies against rM1 protein were lower (1:100 to 1:3200) (Fig. 2). Additionally, none of the transgenic mice developed antibodies against either porcine cardiac myosin (Fig. 2) or human myocardium-derived proteins (Fig. 3) indicating the absence of cross-reactivity about with cardiac proteins. All the mice were followed for one year before they were sacrificed. The amount of IgG was evaluated at 1, 4, 8, and 12 months. Our results showed a decreased amount of IgG present in immunized mice after 4 months (Fig. 4), and most of the mice maintained low reactivity IgG titers until 1 year post-immunization (Fig. 4). We analyzed the humoral immune response of HLA class II Tg-mice against 8 StreptInCor-derived overlapping peptides that cover the entire vaccine epitope sequence and encompassed the possibilities of processing and presentation by antigen-presenting cells (APCs) as previously described [22]. Our results were similar to those observed in humans. Both, HLA-DR and -DQ Tg-mice recognized most of the peptides (Table 1).

g. from the World Health Organization [WHO] and EMA [8] and [9]), they may have to be adapted according

to the specificity of each vaccine. In the US, ‘Investigational New Drug’ (IND) submission is a major milestone in the vaccine development process. Before starting clinical trials, vaccine developers must submit pre-clinical Cell Cycle inhibitor data and the agenda for future clinical trials of their IND to the US Food and Drug Administration (FDA). The information requested is intended to put the product development plan into perspective so that the US FDA can anticipate the needs of the vaccine developer. In Europe, regulatory permission to conduct a clinical trial, including authorisation from relevant independent ethics committees and/or institutional review boards, must be obtained from the competent authorities of the EU Member State where the clinical trial is being performed. This authorisation, however, is not to be considered as scientific advice on the development programme of the Investigational Medicinal Product (IMP) that is being tested. Scientific advice can be obtained independently, on a voluntary and, with some exceptions, on a fee-for-service basis from PCI-32765 clinical trial EMA and/or from National Regulatory Agencies. In the absence of such advice, it is possible that EMA may consider that the trial design,

assays, biomarkers, endpoints or comparators are neither relevant nor sufficient to register the product. Regulatory agencies such as EMA, US FDA and international organisations such as WHO base their guidelines/evaluation criteria on the scientific evidence the obtained by their own services or from external expert groups. EMA, for instance, relies mainly on data provided by external research groups. With the aim to provide EMA with the scientific evidence it needs to address issues impacting the licensure of new and improved vaccines, EVRI will establish expert groups to address emerging issues regarding regulatory approval of vaccines such as assay validation, standardisation

and harmonisation; validation of biomarkers and endpoints for clinical trials; reference animal models; comparative studies. It will also be the link between those groups and EMA. During the preparation and implementation stages, discussions with EMA will be conducted in order to specify the needs and define the services to be provided by EVRI. Vaccinology is multidisciplinary and multi-professional by nature. It covers basic research in immunology and microbiology at one end of the vaccine development process, translational research and product development in the middle, and logistics, clinical delivery and public health education at the other end. Some aspects of vaccinology are included in various curricula: medicine, biological sciences, pharmaceutical sciences, nursing, midwifery, and biotechnology. Given the huge impact of vaccinology on global health, it merits recognition as a discipline in its own right.

When applied to the present study, the protective efficacy of Ty21a would increase in the order Salmonella Paratyphi A → Salmonella Paratyphi B → Salmonella Typhi. A lower efficacy against Salmonella

Paratyphi than Salmonella Typhi appears consistent Trametinib in vitro with previous reports from field trials and from travelers [17] and [18]. Along with the increasing efficacy against typhoid fever, an increasing number of vaccine doses is expected to be associated with an increase in the cross-protective efficacy: even though a significant protection against typhoid fever is achieved already with three vaccine doses, the levels of cross-protection against paratyphoid fever appear somewhat lower in field trials [17], consistent with the lower numbers of plasmablasts in this study. Administration of four doses, as recommended in the US, could result in a further increase in the cross-protective efficacy. Even with three doses, if the response in an individual would be too weak to confer full cross-protection, the question remains whether the level of antibodies achieved would be enough to contribute to a milder outcome of the learn more disease than in unvaccinated persons. The homing

