Our study does not include antigenic and genetic data of circulating strains so we cannot comment on suboptimal antigenic match between the 2011–2012 vaccine and circulating strains in Valencia. Further studies should be conducted over several influenza seasons to assess the variability of selleck chemicals llc comparative vaccine effectiveness with the degree of antigenic match between vaccine and circulating viruses. We are grateful to Julián Librero for

his comments on the various drafts of the manuscript, Isabel Muñoz and Manuel Escolano for their continuous support to the research team during the conduct of this study, the Microbiological Surveillance Network in the Valencia Autonomous Community (redMIVA) for their assistance and for sharing their data and to all the members of the Valencia Hospital Network for the Study of Influenza and Respiratory Virus Diseases. Conflict of interest: JPB, ANS, SMU and JDD work in FISABIO’s Vaccines Research Area, FISABIO has received funding for GSK, Novartis, Pfizer, SanofiPasteur, SanofiPasteur MSD for conducting epidemiological studies on infectious disease epidemiology, vaccine effectiveness, pharmacoeconomics, and safety studies. The Vaccines Research Area is and has been involved in various randomized clinical trials

with www.selleckchem.com/products/AP24534.html GSK, Novartis, Pfizer and MSD vaccines. No conflicts related to

the submitted paper are declared by the rest of the authors. Funding: This work was supported by a grant from the Spanish Ministry of Health to support independent clinical research, Order SPI/2885/2011, October 20, 2011 [grant number EC11-480]. “
“Neonatal vitamin A supplementation (NVAS) is currently under investigation as a public health intervention to combat vitamin A deficiency and mortality in areas afflicted by vitamin A deficiency. We have studied the effect of NVAS on infant mortality in three randomized trials in Guinea-Bissau. One trial randomized normal birth weight neonates (≥2500 g) 1:1 to 50,000 IU vitamin A or placebo (VITA I, 2002–2004) [1]. A second trial randomized low birth weight neonates Liothyronine Sodium (<2500 g) 1:1 to 25,000 IU vitamin A or placebo (VITA II, 2005–2008) [2]. A third trial randomized normal birth weight neonates 1:1:1 to 50,000 IU vitamin A, 25,000 IU vitamin A or placebo (VITA III, 2004–2007) [3]. We observed that NVAS interacted with subsequent routine vaccinations in a sex-differential manner; the effect of NVAS tended to be negative in females once they started receiving the diphtheria–tetanus–pertussis vaccine (DTP) recommended at 6 weeks of age [2] and [4]. From 2003 to 2007 a trial randomizing children to early measles vaccine (MV) at 4.

Of the nine peptides in this group, eight elicited IFNγ ELISpot responses in PBMCs from HIV-1-infected subjects possessing A2 alleles: ENV-1002 (AVLSIVNRV) [49], ENV-1005 (SLCLFSYHRL) [49], GAG-1013 (ELKSLYNTV) [68], NEF-1015 (WLEAQEEEEV) [69], POL-1008 (ELAENREIL) [70], POL-1010 (DIQKLVGKL) [70], VPR-1019 (ETYGDTWTGV) [71], and VPU-1020 (TMVDMGHLRL) [70]. And finally, eight of the selected HLA-A2 epitopes are still novel for HIV-1 at the time of submission. The following peptides were confirmed to be immunogenic in IFNγ ELISpot assays in PBMC cultures from our HIV-1 infected cohorts: ENV-1001 www.selleckchem.com/products/Adrucil(Fluorouracil).html (GIKPVVSTQL) in both Providence, RI and Bamako, Mali; TAT-1017 (RLEPWKHPG)

and VIF-1018 (KISSEVHIPL) in Providence; and REV-2001 (GVGSPQILV), REV-2002 (ILVESPTVL),

VIF-3006 (KVGSLQYLA), VIF-3007 (SLQYLALTA), and VPU-3009 (KIDRLIDRI) in Bamako. Epitope VPU-3009 did not elicit any positive IFNγ ELISpot responses and has yet to be described as an HIV-1 epitope in other publications even though it bound to HLA-A2 in vitro; PFI-2 mouse this may due to the size of the study cohort or to false positive selection by our immunoinformatics tools. A globally relevant vaccine for HIV-1 continues to remain elusive due to the dynamic and extraordinary diversity of the virus. Virus-specific cytotoxic T-cell responses have been shown to play a vital role in the control of primary and chronic HIV-1 infection [16], [20], [17], [72] and [73], and while T-cell epitopes continuously evolve under immune pressure, early work showed fitness costs limited viral escape from CTL [34]. These findings suggest that a vaccine capable of raising CTL to the most conserved epitopes would have the most success at slowing or halting the progression of disease. This supports our firm belief that critical highly conserved, high-affinity epitopes available for vaccine design lie in restricted regions of the HIV genome that are resistant

