In wt mice significant levels of SIgA were observed locally in the nasal and lung lavages, but also in the peripheral vaginal lavages after i.n. BLP-SV administration, while mice vaccinated i.m. with SV alone showed decreased or absent SIgA levels (Fig. 3A). In contrast to the levels observed in JQ1 wt mice, low to absent SIgA levels

were measured in nasal (Fig. 3B) and vaginal (Fig. 3C) lavages in TLR2KO mice. In addition, very low levels of SIgA antibodies were measured in mucosal lavages when SV alone was administered either i.n. or i.m. The data show that local and peripheral SIgA production after i.n. BLP-SV administration depends on the interaction of BLP with TLR2. Next, we explored if the observed enhanced IAV-specific B-cell response after i.n. BLP-SV vaccination in wt mice compared BI 6727 solubility dmso to TLR2KO mice as shown in Fig. 1 also affected IAV-specific systemic antibody production. We observed an enhanced IAV-specific IgG response in serum of wt mice

after booster vaccination with i.n. BLP-SV in contrast to vaccinated TLR2KO mice, which resembles the IgG response of the SV vaccine in wt mice (Fig. 4A and B). Then, we investigated if IgG class switch to IgG1 or IgG2c after i.n. BLP-SV vaccination also depended on TLR2 interaction. Here, we showed that the BLP-SV-induced class switch to IgG2c depended on the interaction of BLP with TLR2 (Fig. 4C). In contrast, the IAV-specific IgG1 response was not reduced in TLR2KO mice compared to wt control mice (Fig. 4D). We therefore suggest that the increase in IgG1 in the TLR2KO mice after both i.n. BLP-SV and SV immunization might indicate an inhibitory role for TLR2 on class switch to IgG1. Thus, both IAV-specific systemic Th1 cell and subsequent B-cell responses that were associated with enhanced

IgG2c antibody production induced after i.n. BLP-SV vaccination depended on interaction of BLP with TLR2. Earlier studies have demonstrated in vitro that BLPs can activate TLR2 signalling in human TLR-transfected HEK cells and mouse dendritic cells [17]. This implies that TLR2 activation by BLP could be responsible for enhancing adaptive immune responses in vivo, but formal proof for this was lacking. Previous studies showed that the effect of TLR2 triggering on the outcome of the immune second response in vivo is variable and depends on several unknown factors: TLR2 can form heterodimers with other TLRs, specifically TLR1 and TLR6 [18] and [19] and TLR2 is expressed by a plethora of immune cells [21], [22], [23], [24], [25] and [26]. Furthermore, the immunostimulatory activity of BLPs in vivo could be the result of activation of innate receptors different from TLR, for example, NOD receptors. Here, we provided clear evidence for an essential role of TLR2 in the BLP-dependent activation of the IAV-specific adaptive immune responses in vivo upon nasal vaccination. Moreover, we showed that both local and systemic IAV-specific IFN-? T-cell (Fig. 1A and C) and B-cell responses (Fig.

3C) was smaller than those in serum from poly(I:C)-immunized mice ( Fig. 3A), implying that general humoral components in saliva reduced KSHV infection to 293 cells. Consequently, these data suggest that the body fluids from KSHV-immunized mice are able to reduce the efficacy of in vitro KSHV infection to 293 cells. Some of the KSHV-encoded proteins were identified as immunogens in human so far [4] and [34]. Among them, six KSHV-encoded proteins, K8, K8.1, ORF26,

ORF59, ORF65, and ORF73 (LANA-1) were synthesized in E. coli as GST-fusion proteins to ascertain immunogens in KSHV-immunized mice [4]. Western blot revealed that GST-K8.1 and ORF59 proteins reacted more strongly with the serum from KSHV-intraperitoneally immunized mice than did other proteins ( Fig. 4A). The serum also produced faint bands in the lanes of K8, ORF26, and ORF65 proteins, but not of ORF73C and ORF73N. Immunofluorescence Selleck VE 822 assays using the serum and anti-KSHV-encoded protein antibodies demonstrated that the stain of the serum overlapped with those of K8.1 and ORF 59 frequently, of ORF26 and ORF65 partially, but not of K8 and ORF73. These data suggest that the serum of KSHV-immunized mice recognized selleck chemicals mainly K8.1 and ORF59 protein, partially ORF26 and ORF65, but not K8 and ORF73. To know whether the KSHV-encoded proteins induce humoral

