Patterns and characteristics of hepatitis C transmission clusters among HIV-positive and HIV-negative individuals in the Australian Trial in Acute Hepatitis C. Clin Infect Dis 2011: 52; 803–811. 105  Fierer D, Factor S, Uriel A et al. Sexual transmission of hepatitis C virus among HIV-infected men who have sex with men – New York City, 2005-2010. MMWR Morb Mortal Wkly Rep 2011: 60; 945–950. 106  Sun HY, Chang SY, Yang ZY et al. Recent hepatitis C virus infections in HIV-infected patients

in Taiwan: incidence and risk factors. J Clin Microbiol 2012: 50; 781–787. 107  de Bruijne J, Schinkel J, Prins M et al. Emergence of hepatitis C virus genotype 4: phylogenetic analysis reveals three distinct epidemiological profiles. J Clin Microbiol 2009: 47; 3832–3838. 108  Danta M, Brown D, Bhagani S et al. Recent epidemic of acute hepatitis C virus in HIV-positive men who have sex with men Rucaparib linked to high-risk sexual behaviours. AIDS 2007: 21; 983–991. Forskolin purchase 109  Van de Laar TJ, Van de Bij AK, Prins M et al. Increase in HCV incidence among men who have sex with men in Amsterdam most likely caused by sexual

transmission. J Infect Dis 2007: 196; 230–238. 110  Schmidt AJ, Rockstroh JK, Vogel M et al. Trouble with bleeding: risk factors for acute hepatitis C among HIV-positive gay men from Germany: a case-control study. PLoS One 2011; 6: e17781. 111  Rockstroh J, Grint D, Boesecke C et al. Increases in acute hepatitis C (HCV) incidence across Europe: which regions and patient groups are affected. 11th International Congress on Drug Therapy in HIV Infection. Glasgow, UK. November 2012 [Abstract 0242]. 112  Vogel M, Page E, Matthews G et al. The use of week 4 HCV-RNA after acute HCV infection (AHC) to predict chronic HCV infection. 17th Conference on Retroviruses and Opportunistic Infections. San Francisco, CA. February 2010 [Abstract 640]. 113  Thomson EC, Fleming VM, Main J et al. Predicting spontaneous clearance of acute hepatitis 4-Aminobutyrate aminotransferase C virus in a large cohort of HIV-1-infected

men. Gut 2011; 60: 837–845. 114  Deterding K, Gruner N, Buggisch P et al. Early versus delayed treatment of acute hepatitis C: final results of the randomized controlled German HEP-NET acute HCV-III study. J Hepatology 2012; 56(Suppl 2): S21. 115  Nomura H, Sou S, Tanimoto H et al. Short-term interferon-alfa therapy for acute hepatitis C: a randomized controlled trial. Hepatology 2004; 39: 1213–1219. 116  Dore GJ, Hellard M, Matthews GV et al. Effective treatment of injecting drug users with recently acquired hepatitis C virus infection. Gastroenterology 2010; 138: 123–135. 117  Lambers FA, Brinkmann K, Schinkel J et al. Treatment of acute hepatitis C virus infection in HIV-infected MSM: the effect of treatment duration. AIDS 2011; 25: 1333–1336. 118  Calleri G, Cariti G, Gaiottino F et al. A short course of pegylated interferon-alpha in acute HCV hepatitis. J Viral Hepat 2007; 14: 116–121. 119  Jaeckel E, Cornberg M, Wedemeyer H et al.

Patterns and characteristics of hepatitis C transmission clusters among HIV-positive and HIV-negative individuals in the Australian Trial in Acute Hepatitis C. Clin Infect Dis 2011: 52; 803–811. 105  Fierer D, Factor S, Uriel A et al. Sexual transmission of hepatitis C virus among HIV-infected men who have sex with men – New York City, 2005-2010. MMWR Morb Mortal Wkly Rep 2011: 60; 945–950. 106  Sun HY, Chang SY, Yang ZY et al. Recent hepatitis C virus infections in HIV-infected patients

in Taiwan: incidence and risk factors. J Clin Microbiol 2012: 50; 781–787. 107  de Bruijne J, Schinkel J, Prins M et al. Emergence of hepatitis C virus genotype 4: phylogenetic analysis reveals three distinct epidemiological profiles. J Clin Microbiol 2009: 47; 3832–3838. 108  Danta M, Brown D, Bhagani S et al. Recent epidemic of acute hepatitis C virus in HIV-positive men who have sex with men ICG-001 cost linked to high-risk sexual behaviours. AIDS 2007: 21; 983–991. Selleckchem Opaganib 109  Van de Laar TJ, Van de Bij AK, Prins M et al. Increase in HCV incidence among men who have sex with men in Amsterdam most likely caused by sexual