Dipeptidyl peptidase to selective pressure, where mutations are slow to evolve and exact a cost on virus replicative fitness. We have called these epitopes the “Achilles’ heel” epitopes of HIV [32]. Due to HIV viral evolution in response to pressure from HLA-restricted immune responses, many highly immunogenic T-cell epitopes may be disappearing from the HIV genome, while highly conserved regions of the genome may also evolve to escape human immune response [74] and [75]. In the work presented here, we have employed immunoinformatics methods to search available HIV sequences for both highly conserved and immunogenic HLA-A2 epitopes. Using this balanced strategy of selecting for both conservation and immunogenicity, 38 total putative A2 epitopes were chosen and then tested in assays with PBMCs from HIV-1 infected subjects in two geographically distinct areas (Providence, Rhode Island, and Bamako, Mali).

These efforts were successful in many regards. The laboratory developed a vaccine to prevent disease caused by two types of adenovirus that the Food and Drug Administration licensed, which has proved important to preventing deaths in the military during crowded conditions. The lab contributed in Z-VAD-FMK developing vaccines against hepatitis A and rotavirus, the most common cause of severe diarrhea among infants. A large number of experimental vaccines for RSV, parainfluenza viruses and dengue viruses from the laboratory have been tested in clinical trials, many of which are ongoing. Vaccine

development is not without its challenges. Chanock and his colleagues were deeply troubled by the adverse outcome of the formalin-inactivated RSV trials in the 1960s, in which children suffered enhanced disease during subsequent infection and some died [5]. This event cast a pall on RSV vaccine development for many years. Appropriate

caution and scientific skepticism tempered the bolder early culture of the laboratory for decades, with recurring reminders of the primum non nocere principle. We recall check details Chanock chastising a colleague, “Whenever I hear someone say ‘This vaccine might not work but there is no way it would hurt anyone’ an alarm bell should go off, because that is exactly what we said about the inactivated RSV vaccine. A large part of Chanock’s success was due to the talents and drive of the many scientists who worked in LID over the years. The laboratory developed through a strong group of leaders as section heads over respiratory, hepatitis, enteric, and dengue viruses. LID served as a beacon for those interested in learning vaccine sciences, and seeded many of the nation’s and world’s medical centers and research institutes with leaders in the field of vaccinology. One of them was recruited by Karzon to be Chief of Pediatric Infectious Diseases at Vanderbilt. Peter F. Wright, MD was largely responsible for building the Vanderbilt program for viral pathogenesis and vaccine evaluation. Chanock’s career was

recognized with some of the highest awards in science, including election to the U.S. National Academy of Sciences and the Danish Royal Academy of Sciences, the Albert B. Sabin Gold Medal, the Robert Koch Prize, the E. Mead Johnson Award, Joseph E. Smadel Medal, the Bristol-Myers Squibb Award, and the U.S. Public Health Service Meritorious Service Medal and Distinguished Service Medal among many others. Through out he maintained a very modest lifestyle, swimming a mile a day, eating carefully, listening to classical music, and connecting closely with his family. He had his peculiarities, especially a prodigious memory. He filed thousands of articles of the research literature in his office by the first author’s name, and retrieved them effortlessly.

, 1999 and McCarthy et al., 2003). Recent UK trends suggest that the rate of increase in obesity prevalence may have slowed (Stamatakis et al., 2010), selleck inhibitor as in some other countries (Han et al., 2010). However, social patterning of overweight and obesity in UK children and adolescents is increasing (Stamatakis et al., 2010). Many studies of obesity prevalence have taken place, but there is a dearth of evidence on the ‘natural history’ of obesity ( Whitaker, 2002 and Reilly et al., 2007). Only a few studies have reported on the