immunity in mice, these proteins with poly(I:C) were immunized intranasally and intraperitoneally to mice. IFA using KSHV-infected cells Thymidine kinase revealed that intranasal and intraperitoneal immunization with the protein induced serum IgG and IgA to KSHV in the mice (Fig. 5A and B). Intranasal immunizations with the proteins also induced IgA to KSHV in the NW and saliva, as effectively as immunization with KSHV particles and ORF73 protein (Fig. 5C and D). The neutralization assay revealed that the serum from mice intraperitoneally

immunized with GST-K8.1 reduced the numbers of KSHV-infected 293 cells in this assay (P < 0.05), whereas the serum from mice intraperitoneally immunized with ORF59 and ORF73 proteins did not reduce them significantly (P = 0.55, Fig. 6A). Neutralization activity of body fluid of K8.1-immunized mice was also shown in the NW of mice intranasally immunized with K8.1 protein (P < 0.01, Fig. 6B). These data suggest the neutralization activity of the antibodies to K8.1 in vitro. In the present study, we demonstrated that KSHV immunization resulted in cellular and humoral immune response in mice. Spleen cells from KSHV-immunized mice produced IFN-γ, and the serum, NW and saliva of KSHV-immunized mice neutralized KSHV infection to 293 cells in vitro. The serum of KSHV-immunized mice recognized KSHV-encoded K8.1 and ORF59 proteins. The serum and NW from K8.1-immunized mice neutralized KSHV infection to 293 cells in vitro as effectively as the serum from KSHV-immunized mice. These results suggest a possibility of mucosal vaccine using inactivated KSHV particles or recombinant K8.

This suggests that NFC as an injectable drug releasing biomaterial is indeed more suitable for larger compounds, such

as macromolecular protein and peptide drugs. Additionally, protein drugs suffer from delivery problems, which need to be overcome for effective treatment (Jain et al., 2013). As an injectable hydrogel, NFC could solve some of the challenges related to the delivery of biopharmaceuticals. The pharmacokinetic models that we constructed could be used to further evaluate the release properties of NFC or other biomaterials in conjunction with SPECT/CT imaging. In our study the deconvolution and Loo–Riegelman models described the amount ready to be absorbed, which relates to the release rate of the compound. This could be useful in further analyzing poorly absorbing compounds (such as the HSA in our case), and can be used to complement drug-biomaterial studies when small-animal imaging is in use. This is especially true in situations where poor absorption Palbociclib mouse is the reason for an apparent slow rate of release, which might be an erroneous indication by the SPECT/CT. Therefore, the detected activity at the injection site might not be because of slow rate of release from the biomaterial, but actually

due to very poor absorption. As we proposed earlier, the high biodurability of NFC suggests that as for a non-biodegrading material, it could have a potential use as a long-term drug releasing biomaterial; ideal as an extended release product for chronic diseases. In addition, NFC hydrogels imbedded with therapeutic compounds could find a potential application as a local

delivery biomedical device. Topical and selleck screening library subcutaneous conditions could be treated with easily injectable NFC hydrogels that can be later enzymatically removed. The steady and continuous release of drug from the hydrogels could be further improved through formulation processes, in addition, nanofibrillar cellulose has not shown cytotoxic properties in previous Suplatast tosilate studies (Vartiainen et al., 2011, Alexandrescu et al., 2013 and Pitkänen et al., 2010), which supports the idea of NFC as a potential biomaterial. However, it should be noted that studies considering the safety of plant-derived NFC in humans have not been done and especially with possible long-term exposure, this should be investigated thoroughly. The possible chemical interactions between proteins and NFC should be investigated individually. NFC contains many hydroxyl groups as well as some carboxyl groups which might interact with the drug compounds imbedded within the matrix; therefore making the predictions of release profiles difficult for different compounds. However, considering the current increase of interest in pharmaceutical research towards the possibilities of macromolecular protein and peptide drugs, NFC might offer an additional method for parenteral delivery, as the effective delivery of protein drugs has been one of the main challenges in pharmaceutical sciences (Kumar et al., 2006).