profiles of Salmonella Typhi- and Salmonella Paratyphi B-specific cross-reactive plasmablasts in the vaccinees were similar to one another and also similar to the pathogen-specific plasmablasts in enteric fever. In both groups, a pronounced targeting to the intestine was observed, as interpreted by the very high expression of intestinal HR, α4β7 and lower expression of l-selectin. Such a profile appears beneficial with respect to the

intestinal transmission route both of the vaccine and of the enteric fever. The similarities between natural infection and Ty21a in eliciting a gut-directed cross-reactive immune response against Salmonella Paratyphi add to the view that Ty21a closely imitates a natural typhoid infection. In conclusion, this study is the first to show that the Ty21a vaccine and enteric fever both elicit cross-reactive humoral immune responses to both Salmonella Paratyphi A and B. The potential cross-protection Methisazone against paratyphoid fever conferred by these immune mechanisms encourage further efficacy studies. As there are no vaccines against paratyphoid fever in clinical use, even a partial protection with a currently available vaccine would be valuable. The study was partly supported by the specific Finnish governmental subsidy for health science research (SP) and partly by Crucell Switzerland AG (formerly Berna Biotech). The funding sources had no involvement in study design, data collection, analysis, interpretation of data, writing of the report or in the decision to submit the article for publication. We thank Dr.

[5] trial, and (2) the proportion of mild, moderate and severe varicella among vaccinated NVP-BKM120 solubility dmso individuals [5] and [21]

(see Appendix A for model fit). Five different vaccine efficacy model structures were investigated, by setting parameters such as the proportion of primary failures (F) or the degree of protection in vaccinated susceptibles (1-b) to 0. For each vaccine efficacy model structure, we identified, using weighted least squares, the combination of parameter values that maximised the goodness of fit. For our base case scenario, we chose the parameter combination that produced the best overall goodness of fit (see Table 1 for values and appendix for model fit). In the sensitivity analysis, we used: (1) the remaining four good fit vaccine efficacy parameter combinations, and (2) the worst and base case scenarios

from Brisson et al. [9]. Model predictions are based on vaccine coverage estimates from the province of Quebec, Canada. Quebec introduced an infant vaccination program in 2006, with a 5 year catch-up campaign in preschool and grade 4. For our base case, we assume that coverage is 90% in 1-year olds, and that 19% and Venetoclax in vitro 6% of 5 and 9 year olds are vaccinated each year. We investigated the impact of adding a second dose of varicella vaccine in 2010 (4 years after the introduction of 1-dose varicella vaccination) using three scenarios: (1) infant program (2 doses given at 1 year of age, 90% coverage), The base case model qualitatively reproduces U.S. varicella surveillance data (Fig. 2(a)). In addition, the base model predictions are in line with surveillance data from Washington State, which shows a very small increase in zoster incidence following varicella vaccination (Fig. 2(b)). However, our model does not support findings from Massachusetts Parvulin [29], which report nearly a two-fold increase in zoster incidence following varicella vaccination, in the period 1999–2003 (Fig. 2(b)). The model predicts a small increase in zoster incidence in the first years following the start of vaccination because of the relatively slow decline in varicella cases (i.e. population continues to be significantly

exposed to VZV). Following the start of 1-dose mass infant varicella vaccination (with catch-up in 5 and 9 year olds), the base case model predicts an immediate steep decline in cases, which lasts for more than 10 years (Fig. 3(a)). During this time, susceptibles (primary failures, individuals not vaccinated) slowly accumulate and once a threshold of susceptible individuals is reached, an epidemic occurs. After this epidemic period, the infection settles into a new equilibrium with a 40% lower number of annual varicella cases than before vaccination. However, 80% of varicella cases at equilibrium are breakthrough infections, which are generally considered to be mild. Of note, the base model predicts that the mean age at infection will increase over time since the start of the vaccination program.