transmission. J Infect Dis 2007: 196; 230–238. 110  Schmidt AJ, Rockstroh JK, Vogel M et al. Trouble with bleeding: risk factors for acute hepatitis C among HIV-positive gay men from Germany: a case-control study. PLoS One 2011; 6: e17781. 111  Rockstroh J, Grint D, Boesecke C et al. Increases in acute hepatitis C (HCV) incidence across Europe: which regions and patient groups are affected. 11th International Congress on Drug Therapy in HIV Infection. Glasgow, UK. November 2012 [Abstract 0242]. 112  Vogel M, Page E, Matthews G et al. The use of week 4 HCV-RNA after acute HCV infection (AHC) to predict chronic HCV infection. 17th Conference on Retroviruses and Opportunistic Infections. San Francisco, CA. February 2010 [Abstract 640]. 113  Thomson EC, Fleming VM, Main J et al. Predicting spontaneous clearance of acute hepatitis Fenbendazole C virus in a large cohort of HIV-1-infected

men. Gut 2011; 60: 837–845. 114  Deterding K, Gruner N, Buggisch P et al. Early versus delayed treatment of acute hepatitis C: final results of the randomized controlled German HEP-NET acute HCV-III study. J Hepatology 2012; 56(Suppl 2): S21. 115  Nomura H, Sou S, Tanimoto H et al. Short-term interferon-alfa therapy for acute hepatitis C: a randomized controlled trial. Hepatology 2004; 39: 1213–1219. 116  Dore GJ, Hellard M, Matthews GV et al. Effective treatment of injecting drug users with recently acquired hepatitis C virus infection. Gastroenterology 2010; 138: 123–135. 117  Lambers FA, Brinkmann K, Schinkel J et al. Treatment of acute hepatitis C virus infection in HIV-infected MSM: the effect of treatment duration. AIDS 2011; 25: 1333–1336. 118  Calleri G, Cariti G, Gaiottino F et al. A short course of pegylated interferon-alpha in acute HCV hepatitis. J Viral Hepat 2007; 14: 116–121. 119  Jaeckel E, Cornberg M, Wedemeyer H et al.

A total of 839 individuals were invited to participate in the study. Of these, 722 were recruited (50.7% women). The overall HIV prevalence in the community was 39.9% [95% confidence interval (CI) 35.9–43.8%]. By age, the prevalence was 23.2% (95% CI 17.9–28.6%) in individuals aged 18–27 years, 41.2% (95% CI 35.6–48.3%) in those aged 28–37 years and 44.8% (95% CI 38.4–51.2%)

in those aged 38–47 years. HIV prevalence was higher among women than men in all age groups. The overall HIV prevalence estimate for women in the community (43.1%; 95% CI 37.6–48.5%) was 1.4 times higher than that for those attending the ANC (29.4%; 95% CI 26.7–32.0%). The high HIV prevalence found in this region suggests that the epidemic is in a mature stable phase. The lower rates in the ANC than in the community suggest that ANC evaluations may underestimate community HIV prevalence. Resources to monitor HIV infection dynamics are needed to Apitolisib research buy guide targeted control strategies in countries in which the epidemic exacts the greatest toll. Despite recent advances in the development of prevention strategies and the global scale-up of HIV antiretroviral drugs, the control of the HIV/AIDS epidemic continues to be challenging, especially in sub-Saharan Africa, where approximately 22.5 million (68.5%)

of the 32.8 million people infected with HIV world-wide live [1]. Although the number of new infections slightly decreased in 2008, recent estimates from sub-Saharan countries NU7441 indicate a modest increase in the HIV prevalence, which can probably be attributed to improved access to antiretroviral treatments and consequent increased survival [2]. Accurate community-based HIV prevalence estimates are needed to assess the evolution of the epidemic in specific settings to allow adequate monitoring and evaluation of control strategies. HIV prevalence data derived from antenatal clinics (ANC) have traditionally been used to monitor HIV epidemic trends in many countries, as the prevalence in pregnant women is assumed to correlate well with HIV prevalence mafosfamide in other adults aged 15–49 years

in the general population [3]. However, since 1998 the Joint United Nations Programme on HIV/AIDS (UNAIDS) has also recommended that population-based surveys should be conducted to enable the population to be more widely represented and to compensate for potential biases in the ANC estimates, such as their poor general representativeness [3-6]. Monitoring basic epidemiological HIV infection data is especially important in southern African countries, as they bear the brunt of the HIV/AIDS pandemic. Mozambique is one of the 10 countries with the highest HIV prevalence in the world, with 1.4 million [95% confidence interval (CI) 1.2–1.5 million] people living with HIV according to UNAIDS estimates [1, 7]. Since 1988, a national surveillance system has been monitoring HIV prevalence through ANC sentinel sites [4].