3). For all vaccines, most solicited reactions were generally mild or moderate and resolved within 3–7 days (data not shown). Injection-site reactions were reported by similar proportions of older adult subjects receiving the 15 μg (76.5%) or 21 μg (77.3%) ID vaccines, but they were reported more often PLX4032 clinical trial by subjects

immunized with the ID vaccines than by those receiving the HD (49.5%) or SD (34.5%) IM vaccines (Table 5). Among SD vaccine recipients, the proportion reporting injection-site reactions was higher for younger adults (64.3%) than for older adults (34.5%). The most common injection-site reaction reported with the ID vaccines was erythema, followed by induration, swelling, and pruritus, all of which were more common with the ID vaccines than with the IM vaccines (i.e. the SD and HD vaccines) (Fig. 4A). In contrast, injection-site pain was reported less often by older adults immunized with an ID vaccine than by older adults immunized with the HD vaccine or younger adults immunized with the SD vaccine. Grade-3 erythema

and swelling were reported more often by subjects immunized with an ID vaccine than by subjects immunized with an IM vaccine, although the proportions did not appear to differ between the 15 and 21 μg groups. The proportion of older adult subjects reporting solicited selleck kinase inhibitor systemic reactions was similar for all vaccines, although myalgia (24.8%) was reported most often by those immunized with the HD vaccine (Fig. 4B). The proportions of subjects reporting myalgia, headache, and malaise were highest in younger adults receiving SD vaccine. One subject in three of the groups experienced an immediate unsolicited reaction (within 30 min of vaccination): Thalidomide one older adult subject immunized with the 15 μg ID vaccine reported moderate dizziness lasting one day; one older adult subject immunized with SD vaccine reported moderate jaw pain lasting one day; and one young adult immunized with the SD reported a mild sore throat lasting eight days (Table 5). Only four subjects reported severe treatment-related unsolicited non-serious AEs. One older adult subject immunized with the 21 μg ID vaccine

reported a severe injection-site rash; one older adult subject immunized with the HD vaccine reported severe vomiting on the day of vaccination; one older adult subject immunized with the HD vaccine reported severe cough beginning 9 days after vaccination; and one younger adult immunized with the SD vaccine reported severe diarrhea and vomiting beginning on the day of vaccination. No treatment-related serious adverse events or treatment-related deaths occurred during the study. Vaccination acceptability was similar for all groups (Table 6). Although roughly two-thirds of the subjects in all groups reported feeling the needle puncture during vaccination, most of the subjects in each group reported experiencing “no pain” or “hardly any pain” (range: 77.6% [21 μg ID] to 86.2% [HD]).

tuberculosis strains isolated from TB patients had been increasing at an alarming rate. 1 One of the intrinsic factors contributing to INH resistant in M. tuberculosis is the underlying architecture of the bacterial cell envelope. 2 and 3 The cell wall of M. tuberculosis is double-layered, comprising of an inner electron-dense layer of peptidoglycan and an outer electron-transparent Selleckchem SAR405838 layer containing mycolyl arabinogalactan complex and peptidoglycan. 4 In brief, the arabinogalactan chains covalently bond to cross-linked peptidoglycan via phosphoryl-N-acetylglucosaminosyl-rhamnosyl

linkage units and then the arabinogalactan in turn is esterified to α-alkyl, β-hydroxy mycolic acids. 5 and 6 Studies reported that the outer layer functions as

an exclusion barrier towards hydrophilic drugs, especially INH. 2 and 3 Thus, the cell wall structure and INH penetration through the lipid domain provide opportunities for rational strategies for development of more effective and less toxic new anti-TB drugs which focused on drug lipophilicity. Previous studies have shown that chemical modifications of INH by increasing its lipophilic property resulted in enhanced activity of INH against M. tuberculosis. NLG919 in vitro 2 and 7 Encouraged by these studies, three lipophilic INH derivatives were synthesized and investigated for their in vitro anti-TB activities. We speculated that these new INH derivatives should easily penetrate the bacterial cell envelope to exert a better inhibitory activity on the growth of the bacteria. This study was also carried out to study the interactions between these INH derivatives with four most common first-line anti-TB drugs: INH, streptomycin (STR),