Actually, this is true only in previously exposed, adult

VX-809 molecular weight individuals in which a BCG vaccination scar was present along with a history of living in a setting of environmental mycobacteria, such as Brazil. We were not, however, able to reproduce those findings in monocytes from naïve individuals; rather, necrosis was quite evident, particularly at 24 h of infection. The reasons behind this are speculative; perhaps this is due to a higher amount of circulating immature immune cells or to a lack of exposure to mycobacterial antigens. In fact, because of decreased production of Th1-cell-associated cytokines, it is thought that the neonatal innate immune system is generally impaired or depressed. The bias against Th1-cell-polarizing cytokines leaves the newborn susceptible to microbial

infection and contributes to impairment of the neonatal immune responses to most vaccines, thereby frustrating efforts to protect this vulnerable population [15]. The ability of pro-inflammatory cytokines to induce spontaneous abortion is likely to be an important reason for the strong bias of the maternal and fetal immune systems of many mammalian species towards Th2-cell-polarizing cytokines [Reviewed by 16]. After birth, there is an age-dependent maturation of the immune response. http://www.selleckchem.com/products/Erlotinib-Hydrochloride.html Thus, the higher necrosis levels in these subjects might reflect still very immature monocytes in which BCG could behave as a moderate virulence organism. In fact, in immune compromised individuals, such as those co-infected with HIV, BCG is considered a life-threaten organism due to impairment of the immune response [17]. In

an attempt to better explore the apoptosis and necrosis findings, we also measured levels of pro-inflammatory cytokines, the key components during cell-death induction. TNF-α is a pleiotropic cytokine during Th1 immune responses and it is also closely connected to mechanism of cell death, given this cytokine is intrinsic ability to activate caspases and thus induce apoptosis Ribonucleotide reductase [Reviewed by 18]. This topic was considered in a previous study, where M. avium-induced macrophage apoptosis was dependent on the function of TNF-α because it was inhibited by the presence of anti-TNF-α antibodies [5]. In fact, true TNF-α bioactivity was actually reduced in supernatants from M. tuberculosis-infected cell cultures due to neutralization when soluble TNFR2, but not TNFR1, was released during macrophage infection [Reviewed by 6]. Accordingly, we observed a significant and progressive increase in the levels of TNF-α and IL-1β during in vitro BCG infection of monocytes from HD individuals that was consistent with the increased rate of apoptosis in this group. This phenomenon was also supported by the fact that the apoptosis levels were not dominant in the immature, naïve group. There, TNF-α level is unchanged, while IL-1β tends to increase over the time during BCG infection.

Protease and phosphatase inhibitors (Calbiochem, San Diego, CA) were added to RIPA buffer Bafilomycin A1 chemical structure at 1:100 for a final concentration of 0.1%. Protein concentrations were determined using the BCA colorimetric method against

known concentrations of BSA (Pierce, Rockford, IL). For SDS-PAGE, lysates were made 2 mg/ml with laemmli reducing sample buffer, heated at 95 °C for 5 min, centrifuged at 15,000 × g for 1 min and left on the bench to come to room temperature. Protein standards (BioRad, Hercules, CA) were loaded next to each 40 μg of lysate and resolved on NuPAGE 4–12% Bis/Tris gels (Invitrogen). Gels were equilibrated for 30 min and proteins were then transferred to nitrocellulose (Amersham, Uppsala, Sweden) at 5 V constant voltage overnight in Towbins Transfer Buffer using semi-dry transfer (BioRad). The membranes were blocked in 5% NFDM/TTBS at room temperature Epigenetics Compound Library for 1 h with constant rocking. Membranes were then cut down into eight identical blots each with a molecular weight standard (BioRad) run adjacent to 40 μg of lysate. Each membrane was incubated at room temperature for 1 h in normal, pre- or post-vaccination sera diluted 1:1000 in 5% NFDM/TTBS. Membranes were washed six times for 10 min each in TTBS. Membranes were then incubated at room temperature for 1 h in rabbit anti-canine IgG HRP-conjugated secondary antibody (Jackson Immunoresearch,

West Grove, PA) at 1:50,000 in 5% NFDM/TTBS and washed as described above. Immunoreactive bands were then detected using ECL Western Blotting Detection System (Amersham) by exposing membranes to HyBlot CL autoradiography film (Denville Scientific, Metuchen, NJ). Sections were cut at 5 μm using a microtome, mounted onto CapGap slides, and rehydrated according to standard protocols. Mounted slides were pretreated with a citrate buffer, 6.0 pH, in a Black & Decker (Hampstead, MD) steamer for 30 min, with a 10 min L-NAME HCl cool down. Standard 2D immunostaining procedures using peroxidase-labeled streptavidin and DAB chromagen on an automated TechMate 500 capillary gap immunostainer

(Ventana Medical Systems, Tucson, AZ) were used. Hematoxylin counterstaining was used to provide cytological detail. Rabbit anti-bovine GFAP antibody was used at a 1:20,000 dilution (Dako, Carpenteria, CA). The tumor was negative for neuronal markers (NeuN and synaptophysin). Two M.D. neuropathologists and 5 veterinary pathologists concurred that the neoplasm was a diffuse astrocytoma, gemistocytic subtype (WHO grade II) based on the histological and immunohistochemistry results. This work was supported by grants from the National Institutes of Health/National Institute of Neurological Disorders & Stroke (NIH/NINDS)NIH IR21-NS055738 (JRO), American Cancer SocietyRSG-09-189-01-LIB (JRO), Randy Shaver Cancer Research and Community Fund (JRO), Children’s Cancer Research fund (JRO and GEP).

