In some cases, such as in Rwanda, no expansion was deemed necessary. In other countries national-level interviewees reported that there had been an expansion or modernisation of the cold chain in preparation for the introduction, although this was generally at the national and sub-national levels, rather LDN-193189 in vivo than in facilities. There was a discrepancy between some national- and facility-level

responses, with the former reporting cold chain expansion whilst the latter reported none. It is not clear whether this discrepancy was because expected expansions had not occurred, or whether facility staff had not realised that new equipment received (sometimes up to a year earlier) was for a particular vaccine introduction. In four countries, the presentation of other vaccines had changed (pentavalent in Cameroon, Kenya and Mali, and PCV in Rwanda), which reduced their cold chain requirement, making capacity available for the new vaccine. Finally, some districts and a minority of facilities reported using adaptive strategies, such as more frequent vaccine deliveries, in order to manage their cold chain space. “There is a problem with the cold chain because the volume [of vaccines] is bigger and districts

are struggling with the cold chain… there is no space. They find more [the health centres] have to take small quantities; we send them the remainder when there is an opportunity. This creates a risk of stock outs Guatemala was an exception in that no assessment was conducted before the introduction and there was no nationally-organised cold chain expansion. Some equipment was reported to have been procured at sub-national levels after the introduction. Interviewees in most countries reported no effect on regulatory policies, with some exceptions. In Kenya, WHO worked to strengthen the country’s Pharmacy and Poisons Board in order to register the new vaccine. It was felt that this would be beneficial for future vaccines. In Mali, the national regulatory process was bypassed for both Men A and PCV vaccines. In almost doing so, some interviewees argued that this weakened national ownership and

domestic regulatory processes. In most countries the new vaccines were not thought to have affected the functioning of their ICCs. However, in Mali (for Men A) and in Rwanda, membership of the committees was extended to additional stakeholders. In Ethiopia some interviewees felt that the ICC had been strengthened by the introduction, particularly because of highly active thematic sub-committees. Vaccination is, in general, well accepted and this was the case for the new vaccines too, with high acceptance and demand reported. Only a minority of facilities reported that they had experienced any resistance from the community regarding the new vaccine – this was most common in Rwanda for the HPV vaccine, or because of a fear of the effect of receiving two vaccinations at once (e.g. in Ethiopia, where PCV and pentavalent were given at the same time).

The source of the increased TNF-α in the maternal circulation in pre-eclampsia is uncertain, however, Ibrutinib in vitro although the placenta is an obvious candidate. Oxidative stress in vitro and in vivo leads to increased tissue concentrations and secretion of the cytokine [7], [8] and [56], and higher concentrations have been reported in pre-eclamptic placentas compared to normal controls [57]. In contrast, a detailed study of non-laboured pre-eclamptic placentas involving sampling from eight independent sites revealed no differences at the mRNA or protein levels compared to controls [58]. These authors concluded that there must be an alternative source of TNF-α, and speculated that

this may be activated maternal leucocytes or the endothelium itself. Despite the widespread recognition that maternal endothelial cell activation represents the second stage of the syndrome, no morphological studies appear to have been

performed on peripheral endothelial cells from women with pre-eclampsia. It is therefore impossible to determine at present whether ER stress occurs in these cells, and whether this could contribute to the raised levels of TNF-α. In contrast, there are several reports describing dilation of the ER in the endothelial cells of the umbilical vessels, indicating a loss of ER homeostasis [59] and [60]. If the same pathology affects the endothelial cells in both circulations during pre-eclampsia, as some authors suspect [61], then it may be that ER stress is not restricted to the placenta in pathological pregnancies. selleck chemicals llc Further

investigations are required to explore this possibility. Endoplasmic reticulum stress represents one component of a set of integrated cellular responses to stress. There are complex interactions between 3-mercaptopyruvate sulfurtransferase it and oxidative stress, and it is likely that in many pathologies the two will co-exist. The extensive secretory activity of the syncytiotrophoblast renders it vulnerable to ER stress, and molecular and morphological evidence confirms high levels in placentas from cases of early-onset pre-eclampsia. There will be many consequences for placental development and function, including a reduction in cell proliferation leading to growth restriction, and activation of pro-inflammatory pathways. Potential therapeutic interventions for pre-eclampsia must therefore be designed to address trophoblastic stress in its entirety, rather than individual stress response pathways. The authors gratefully acknowledge the support of the Wellcome Trust (069027/Z/02/Z and 084804/2/08/Z) for their research. “
“Urology Practice will focus on clinical trends, challenges and practice applications in the four areas of Business, Health Policy, the Specialty and Patient Care.