incidence of child and adolescent obesity ( Andersen et al., 2010, Gortmaker et al., 1996, Hesketh et al., 2003, Nader et al., 2006 and Plachta-Danielzik et al., 2010), and none have reported on incidence across childhood and adolescence. Evidence on incidence of overweight and obesity by age group would be helpful to prevention strategies: periods of highest incidence might merit highest priority in preventive interventions. buy ON-01910 A recent review ( Nichols and Swinburn, 2010) found that decision-making in choice of target population for obesity prevention is rarely explicit. Specific periods of childhood and adolescence

might be particularly important to the establishment of health behaviours related to obesity, and identifying whether incidence of obesity is highest in early childhood (e.g. 3–7 years), mid–late childhood (7–11 years), or adolescence (beyond 11 years) could inform preventive interventions. The primary aim of the present study was therefore to estimate the incidence of overweight Phosphatidylinositol diacylglycerol-lyase and obesity across childhood and adolescence in a large, contemporary, cohort of English children. A secondary aim was to examine the persistence of overweight and obesity. ALSPAC (The Avon Longitudinal Study of Parents and Children) is a large prospective cohort study of children born in the South-West of England

in 1991/1992; study design and methods are described elsewhere (Ness, 2004 and Golding and the ALSPAC Study Team, 1996). Briefly, 14,541 pregnant women with an expected date of delivery between April 1991 and December 1992 were enrolled, resulting in 13,988 participating children alive at one year. Detailed information has been collected using self-administered questionnaires, data extraction from medical notes, linkage to routine information systems and at research clinics for children. A 10% sample of the ALSPAC cohort, the Children in Focus (CiF) group, attended research clinics at 4, 8, 12, 18, 25, 31, 37, 43, 49, and 61 months where detailed physical examinations were undertaken. The CiF group was broadly socio-economically representative of the entire ALSPAC cohort and the UK (Reilly et al., 2005). From age 7, the entire ALSPAC cohort was invited to attend regular research clinics.

We suggest conducting further prospective studies with longer follow-up periods and with more accurate diagnosis. In conclusion, this prospective cohort study demonstrated that the incidence of RRI in recreational runners was 31% or 10 RRIs per 1000 hours of running exposure. The most

frequent check details type of injury was muscle injury and the most affected anatomical region was the knee. The relevant risk factors for RRI in recreational runners were identified in this study as previous RRI and speed training, while the protective factor identified was interval training. eAddenda: Appendix 1 and 2 available at jop.physiotherapy.asn.au Ethics: The Ethics Committee of the Universidade Cidade de São Paulo approved this study (number 13506607). All participants gave written informed consent before data collection began. Competing interests: None declared. Support: None. Luiz

Carlos Hespanhol Junior is a PhD student supported by CAPES (Coordenação de Aperfeiçoamento de Pessoal de Nível Superior), process number 0763-12-8, Ministry of Education of Brazil. We thank CORPORE Brasil for their assistance in the recruitment of the study participants, as well as Aline Carla Araújo Carvalho, Bruno Tirotti Saragiotto and Tiê Parma Yamato for their BIBF-1120 help in the data collection, and Professor Jos Twisk for statistical advice. “
“To assist clinicians looking for authoritative assistance with clinical problems, the journal publishes an annual

index of content from the most recent two years of Appraisal pages. This index includes content from Volumes 58 and 59 of Journal of Physiotherapy. Content is indexed under the PEDro codes: subdiscipline, intervention, problem, and body part. It is identified by Appraisal section and Volume and page number. Some content is indexed under more than one code. Cardiothoracics. Continence & Women’s Health. Ergonomics & Occupational Health. Gerontology. Musculoskeletal. Neurology. Paediatrics. Other. Behaviour Modification. Education. Fitness Training. Respiratory Therapy. Strength Training. Stretching, Mobilisation, Manipulation, Massage. Difficulty with Sputum Clearance. Impaired Ventilation. Muscle Weakness. Pain. Reduced Exercise Tolerance. Other. Head & Neck. Upper Arm, Shoulder PDK4 or Shoulder Girdle. Hand or Wrist. Chest. Thoracic Spine. Perineum or Genito-Urinary System. Thigh or Hip. Lower Leg or Knee. Whole Body/Other. “
“Clinical trial registration involves placing the protocol for a clinical trial on a free, publicly available and electronically searchable register. Registration is considered to be prospective if the protocol is registered before the trial commences (ie, before the first participant is enrolled). Prospective registration has several potential advantages. It could help avoid trials being duplicated unnecessarily and it could allow people with health problems to identify trials in which they might participate.