The primary endpoints of the study were antibody titers to yellow fever in mIU/mL and categories (seropositive: selleck screening library titer higher than

2.7 log10 mIU/mL or reciprocal dilution higher than 10). Seroconversion was defined as quadrupling of pre-vaccination antibodies against yellow fever. Serologic testing for rubella antibodies (ELISA, Enzygnost® Anti-Rubella-Virus/IgG, Dade Behring, Germany) and for mumps antibodies (ELISA, Enzygnost® Anti-Parotitis-Virus/IgG, Dade Behring, Germany) were performed at the Respiratory Virus Laboratory of Instituto Oswaldo Cruz (FIOCRUZ, Rio de Janeiro), and the results expressed in International Units per milliliter of serum (IU/mL). The primary endpoints for rubella were post-vaccination antibody titers in IU/mL and categories (non-reactive: <4.0 IU/mL; inconclusive: 4.0–6.5 IU/mL; reactive: >6.5 IU/mL). For mumps, sera with antibody titers ≥231 U/mL were considered reactive, implying that borderline BEZ235 supplier titers were considered seropositive. Both for rubella and for mumps, seroconversion was defined as seropositivity in subjects who were non-reactive before vaccination. The proportion of seroconversion, the

geometric mean titer (GMT) and proportion of adverse events after vaccination were compared across groups defined by types of yellow fever vaccine and interval between vaccinations. The statistical significance of differences in proportions was analyzed by chi-square test, whereas for the differences in the means of antibody

titer logarithms the Student’s t test was used. Reverse cumulative distribution plots were constructed to display the complete range of serologic data. The level of significance was 5%. Data were analyzed using SPSS version 13.0 (SPSS, Inc., Chicago, IL). The complete cohort (“intention-to-treat”) from for analysis of adverse events included children with data on reactogenicity, even those who failed to adhere to the study protocol. For the analysis of immunogenicity, the cohort consisted of all subjects randomized to YFV types, keeping subjects in the groups to which they were randomly assigned. The interaction of the MMR vaccine and yellow fever was evaluated by comparing the proportions of seroconversion for yellow fever in individuals in subgroups defined by the interval between vaccinations. Children without post-vaccination serological test, or who violated eligibility criteria were disregarded in “per-protocol analysis”. With this approach, analysis of immune response considered the vaccine actually administered, regardless of randomization group. The probability of seroconversion was adjusted for the covariates of interest (age, sex, pre-vaccination seropositivity, time between pre- and post-vaccination blood collection, and comorbidity) in a logistic regression model.

These findings provide exciting insight into the biology of resilience as well as a potential therapeutic avenue. In addition to dopaminergic innervation from the VTA, the NAc also receives glutamatergic innervation from the PFC, GSK J4 molecular weight amygdala, thalamus and hippocampus. Decreased PFC activity, as measured by cerebral blood flow and glucose metabolism, is the most robust finding reported by human imaging studies of depressed patients (Mayberg, 2009). Findings from rodent

models are generally consistent with those in humans and suggest that stress leads to hypofrontal function. First, chronic stress leads to significant atrophy and synapse loss on glutmatergic neurons in the PFC (Christoffel et al., 2011b, McEwen and Morrison, 2013 and Duman and Li, 2012). Importantly, loss of synapses has also been observed in the PFC of humans with MDD (Kang et al., 2012). Covington et al. (2010) reported decreased expression of the immediate early genes (IEGs) zif268 (also termed egr1) and arc in human postmortem prefrontal cortical tissue of unmedicated depressed patients. IEG expression was also reduced in the ventromedial Selleckchem SAR405838 PFC of susceptible mice, but was unchanged in resilient mice following CSDS. As IEG expression is considered a representation of brain activity, these results suggest that activity is reduced in susceptible mice and depressed patients, but maintained in resilient mice. Optogenetic stimulation of the mPFC of susceptible