Serum samples collected at week 4 were examined by pseudo-neutralization assay. For separate inoculation experiments, mice (n = 4 per group) were immunized intramuscularly with Trivalent-1, Separate 16, Separate 18, Separate 58 and corresponding monovalent

vaccines, respectively. Trivalent-1 vaccine and monovalent vaccines were inoculated at one site, while “Separate” SAR405838 vaccines were inoculated at two sites. “Separate 16” indicated that HPV 16 L1 VLPs were injected at left leg separately, while HPV 18 L1 VLPs and HPV 58 L1 VLPs were mixed and injected at right leg. “Separate 18” meant that HPV 18 L1 VLPs were injected at left leg, while other two types at right leg. “Separate 58” also had similar meaning. Serum samples were collected at week 4 and 6 and detected by pseudo-neutralization assay. Production of pseudoviruses were produced according to previous studies [34], [35] and [36]. To be specific, 293TT cells (provided by Prof. John Schiller) were co-transfected with L1, L2 expression vectors (p16SHELL and p18SHELL, provided by Prof. John Schiller; p58SHELL, provided Staurosporine concentration by Prof. Tadahito Kanda) and reporting plasmid (pEGFP-N1, Clonetech). Cells were harvested 48 h after transfection, lysed with cell lysis buffer [0.5% Brij58 (Sigma–Aldrich), 0.2% Benzonase (Merck), 0.2% Plasmid Safe ATP-Dependent DNase (EPICENTRE

Biotechnologies) DPBS-Mg solution], and incubated at 37 °C for 24 h. The cell lysate was extracted with 5 M NaCl solution, and then examined for the titers. The titers of pseudoviruses were defined as the dilution factors at TCID50 (tissue culture infective dose). 2000 TCID50/50 μl pseudoviruses were determined as the inoculating dose for neutralization assay. 293TT cells were incubated at 37 °C in 96-well plate at a density of 1.5 × 104 cells per well for 6 h. Sera were diluted according to a 5-fold dilution. Pseudoviruses were diluted to 2000 TCID50/50 μl. 60 μl pseudoviruses diluent and 60 μl serially diluted sera were mixed thoroughly and incubated at 4 °C for 1 h in a dilution plate. The negative

control was prepared by mixing of 60 μl pseudoviruses diluent and 60 μl culture media. 100 μl of mixture per well were added to the cell culture plate and incubated at 37 °C CYTH4 for 72 h. Cells were digested with trypsinase and transferred to cell sorting tube. The fluorescent cells were detected by FACS (fluorescence activated cell sorting). The percent infection inhibition was calculated with following formula: Percent infection inhibition (%)=1−the proportion of fluorescent cells in the sera incubated samplethe proportion of fluorescent cells in the negative control sample×100 The endpoint titers were calculated as the base 10 logarithm of the highest sera dilution with percent infection inhibition higher than 50%.

Several of the vaccine recipients experienced fevers classified

as grade 3, based on the current adverse event grading scale. Viral shedding that occurred in a subset of the recipients appeared to coincide with sore throat and/or fevers. Based on these findings, clinical testing of V3526 was discontinued. Since a high frequency of adverse reactions has been associated with live-attenuated VEEV vaccines [9], [10] and [16], licensure of a live-attenuated vaccine will likely be faced with significant regulatory obstacles relating to safety. Our strategy to develop a VEEV vaccine was revised to focus on a non-infectious virus vaccine. The use of C84 was not considered for further Selleckchem Navitoclax development because the Department of Defense, in 1996, deemed this vaccine in need of improvement. C84 was last selleckchem manufactured between 1980 and 1981 and the limited supply of C84 vaccine has been in storage for over