C. perfringens toxinotype B is the etiologic agent of dysentery in newborn lambs and haemorrhagic enteritis and enterotoxemia in goats, calves and foals [2] and [3]. More recently, toxinotype B has been detected in a human with a clinical presentation of multiple sclerosis, providing clues for environment triggers of the disease [4]. C. perfringens toxinotype D affects mainly sheep and lambs but also causes infections in goats and calves [2] and [3]. The most important factor in initiating disease is the disruption of the microbial

balance in the gut due to overeating carbohydrate rich food, which causes proliferation of C. FK228 ic50 perfringens and consequent overproduction of the toxin [2] and [5]. Overproduction of Etx causes increased intestinal permeability, facilitating entry of the toxin into the bloodstream and its spread into various organs, including the brain, lungs and kidneys. While infection of the central nervous system results in neurological disorders, the fatal effects on the organs often lead to sudden

death [6] and [7]. For full activity of the toxin, proteolytic processing is required, with carboxy-terminal and amino-terminal peptides removed. Toxin activation typically occurs in the gut either by digestive proteases GPCR Compound Library high throughput of the host, such as trypsin and chymotrypsin [8], or by λ-protease produced by C. perfringens itself [9] and [10]. To prevent Etx-induced enterotoxemia in domesticated livestock, a number of commercial vaccines are available that have been used extensively over the past decades. These vaccines are based on either formaldehyde treated C. perfringens type D culture filtrate or formaldehyde-inactivated recombinant wild type toxin [11] and [12]. These vaccine preparations have several disadvantages: (1) complete removal of free formaldehyde is required to avoid possible toxic side effects, (2) toxoiding using formaldehyde can

show considerable batch to batch variation in immunogenicity of these vaccines [12], (3) inflammatory responses following vaccination can lead to reduced feed consumption [13] and (4) reversion Liothyronine Sodium to toxicity may occur in incompletely inactivated bacterial toxins. Therefore, there is a need to identify Etx variants with reduced toxicity relative to wild type toxin. One approach to solving this problem is to develop recombinant vaccines based on site-directed mutants with markedly reduced toxicity. Amino acid residues Y30 and Y196 have previously been identified to play key roles in cell binding and thus, cytotoxicity of Etx [14] and [15]. Therefore, this study aimed to determine the potential of a site-directed mutant of Etx with mutations Y30A and Y196A combined, termed Y30A-Y196A, to be exploited as a recombinant vaccine against enterotoxemia. The gene encoding epsilon prototoxin, etxD, from C.

This calls for improved methods for protection of farmed salmon against virus diseases. The discovery of type I IFNs in fish opens a possibility for using them in prophylaxis against virus infections in fish. Type I IFNs are induced upon host cell recognition of viral nucleic acids [2], and protect other cells against infection by inducing numerous antiviral proteins such as Mx, ISG15, IFIT5 (ISG58) and Viperin [3], [4] and [5].

In fish, four selleck compound type I IFN subtypes, named IFNa, IFNb, IFNc and IFNd, have so far been characterized [6] and [7]. IFNa and IFNd contain 2 cysteines (2C-IFNs) while IFNb and IFNc contain 4 cysteines (4C-IFNs). The largest cluster of IFN genes has been found in Atlantic salmon, encoding two IFNa, four IFNb and five IFNc genes [6]. Atlantic salmon IFNa, IFNb and IFNc and IFNd have only 22–37% amino acid sequence identity and show major differences in cellular expression properties and antiviral activities [6] and [8]. IFNa1 and IFNc induced similar strong antiviral activity against IPNV and induced similar transcript levels of antiviral genes in cell lines,