mice had an antidepressant effect, reversing social avoidance and anhedonic behavior, and indicating that burst firing in mPFC neurons promotes behavioral resilience. Optogenetic induction of burst firing also increased expression of the IEG

c-fos. The many NAc is another region of brain reward circuitry that undergoes significant stress-induced remodeling of glutamatergic synapses. Following CSDS, susceptible, but not resilient, mice have an increased density of glutamatergic synapses on NAc MSNs, which correlates with increased mini excitatory postsynaptic potential (mEPSP) frequency (indicative of more functional glutamatergic synapses or altered presynaptic release). Data from our lab using circuit specific optogenetic tools to stimulate glutamatergic neurons terminating in the ventral striatum (vStr), find that glutamatergic projections from the intralaminar thalamus (ILT) promote susceptibility to CSDS whereas stimulation of projections from the PFC exert opposite effects (Christoffel, D.J. et al., Soc. Neurosci. Abstr. 705.08, 2013). Both chronic, viral-mediated expression in the ILT of tethered toxins (tToxins, designed to inhibit excitatory transmission by selectively blocking calcium influx at the pre-synaptic voltage gated Ca2+ channels Cav2.1 and Cav2.2) and rapid optogenetic inhibition of ILT–vStr terminal projections prevented social avoidance and reduced MSN stubby spine density (a parameter that is known to positively correlate with social avoidance).

The number of serotypes causing RVGE of any severity during Year 2 in the HRV_2D, HRV_3D and placebo groups were 3, 1, and 5, respectively for G1P [8]; 2, 2, and 4 respectively for G2/P [4] or P [6]; and 1 case of G12P [6] in a HRV_2D recipient. The ATP analysis for seroconversion consisted of 205 subjects from Cohort 1 (70 subjects in the HRV_2D group, 66 subjects in the HRV_3D group and 69 subjects in the placebo group) from whom blood had been obtained prior to the first dose and 1 month following the third dose of study vaccine. The seroconversion rate MS-275 research buy in the HRV_3D group was moderately higher (66.7%; 95% CI: 54.0–77.8%), although not significantly, than in the HRV_2D group (57.1%; 95% CI: 44.7–68.9%)

(Fig. 2). Similarly, a trend toward higher GMCs was observed in the HRV_3D group (94.3 U/mL; 95% CI: 56.5–157.4 U/mL) than the HRV_2D group (59.4 U/mL; 95% CI: 37.5–93.9 U/mL). This analysis confirmed protection against severe RVGE by Rotarix over 2 consecutive rotavirus seasons in South African children for the combined endpoint of infants who had received either a 2-dose or 3-dose HRV schedule during infancy. The 59% reduction of severe selleck products RVGE

over 2 consecutive rotavirus seasons in the pooled cohort of HRV recipients was lower than the point-estimate observed during the first rotavirus season (77%; 95% CI: 56–88), which also included a combined analysis of Cohort 1 and Cohort 2 subjects enrolled in the study in South Africa. Interestingly, these results are similar to that observed in another vaccine study in 3 African countries with the pentavalent rotavirus vaccine [4]. In that study, efficacy against severe rotavirus diarrhea during the first two years of age in 3 African countries, was 39.3%; although vaccine efficacy against severe rotavirus diarrhea in the first year of life was 64.2%. This is distinct from the situation reported in Latin America, the US, Europe, or middle-income countries in Asia, where the level of clinical protection was maintained at very similar levels

over 2 years [7], [8], [9] and [10]. One of the Phosphatidylinositol diacylglycerol-lyase possible explanations for this difference, besides the higher immunogenicity and higher point-estimate of efficacy in the European and pan-American studies, is the age at which children are infected with rotavirus. In Africa, rotavirus infections occur commonly in young infants between 3 and 12 months of age, where >75% of children with severe rotavirus gastroenteritis from hospital-based studies are observed [13], [21], [22] and [23] and only approximately 10% of rotavirus disease requiring a visit to hospital or the outpatient clinic was in the 12- to 18-month-old group in several African countries [24]. On the other hand, studies from Europe indicate that while rotavirus infection peaks in children 6–24 months of age [25], 40% of infection occurs in the group 12–23 months of age [26].