29 years and the recent potency and stability of this vaccine are unknown. Manufacture of new lots of C84 is unlikely to occur because this would require re-derivation of the TC-83 stock, followed by GMP production of the TC-83 in a certifiable cell line and further development of the entire TC-83/C84 manufacturing process. In addition, a technical review of the C84 manufacturing records failed to identify a credible source document describing the actual manufacturing process and testing scheme therefore this would also need to be devised. Having a large inventory of GMP manufactured V3526 originally

reserved for the clinical testing, the decision was made to inactivate V3526 for the production of VEEV vaccine candidates that would ultimately replace C84 and be used as a primary vaccine to protect personnel at risk to accidental or intentional VEEV exposure. Studies were initiated using formalin to inactivate V3526 with the intent of producing a vaccine with a significantly reduced adverse reaction profile compared to second V3526, but one that retains potential as a protective immunogen against VEEV infection and performs similarly or better than C84. Formalin inactivation of virus has been successfully used to develop safe and efficacious human and veterinary vaccines since 1955 [17] and most recently, an inactivated vaccine for Japanese encephalitis virus [18]. The use of formalin inactivation for virus vaccine development is attractive from a safety perspective in that the virus cannot revert to virulence, since there is no virus replication during immunization. The use of formalin to inactivate viruses is also attractive from a manufacturing perspective as the inactivation process is relatively simple to develop. In the development of a formalin inactivated VEEV vaccine candidate, we recently developed a method to inactivate V3526 using formalin and established a system of prioritized assays to evaluate residual infectivity and preservation of immunologically essential epitopes [19].

Yield: 76%, m.p. 176-178 °C; IR (KBr, cm−1): 3069 (Ar C–H stretch), 2841 (Aliphatic C–H stretch), 1581–1550 selleck chemical (Amidine C N stretch), 1479–1455 (Aromatic C C stretch), 1170 (C–N stretch); 1H NMR (CDCl3, 400 MHz) δ: 3.63 (s, 2H), 2.29–2.5

(broad, 8H, pip), 7.18–7.23 (m, complex, Ar–H), 7.23–7.49 (m, complex, Ar–H). Yield: 69%, m.p. 190–192 °C: IR (KBr, cm−1): 3065(Ar C–H stretch), 2835 (Aliphatic C–H stretch), 1605–1560 (Amidine C N stretch), 1490–1465 (Aromatic C C stretch), 1189 (C–N stretch) 1H NMR (CDCl3, 400 MHz) δ: 4.26 (s, 2H), 2.38–2.74 (broad, 8H, pip), 7.22–7.49 and 7.49–7.6 (m, complex Ar–H). Yield: 72%, m.p. check details 178–179 °C: IR (KBr, cm−1): 3061 (Ar C–H stretch), 2856 (Aliphatic C–H stretch), 1578–1540 (Amidine C N stretch), 1487–1445 (Aromatic C C stretch), 1210 (C–N stretch) 1H NMR (CDCl3, 400 MHz) δ: 4.22 (s, 2H), 3.24–3.29 (8H, pip), 6.97–7.29 (m, complex, Ar–H). Yield: 80%, m.p. 167–169 °C: IR (KBr, cm−1): 3058 (Ar C–H stretch), 2867 (Aliphatic C–H stretch), 1587–1540

(Amidine C N stretch), 1467–1450 (Aromatic C C stretch), 1205 (C–N stretch) 1H NMR (CDCl3, 400 MHz) δ: 3.77 (s, 2H), 2.37–2.73 (8H, pip), 3.5 (s, 3H), 6.98–7.40 (m, complex, Ar–H). Yield: 75%, m.p. 188–191 °C: IR (KBr, cm−1): 3064 (Ar C–H stretch), 2847(Aliphatic C–H stretch), 1597–1550 (Amidine C N stretch), 1479–1450 (Aromatic C C stretch), 1190 (C–N stretch) 1H NMR (CDCl3, 400 MHz) δ: 4.26 (s, 3H), 2.74–3.24 (8H, pip), 3.8 (s, 3H), 7.23–7.6 (m, complex, Ar–H). Yield: 69%, m.p. 156–158 °C: IR (KBr, cm−1): 3064 (Ar C–H stretch), 2847 (Aliphatic see more C–H stretch), 1597–1550 (Amidine C N stretch), 1479–1450 (Aromatic C C stretch), 1190 (C–N stretch); 1H NMR (CDCl3, 400 MHz) δ: 3.66 (s, 2H), 3.23–3.38 (8H, pip), 2.31 (s, 3H), 7.22–7.6 (m, complex, Ar–H). Yield: 78%, m.p. 160–162: IR (KBr, cm−1): 3060 (Ar C–H stretch), 2847 (Aliphatic C–H stretch), 1597–1550 (Amidine C N stretch), 1479–1450