IFNb was less active and IFNd showed no antiviral activity [8]. IFNa1, IFNb and IFNc provided only transient inhibition of ISAV replication in TO cells [9]. In humans, pegylated recombinant IFN-α, mostly in combination with ribavirin, is used for treatment of chronic hepatitis C virus infections [10]. IFN-α treatment has also shown protective effects against influenza virus infection in mammals and chicken [11], [12] and [13]. However, IFN prophylaxis to Linifanib (ABT-869) combat virus diseases Autophagy inhibitor in domestic animals and human has apparently had limited success due to the costs of recombinant IFNs, their rapid degradation in the body and side effects. Reports on effects of IFNs against virus infection in live fish are scarce. Treatment of rainbow trout with recombinant Atlantic salmon IFNa2 injected intraperitoneally (i.p.) provided protection against IHNV infection for up to 7 days, which is not enough for prophylaxis of farmed

fish [14]. In the present work we have used a more novel approach by studying antiviral effects of intramuscular (i.m.) injection of IFN expressing plasmids in Atlantic salmon. The results showed surprising differences among IFNa, IFNb and IFNc plasmids in their ability to induce systemic expression of antiviral genes and to protect salmon from infection with a high virulent strain of ISAV. Notably, i.m. injection of IFNc plasmid provided systemic up-regulation of antiviral genes in salmon for at least 8 weeks accompanied by a high level of protection against ISAV infection. Atlantic salmon (Salmo salar L.) presmolts (35–45 g) of the strain Aquagen standard (Aquagen, Kyrksæterøra, Norway) were kept at Tromsø Aquaculture Research Station, Norway in 300 l tanks supplied with fresh water at 10 °C and were fed commercial dry food. Prior to treatments, the fish were anesthetized with 0.

Une étude réalisée en Angleterre n’a pas mis en évidence de différence de survie entre Blancs et Noirs, 38 mois vs 34 mois [30]. D’autres travaux ont identifié une survie plus courte des sujets non Blancs [20] ou issus de l’Afrique du nord ou des Balkans [31] par rapport aux sujets Blancs. Toutefois, ces études restent limitées par les outils utilisés (modalités de détermination des origines ethniques, de classification de sujets Blancs/Noirs)

MG-132 solubility dmso et la possibilité d’un accès différentiel des groupes ethniques aux soins. Le début bulbaire de la maladie est associé avec un pronostic péjoratif par rapport à un début spinal [19], [20], [21], [24], [25] and [28]. Une atteinte respiratoire initiale qui reste une forme de présentation rare est également un facteur

défavorable pour la survie [32]. Un plus long délai entre la date des premiers symptômes et la date de diagnostic est associé à un meilleur pronostic [14], [20], [22], [26] and [33], probablement parce qu’une présentation de la maladie d’emblée et rapidement grave induit un recours aux soins et un diagnostic plus précoce. Les formes familiales génétiques ont des profils variables selon les mutations. Vingt gènes sont impliqués actuellement find more expliquant 60 à 70 % des formes génétiques. Les mutations C9ORF72 et FUS sont associées à une durée de survie plus courte. Parmi les mutations SOD1, la mutation A4V provoque une forme très rapide par comparaison aux mutations D90A. Des profils phénotypiques particuliers peuvent être mis en évidence en fonction de la mutation incriminée et du mécanisme physiopathologique impliqué : perturbation du transport axonal et du cytosquelette (dynactine, PFN1 et from Eph A4), conformation spatiale de la protéine mutée (SOD1, TDP43, FUS), action sur le protéasome et mécanisme d’autophagie (ubiquilline-p62), action sur le métabolisme des ARN (TDP43, FUS, C9ORF72). Quelques études ont permis de montrer l’association entre un état psychologique

altéré (stress, dépression, colère, manque d’espoir) et une survie plus courte. Ainsi, par rapport au groupe de patients défini par un score psychologique compris dans le tertile élevé (absence d’atteinte), les patients avec une atteinte psychologique (score psychologique dans le tertile le plus bas) avaient un RR de décès de 2,24 (1,08–4,64) (p = 0,02) après ajustement sur les facteurs pronostiques habituels. Dans une autre population, une humeur dépressive était également associée avec une progression plus rapide et une survie plus courte [34]. De même, parmi les 8 dimensions et 2 scores synthétiques du questionnaire de qualité de vie SF36, 3 dimensions étaient significativement associées à la survie de patients atteints de SLA : santé générale, limitations (du rôle) liées à la santé physique, fonctionnement ou bien-être social [20].