rifampicin (RIF), and ethambutol (EMB). It is hoped that the findings of this study will point to a promising lead compound for future development of alternative therapeutic for INH resistant M. tuberculosis strains. The INH-C16, INH-C17 and INH-C18 were synthesized following the procedure by Besra et al.8 Dry dichloromethane and 4-dimethylaminopyridine (1.2 eq.) were added to hexadecanoyl chloride, heptadecanoyl chloride and octadecanoyl chloride for synthesis of INH-C16, INH-C17 and INH-C18 respectively, followed by INH (1.1 eq.). Each reaction mixture was stirred the at ambient temperature overnight. It was then washed with 2% diluted hydrochloric acid and water. The organic layer obtained was dried over anhydrous magnesium sulphate. The solvent was removed under reduced pressure to afford the crude product, which was purified by column chromatography. Product confirmation was achieved by standard procedures involving IR, 1H NMR, 13C NMR, and mass spectroscopy. Fig. 1 displays the chemical structures of INH-C16, INH-C17 and INH-C18 as compared to INH. INH, STR, RIF, and EMB were obtained commercially from Sigma–Aldrich Chemical Company, United Kingdom. Stock solutions of INH, STR, and EMB were prepared by dissolving in distilled water to obtain a concentration of 1 mg/mL, 3.

The lack of consistent guidance

on the use of placebo controls raises significant ethical concern. On the one hand, investigators and sponsors may avoid conducting placebo-controlled trials when an efficacious vaccine exists, even if PF-01367338 in vitro such trials are scientifically necessary and potentially justifiable. On the other hand, a lack of clear guidance may result in the conduct of placebo-controlled trials that are ultimately unethical. Against this backdrop, the WHO Department of Ethics and Social Determinants convened an expert consultation to provide recommendations on the use of placebo controls in vaccine trials in cases where an efficacious vaccine already exists. The focus was on large-scale clinical trials that test vaccines in Phases III and IV of development (i.e. where preliminary testing of safety and immunogenicity, and sometimes efficacy, has been completed in Phase I and II trials). The panel, consisting of 20 experts from selleck chemicals 11 countries, met to discuss relevant issues and develop recommendations in consultation with key stakeholders in international vaccine research (Appendix). The present paper develops the discussion and conclusions from that meeting [13]. Given the high burden of infectious diseases, especially in LMICs, there is an

ethical imperative to develop and test new vaccines. The recommendations from the panel therefore aim to facilitate the conduct of vaccine research

that is ethical, scientifically valid, and designed to meet important public health needs. While this paper focuses specifically on the use of placebo controls, similar considerations apply to open designs in which a placebo is not used, but an unvaccinated control group is included. The following recommendations assume that other common requirements for ethical research are respected [4] and [5]. In particular: Investigators and sponsors consult and collaborate with local stakeholders in all phases of the research; research participants, or their legal representatives, give voluntary and informed consent to study participation; participants are free to withdraw from research at any time, for any reason, without MTMR9 penalty; the research addresses an important health problem and is responsive to local health needs; the study design used minimizes risks and enhances potential clinical benefits for participants; the benefits and burdens of the research are justly distributed; and sponsors, in consultation with national or local authorities, make provisions to ensure reasonable post-trial access to interventions proven most efficacious to the population from which the research participants were drawn. To navigate the difficult ethical terrain of using placebo controls in vaccine trials, it is helpful to identify the conditions under which placebo use is clearly acceptable and clearly unacceptable.

6 ± 5.0 to 66.8 ± 2.0). Considering the fact that in erythroid-induced K562 cells the growth efficiency is lower (see Tables 1 and 2), these evidences support

the concept that benzidine-negative cells at day 6 still can differentiate even in the absence of irradiated compounds in the medium (this “commitment-like” effect is present in several inducers of K562 cell differentiation). In any case, the data suggest that the induced differentiation observed at day 6 is irreversible. Since 5′-methylpsoralen (5′-MP), 4′,5′-DMP and 5,5′-dimethylpsoralen (5,5′-DMP) for psoralens and 4,6,4′-TMA for angelicins were the most active compounds, further experimental activity was carried out with these molecules. Moreover, the lower UV-A (1 J/cm2) dose was this website chosen to minimize the phototoxic effect. The mechanism by which erythroid differentiation Metabolism inhibitor induced by furocoumarin takes place is still

unknown. However, the DNA photobinding is considered the main effect for the photoantiproliferative activity of the PUVA therapy. Thus, some preliminary experiments were carried out to verify whether furocoumarin DNA photodamage could be involved also in the erythroid differentiation process. K562 cells were irradiated in the presence of the tested compounds and of the inhibitors of some phosphoinositide kinase-related kinases, such as DNA-dependent protein kinase (DNA-PK), ataxia telangiectasia mutated (ATM) and the ataxia- and Rad3-related protein (ATR), which can be activated after different kinds of DNA damage not [27]. In particular, wortmannin was used as inhibitor of the catalytic subunit of the PI3-kinase family of enzymes [28], and caffeine as inhibitor of ATM and ATR but not of DNA-PK [29]. Cell viability was not affected