(Aromatic C C stretch), 1190 (C–N stretch); 1H NMR (CDCl3, 400 MHz) δ: 2.21 (s, 2H), 3.24–3.39 (8H, pip), 4.26 (s, 2H), 7.28–7.6 (m, complex, Ar–H). Yield: 55%, m.p. 125–127; IR (KBr, cm−1): 3054 (Ar C–H stretch), 2845 (Aliphatic C–H stretch), 1595–1557 (Amidine C N stretch), 1470–1440 (Aromatic C C stretch), 1179 (C–N stretch); 1H NMR (CDCl3, 400 MHz) δ: 4.26 (s, 3H), 2.74–3.24 (8H, pip), 3.8 (s, 3H), 7.23–7.6 (m, complex, Ar–H). The mice (22–25 g) were divided into twelve groups, each group contain five animals.

In the CSDS model, a C57BL/6J mouse is repeatedly subordinated by a larger,

aggressive CD-1 mouse for 10 consecutive days (Golden et al., 2011). Each physical bout is followed by overnight sensory contact with the aggressor through a plastic partition. Following CSDS, approximately 2/3 of experimental mice, termed “susceptible,” develop a constellation of depression-like behaviors including social avoidance and anhedonia (Krishnan et al., 2007 and Donahue et al., 2014) as well as metabolic syndrome marked by dysregulated feeding peptides, weight gain and insulin insensitivity (Chuang et al., 2010 and Lutter et al., 2008). Conversely, the remaining 1/3 of mice, termed “resilient,” develop a much milder phenotype, including elevated corticosterone and increased anxiety-like behavior (Krishnan et al., 2007). Similar to human depression, CSDS-induced depression- and anxiety-like behavior

AC220 price can be reversed by chronic, but not acute, administration of antidepressants (Berton et al., 2006 and Tsankova et al., 2006). Importantly, a number of biomarkers identified in humans with MDD are similarly disrupted in susceptible mice following CSDS, further highlighting its utility in studying depression mechanisms (Krishnan et al., 2007, Golden click here et al., 2013 and Robison et al., 2014). The learned helplessness (LH) model is an acute stress paradigm that, similar to CSDS, produces heterogeneous responses, enabling researchers to delineate stress susceptible and resilient animals (Krishnan and Nestler, 2011). The proportion of animals exposed to the

LH paradigm that demonstrate phenotypic resilience ranges from 10% to 80% (Cryan and Mombereau, 2004). In this model, rodents are exposed to repeated inescapable foot shocks followed by a test period in which an easy escape mechanism is made available during shock exposure. Compared to control animals trained with escapable shocks and resilient animals, susceptible animals demonstrate “helplessness,” measured as longer escape latency or failure to escape (Seligman and Beagley, 1975). Like CSDS, the LH paradigm produces numerous behavioral for and physiological changes including weight loss, HPA axis dysfunction, circadian alterations, and reductions in hippocampal synaptic spine number (Krishnan and Nestler, 2011). A weakness of the model is that LH-induced changes are short-lived, usually lasting only 2–3 days and can be reversed with acute antidepressant treatment (Cryan and Mombereau, 2004). Appropriate response to stress involves the coordinated activity of the autonomic nervous system (ANS) and the HPA axis as well as the neural circuits in the hypothalamus, brainstem and forebrain that control their activity (for a comprehensive review, see Ulrich-Lai and Herman, 2009).

However, schistocytes not only are present in TTP, but may be encountered in other TMA’s as well, including SLE [4]. Martin and colleagues performed

a prospective study which included eighteen women diagnosed with HELLP syndrome [16]. These women were treated with plasma exchange postpartum because of 1) persistent evidence of atypical HELLP syndrome > 72 h after delivery (n = 9) or 2) evidence of worsening HELLP syndrome at any time postpartum in association with single- or multiple-organ injury (n = 9). Only patients with class 1 HELLP syndrome (platelet count ≤ 50 × 109/L; ASAT or ALAT ≥ 70 U/L; LDH ≥ 600 U/L) and progressive anaemia with abnormal red blood cell forms were included. Two out of nine patients from the second arm (with worsening HELLP syndrome) died despite the therapy. All patients in the first arm responded well to plasma exchange. GDC-0449 price An earlier study recommended that in case of doubt between

ongoing HELLP syndrome and TTP after delivery, one should wait at least 72 h before considering plasmapheresis [17]. McMinn & George support the ‘72-hour policy’ [18]. They provide additional clinical features for starting with plasma treatment, especially in pregnant or postpartum women who are more likely to have TTP-HUS. They recommend to start with plasma therapy if: – Severe thrombocytopenia and microangiopathic haemolytic anaemia progress for more than three days following delivery. Forskolin nmr TTP that occurs during pregnancy carries the risk of relapse after delivery as well as in subsequent pregnancies. Patients should be instructed about recognizing symptoms and reporting them immediately to a physician [7]. Relapses are common among those with congenital ADAMTS13 deficiency (approximately 40% will relapse), but very rare among patients without congenital ADAMTS13 deficiency.