He was accepted as a resident in the Mayo Foundation and Graduate School at the University of Minnesota, Erlotinib nmr serving from 1957 to 1961, and he became board certified in Anatomic and Clinical Pathology. Dr. Titus earned a Ph.D., degree in pathology from the University of Minnesota, Mayo Graduate School of Medicine in 1962 (under the mentorship of Jesse E. Edwards, M.D.). He served as Associate Professor of Pathology and as a consultant in pathology at the Mayo Graduate School of Medicine from 1961 to 1972 and became a professor there in 1972. He was also coordinator of the Pathology

Training Programs from 1964 to 1972. In 1972, he was recruited to The Baylor College of Medicine in Houston, TX, to become the W.L. Moody, Jr., Professor and Chairman of the Department of Pathology, a position that he held until 1987. He served concurrently as Chief of the Pathology Service at The Methodist Hospital and Pathologist-In-Chief of the Harris County Hospital District. In 1987, upon the retirement of Dr. Jesse E. Edwards from the Registry of Cardiovascular Diseases United Hospital, St. Paul,

MN, which houses a collection of more than 20,000 heart specimens and 85,000 photographic slides, Dr. Titus was recruited as the second director. He also was a Professor of Pathology CP-673451 cell line on the University of Minnesota Medical School faculty. During his oxyclozanide time at the Registry, he continued to serve as Adjunct Professor at the Baylor College of Medicine. Although Dr. Titus retired in 2004, he continued to serve as senior consultant to the Jesse E. Edwards Registry of Cardiovascular Disease. Dr. Titus made many contributions to our discipline, its knowledge base, and the mentorship of its participants.

He fostered an early understanding of the normal AV conduction system, sudden cardiac death, the surgical anatomy of congenital heart disease. He published studies on how the AV conduction system was distorted in congenital heart disease and particularly in septal defects, and, in collaboration with cardiac surgical pioneers and other pathologists, he contributed to the development of the surgical and catheter-based repair of congenital heart disease and the pathological anatomy of both valvular heart disease and valve replacement by homograft and prosthetic valves. With pathologists, he collaborated on the earliest studies of the early diagnosis of myocardial infarction by the triphenyl tetrazolium chloride (TTC) macroscopic staining technique and the pathology of coronary artery bypass graft surgery. Dr. Titus was instrumental in the founding of the Society for Cardiovascular Pathology (SCVP) in 1985 and served on and as an enthusiastic and wise advisor to its Executive Council for many years. In 1993, Dr.

At a mean TIV coverage rate of 83% (range, 53–100%), indirect protection of non-recipients of the influenza vaccine had a protective effectiveness of 61% (95% confidence interval, 8–83%; P = .03). The overall protective effectiveness (direct and indirect protection) check details was estimated to be 59% (95% CI, 5–82%; P = .04). Bearing in mind that this randomised controlled study was over a single season, used TIV rather than LAIV and targeted a slightly narrow age range, the estimate of indirect protection is consistent with that estimated in this paper. The long-term

impact of vaccination on the dynamics of influenza transmission depends in part on the degree of cross protection between different strains, MAPK inhibitor imparted by the vaccine. This analysis has highlighted the potential importance of herd immunity in preventing influenza in high risk groups. A long-term programme of vaccination may, however, alter the breadth of this herd immunity. The influenza virus evolves away from the herd host immune protection by a process of antigenic shift

and drift [42] and [43]. Each individual host immune system comprises a repertoire of immunities to strains that had previously infected that individual. This natural immunity is long term and has some level of cross-protection against strains not previously experienced by that individual. Thus the natural herd immunity of a population is based on the collective experience of influenza over the last 50 years and is cross-protective to varying degrees against other related strains as well. It can be assumed that vaccine induced immunity is less cross-protective and possibly shorter

lived than natural immunity, although studies of the duration of immunity in naturally exposed individuals and from time series data have proved inconclusive [44] and [45]. If an effective seasonal influenza vaccination strategy were in place for 50 years, the herd immunity of the population will comprise the collective experience of annual influenza vaccination over the last 30 or so years (as the immunity from 30 to 50 years will have waned and natural infection would have been rare). This new herd immunity however will be at a high level, but its antigenic scope may be narrower than the natural herd immunity counterpart, possibly leading to an increased susceptibility to strains that have undergone antigenic drift or shift. Strains that have undergone antigenic shifts have the potential to cause pandemics, as was observed in 2009. These emerging strains typically infect and cause morbidity in younger individuals than those responsible for seasonal influenza [46] and [47]. With the emergence of A(H1N1)v following the 2009 pandemic, this shift in the age distribution of infection towards younger individuals is likely to increase the direct benefits of paediatric vaccination.