by the presence of these two inhibitors (data not shown). As it can be observed in Fig. 3, the amount of benzidine positive cells was significantly reduced, even if not completely abolished, for all tested compounds, when the irradiation was carried out in the presence of those inhibitors. Thus, the processes activated by DNA damage could be involved, at least in part, in the erythroid differentiation process. The effects of furocoumarins on the expression of human globin genes were determined by RT-qPCR analysis using probes amplifying the α-like α-globin and ζ-globin and the β-like ε-globin and γ-globin mRNA sequences. Effects on production of β-globin mRNA were not analyzed, since it is well known that K562 cells do not efficiently transcribe the β-globin genes [10] and [30]. In Fig. 4, globin mRNA expression for 4′,5′-DMP and 4,6,6′-TMA is presented; these two molecules were selected as an example for linear (4′,5′-DMP) and angular (4,6,4′-TMA) most active furocoumarins in inducing erythroid differentiation (Table 1).

The E. coli pellet was suspended and sonicated. The supernatant and precipitate were separated

by centrifugation. To purify r3aB, the supernatant was directly loaded onto a Ni-NTA column (Pharmacia Biotech) to remove almost all of the bacterial proteins. To purify r3AB, the precipitate of cell lysate was collected and dissolved by 8 mol/l urea and then centrifuged. Cyclopamine chemical structure The resultant supernatant was loaded onto Ni-NTA column to remove bacterial proteins. The bound r3AB or r3aB was eluted and then loaded onto Sephadex G-25 column to remove imidazole and change the buffer to saline. The products were analyzed on 12% SDS-PAGE. The r3aB and r3AB at 8 μg/ml were coated on 96-well polystyrene microtiter plates (Yangzi Company, Jiangshu, China), and incubated overnight at 4 °C in 0.01 mol/l PBS (1 mmol/l KH2PO4, 10 mmol/l Na2HPO4, 137 mmol/l NaCl, 2.7 mmol/l KCl, pH 7.4). After washing for three times with washing buffer (PBST, 0.01 mol/l PBS,

0.05% Tween 20), 200 μl of blocking buffer was added (0.01 mol/l PBS, 5% skim milk) followed by incubating at 37 °C for 2 h. The sera were diluted at 1:100 with sample buffer (0.01 M PBST, 5% skim milk), added to wells in duplicate and incubated at 37 °C for 1 h. Afterwards, plates were washed three times followed by the addition of 100 μl Onalespib nmr per well of rabbit anti-bovine IgG/HRP (Sigma) at 1:5000 dilution and incubation at 37 °C for 1 h. After washing three times, the substrate solution of Ophenylenediamine dihydrochloride (OPD) (Amresco) was added and incubated at room temperature for 5 min for color development which was stopped with 50 μl per well of 2 M sulphuric acid. The optical density (OD) of the color in each well of plates was determined at 492 nm on an automated ELISA plate reader. The results were expressed as A492 ± SD. To obtain coating antigens for establishing indirect ELISAs to detect FMDV NSP-specific antibodies ADP ribosylation factor in cattle, recombinant 3AB (r3AB) was expressed in E. coli. The cells expressed r3AB were collected and subsequently sonicated. After separation by

centrifugation, the supernatant and precipitate were analyzed by SDS-PAGE. As shown in Fig. 1a, an abundant band with 37 kDa was revealed in the lane loaded with the precipitate, indicating that r3AB was majorly expressed in inclusion body. To purify the r3AB, the inclusion body was broken by lysis buffer containing 8 mol/l urea and the expressed proteins experienced refolding process by reducing the amount of urea. After purification, the r3AB displayed two bands close to 74 kDa and 37 kDa by SDS-PAGE, indicating that the purified r3AB existed as a mixture of monomers and dimers ( Fig. 1b). To avoid the inclusion body formation and dimers aggregation, a gene coding a truncated 3AB protein (r3aB) by deleting 80 amino acids at N-terminal of 3AB was constructed (Fig. 2a). The only cysteine at 65th residue was eliminated by the deletion.