Most of the relapses of non-congenital TTP occur within the first year and are a single event. Relapses after four years are rarely seen [9]. New onset thrombocytopenia during pregnancy should have a thorough work-up, including a peripheral blood smear to look for schistocytes, to exclude thrombotic microangiopathy’s (TMA’s). Also treatment for TTP should be strongly considered in case of an on-going TMA more than aminophylline 72 h after delivery. The authors declare that they have no conflicts of interests. C.H. Wessel: first draft, drafting, conception, revising, literature search, and final approval. C.E. Andreescu: drafting, revising, treating physician, and final approval. S. Rombout-De Weerd: drafting, revising, attending gynecologist, and final approval. M-D. Levin: drafting, revising, supervision, attending internal medicine physician, and final approval. “
“Pregnancy-associated breast cancer is defined as breast cancer diagnosed during pregnancy or in the first postpartum year. It is the most common cause of invasive cancer in pregnant women and is estimated to occur at a rate of 6.5 per 100,000 live births [1] and [2].

Both methods indicated PDK1 as a sensitive node in the presence of pertuzumab. GSA predicted higher sensitivity to PI3K than LSA. To summarise, most of the parameters identified by LSA in this study represented a subset of GSA derived predictions, but the LSA ranking differed from the GSA ranking. Such differences in the predictions provided by global and local sensitivity methods, as well as the discrepancy between LSA findings presented in different studies, in our opinion, http://www.selleckchem.com/products/Bortezomib.html should not be considered as contradictory, because they originate from

significantly different design and purposes behind local and global types of analysis. Indeed, LSA is normally performed in the proximity of the single solution

identified from the best fitting to a particular dataset, therefore it would be logical to expect that it can help to identify the proteins possessing the most control over the output signal in the particular cell line used for model calibration. For example, LSA of our ErbB2/3 network model could point to the best targets to suppress the pAkt signal in the PE04 NU7441 manufacturer ovarian carcinoma cell line. However, since the model is not fully identifiable, such predictions may not be accurate. In contrast to LSA, GSA works not with a single model solution, but with the whole ensemble of those, generated for N randomly sampled parameter sets. Therefore GSA procedure GBA3 is not intended to find the best targets for inhibition in a particular cell type, but instead it identifies those proteins whose parameters are highly correlated with the output signal of interest in the majority of (but not all) possible network implementations, defined by possible combinations of network parameters. Thus, the GSA of our ErbB2/3 network model points to the proteins, targeting of which is likely to result in a lower pAkt signal in the majority of cells with the same network topology, while the kinetic parameters of individual reactions may differ between the

cells or be uncertain. Because of the differences in technical setup and applicability of LSA and GSA techniques, we suggest that these methods should not be opposed but rather considered as complementary approaches, which, when used together, may allow exploration of a wider range of promising targets and prioritisation for future study. Indeed our GSA procedure predicted that PDK1 could be a promising target to suppress pAkt. In contrast to that conclusion, LSA indicated a very low level of sensitivity to PDK1, both in our study and in Schoeberl et al. (2009) (Schoeberl et al., 2009). Experimental testing of GSA prediction proved that inhibition of PDK1 resulted in a significant suppression of pAkt signal in two cell lines, including PE04, which was used for initial calibration of our model.

The gene encoding FomA was cloned into an E. coli vector-based system [37] for generation Quisinostat purchase of vaccines against bacteria-induced gum inflammation ( Fig. 5) and production of antibodies against VSC emission ( Fig.

6). The E. coli vector-based system has been used in our laboratory to develop various non-invasive vaccines [37]. The E. coli vector (E. coli intact particle) has all E. coli components and exhibits an excellent and natural adjuvant effect that accelerates the evaluation of protein immunogenicity [38]. Most E. coli strains are harmless and are part of the normal flora in human. In addition, an UV-irradiated and non-pathogenic E. coli BL21(DE3) strain was used in this study to construct vaccines targeting FomA. The fact that F. nucleatum is not an indigenous

bacterium in murine oral cavities has hindered the development of animal models of abscesses and halitosis for evaluation of vaccines and drugs against oral infections. In humans, gum pockets appear in an empty space between the root of the tooth and the top edge of the gum. These pockets trap bacteria and are the perfect incubators for bacteria to grow biofilm and produce VSCs. An oral colonization model in which bacteria are administered directly into the mouse oral cavity using PBS selleck products with carboxymethylcellulose [39] and [40] has been commonly used for studying oral infections. Undoubtedly, the model represents the natural route of oral infection. However, the ability to quantify the

bacterial colonization is limited due to the uneven distribution of infected sites. Furthermore, unlike humans, mice do not physically secrete abundant saliva [41]. Thus, it may be inappropriate to use this model for studying the in vivo effect of vaccine-induced secretory immunoglobulin A (S-IgA) on bacterial colonization. Alternatively, injection of F. nucleatum and P. gingivalis into gum tissues of ICR mice recapitulates a model of infection in a gum pocket [22], validating our use of this model for quantification of gum inflammation ( Fig. 4 and Fig. 5) in this study. It has been shown that prior exposure of mice to F. nucleatum modulates host response to Linifanib (ABT-869) P. gingivalis [42]. All the T-cell clones derived from mice immunized with F. nucleatum followed by P. gingivalis were T-helper type 2 (Th2) subsets, while those from mice immunized with P. gingivalis alone belonged to T-helper type 1 (Th1) subsets based on the flow cytometric analysis and cytokine profiles [43]. Other studies have shown that exposure of mice to F. nucleatum prior to P. gingivalis interfered with the opsonophagocytosis function of sera against P. gingivalis [42]. However, our results demonstrated that mice immunized with E. coli BL21(DE3) FomA did not increase the severity of P. gingivalis-induced gum swelling ( Fig. 5A), suggesting that vaccination with F. nucleatum FomA may not alter the host susceptibility to other oral bacteria. After injection of F. nucleatum and P.

Indeed, the Kenya Ministry selleck inhibitor of Public Health and Sanitation intends to introduce rotavirus vaccine by 2013. The trial (Merck protocol V260-015) was funded by PATH’s Rotavirus Vaccine Program with a grant from the GAVI Alliance; the trial was co-sponsored by Merck & Co., Inc. This study, under protocol V260-015, was designed, managed, conducted, and analyzed by the co-sponsors in collaboration with the site

investigators and under the supervision and advice of the Data and Safety Monitoring Board. We wish to thank the study participants and their families, and the entire study team. We wish to acknowledge the assistance from the KEMRI/CDC HIV laboratory http://www.selleckchem.com/products/PLX-4032.html for all HIV diagnostic testing, and the CDC GAP team for assistance in linking the study participants to appropriate HIV care and treatment. We are grateful to Michael J. Dallas and Donna Hyatt at Merck for numerous additional data analyses, and we also thank Michele L. Coia, and Margaret Nelson, also at Merck. We appreciate the support received from Kristen Lewis, J.C. Victor, and A. Duncan Steele at PATH. This manuscript is published with the permission of the

Director, KEMRI. KEMRI/CDC is a member of the INDEPTH Network. Conflict of interest statement: SBR is an employee of Merck and Co., and may own shares in the company. MC was an employee of Merck & Co., and owned shares in the company when

the study was conducted. The findings and conclusions in this report are those of the authors and do not necessarily represent the official position of the Centers for Disease Control and Prevention. No other conflicts of interest are reported. “
“Diarrheal diseases constitute CYTH4 one of the top two killers of infants and young children <5 years of age worldwide, the vast majority occurring in developing countries [1]. It has been estimated that each year rotavirus gastroenteritis (RVGE) is responsible for approximately 2 million hospitalizations and 453,000 deaths among children <5 years, representing 37% of all deaths due to diarrhea in this age group [2]. Although rotavirus (RV) vaccines had been shown to be highly efficacious in preventing severe RVGE in infants and toddlers in industrialized countries [3] and [4], their efficacy in infants and young children in the developing world was questioned by the World Health Organization (WHO). Differences in host populations (e.g., differences in the gut microbiome), associated health conditions (e.g.