We considered that a ‘moderate’ improvement would be enough for typical patients to consider that the intervention in this study is worthwhile. A total of 90 participants would provide 80% power to detect a difference between groups of 6 points on the modified Oswestry scale as significant at a two-sided significance level, assuming a standard deviation of 10 points (Fritz et al 2005, Childs et al 2004). To allow for some loss to followup, we increased the original sample to 100. However, since initial loss to follow-up was very low, study recruitment was closed CX-5461 mw at

89 participants. Analyses were conducted using the intention-to-treat principle including data from all randomised participants wherever it could be obtained. Significance for analyses was set at p < 0.05. Data samples were examined for normality using the Kolmogorov-Smirnov test MK-2206 ic50 and Q-Q plots. Repeated measures ANOVA was used to examine for differences

between groups for Oswestry Disability Index score, VAS, SF-36, and ratings of interference with work and satisfaction with life, with Bonferroni adjustment used for multiple comparisons. Student t-tests were used to compare global rating of change and satisfaction with the intervention between treatment and control groups. The Wilcoxon signed ranks test was used to compare the number of physiotherapy treatments following the intervention period between groups. Pearson’s chi-square test was used to compare groups for the number of participants who were able to manage their acute low back pain without the need to take medication. Between January 2009 and April 2010, 101 volunteers were screened for eligibility. Of these 89 were deemed eligible, gave

informed consent, and were randomised: 44 to the experimental group and 45 to the control group. The flow of participants through the trial, including reasons for exclusion and Rutecarpine loss to follow-up, is presented in Figure 1. The baseline characteristics of participants are shown in Table 1 and the first two columns of Table 2. No important differences in these characteristics were noted between the experimental and control groups. A single physiotherapist with a postgraduate degree in manual therapy and 15 years of experience using Strain-Counterstrain treatment provided all interventions to both experimental and control groups and remained blind to primary and secondary outcome measures throughout the trial. In each group, all participants attended two 30-min intervention sessions per week for two consecutive weeks. All participants received the study intervention as originally allocated.

While G1P [8], G2P [4] and G9P [8] accounted for 64.4% of strains, a number of unusual strains including uncommon G and P combinations such as G1P [4], G2P [8] and bovine-human reassortant strains PS-341 mouse such as G10P [11] were also identified. G3 and G4 rotaviruses were not seen in this population. The common genotypes caused more severe disease than rare or reassortant strains. Higher disease severity has been shown to correspond with greater virus replication by stool

viral load [23]. It would be interesting to quantify the rotavirus shed in stools of children infected with these genotypes and determine if viral load is greater in common genotypes, indicating a replicative advantage possibly resulting in more severe disease. However, it is important to note that

the hospital based study design is biased towards severe cases and a better assessment of severity and genotype can be obtained through a combination of hospital and community based studies. In summary, the study provides an in-depth clinical description of rotavirus Pomalidomide in vitro gastroenteritis and underscores the need for a uniform measure of severity assessment and clinical data collection in vaccine studies. This work was supported by grants from the Indian Council of Medical Research and the Centers for Disease Control and Prevention, Atlanta, USA. Conflict of interest: None to declare “
“Diarrhoea remains an important cause of death in children under five years of age worldwide and accounted for an estimated 1.3 million deaths in 2008. In the Africa region, 19% of the 4.2 million annual deaths were caused by diarrhoea. In addition, 90% of deaths due to AIDS in children occurred in this region [1]. Ribonucleotide reductase Diarrhoeal disease has been identified as a leading cause of morbidity and mortality in

HIV-infected children. Incidence rates for acute diarrhoea, recurrent diarrhoea and persistent diarrhoea were shown to be higher in HIV-infected infants compared to HIV-uninfected infants [2]. In South Africa, HIV-infected children admitted with diarrhoea were more likely to have prolonged diarrhoea, malnutrition, require a longer hospital stay and have a co-diagnosis of pneumonia. They also had a higher frequency of recurrent diarrhoea and recurrent hospital admissions [3], [4] and [5]. Data on the burden of rotavirus disease in HIV-infected children are limited. Globally, rotavirus is the main cause of acute gastroenteritis and accounted for 527,000 under-five childhood deaths in 2004. Rotavirus detection rates ranged from 16 to 66% with a mean detection rate in the Africa regions of 30% [6]. A review of South African studies shows that rotavirus contributes significantly to childhood diarrhoea in South Africa, with a median detection rate of 24% among inpatients [7]. Surveillance data from Gauteng, South Africa shows 23% of children hospitalised with diarrhoea were rotavirus positive [8].