Oseltamivir, a neuraminidase inhibitor, can shorten illness caused by influenza by up to 1.5 days if commenced within 48 hours of symptom onset, and it can therefore be used by travelers for presumptive self-treatment

of flulike symptoms. For some high-risk travelers, CH5424802 price oseltamivir prophylaxis may also be considered. This can be begun either on arrival at the destination or after a suspected exposure.30 However, there is no clear guidance on appropriate uses of antivirals among travelers, and opinion regarding specific indications may vary according to the predicted incidence, morbidity, and mortality of the annual circulating influenza species. Two factors that argue against the widespread use of oseltamivir by travelers are emerging resistance31,32 and the fact that travelers should be wary of self-treatment of influenza-like illnesses with antiviral medications alone, especially when traveling in malarious areas, as a malaria diagnosis should be considered in any febrile illness.30 Given the recent heightened interest in influenza, it is conceivable that now more than ever travelers (and non-travelers) might

respond to public health messages regarding influenza prevention, www.selleckchem.com/products/Y-27632.html or they might deliberately boycott such messages, claiming that public health and the industry exaggerated the risk of influenza. Devising suitable educational messages for travelers about influenza prevention requires information about their baseline influenza knowledge and their perspectives

regarding risk. The studies in this issue provide useful information regarding attitudes and practices to influenza prevention among travelers from the United States to Asia and business travelers, respectively.22,23 They also suggest that, in addition to more widely promoting WHO recommendations for general hygiene precautions for the prevention of influenza, guidelines for seasonal and novel influenza virus prevention need to be clarified internationally. Ideally there should be uniform guidance among international advisory P-type ATPase groups, focusing on both traveler vaccination and on carriage and use of antiviral medications. P. A. L. has received fees for consulting and/or serving on an advisory board from GSK and was paid travel to attend symposia and/or conferences by GSK and Sanofi Pasteur. K. L. states she has no conflicts of interest to declare. “
“Background. Many countries with high prevalence of human immunodeficiency virus (HIV) infection also have substantial Muslim populations. HIV-infected patients who travel to Hajj in Saudi-Arabia may encounter challenges regarding their anti-retroviral therapy (ART). Methods.

The reducing conditions selleck products within the cytoplasm are maintained by two enzymes: thioredoxin/thioredoxin reductase and glutathione/glutathione reductase. Two thioredoxin peroxidases have also been identified, and, in addition,

alkyl hydroperoxide reductase has been shown to convert lipid hydroperoxides to alcohols. Besides mutations in sod (superoxide dismutase) and kat (catalase) genes, mutations in the other genes do not result in particular sensitivity to oxidative stress, suggesting that other, as yet unidentified, redundant systems may exist that protect E. coli from oxidative stress. Herein, we improved a system to form markerless-chromosomal deletions, which resulted in PKC412 ic50 a genome that lacked an additional 10.1% compared with currently available reduced genomes. These large-scale deletion mutants had genomes that were up

to 38.9% smaller than the wild-type genome. The strains were examined for their sensitivity to menadione, which generates reactive oxygen species such as H2O2. All E. coli strains used were derivatives of MG1655. Antibiotic medium 3 (Becton Dickinson) was used in all experiments. The approximate formula in g L−1 is beef extract 1.5, yeast extract 1.5, peptone 5.0, dextrose 1.0, sodium chloride 3.5, dipotassium phosphate 3.68, and monopotassium phosphate 1.32. The deletion unit 14 was combined with the large-scale chromosome deletion mutant Δ10 constructed in previous work and was used to construct Δ11a (Hashimoto et al., 2005). Δ12a was constructed by combining deletion unit 13 with Δ11a. The deletion unit 9-1 was added to Δ12a to construct Δ13a. Δ14a was constructed by combining the deletion unit 20, which has the tetracycline-resistance (TcR) gene as a marker. The deletion units 14, 13, 9-1, and 20 were constructed as described Olopatadine previously (Hashimoto et al., 2005). The deletion unit 15 was combined with Δ14a to construct Δ15-1 and the red-kanamycin-resistance gene (KmR) was introduced into this strain by P1 transduction to construct Δ15-2 (Miller,

1992). The TcR marker within deletion unit 20 was replaced with the gentamycin-resistance gene (GenR) by red-mediated homologous recombination using the linear DNA fragment. Next, red-KmR was replaced with red-TcR and the TcR marker was removed using ‘the 415S Sm system’ (Kato & Hashimoto, 2008) to construct Δ15a. The deletion unit OCL38 (KmR) was introduced into the Δ15a to construct Δ16aK (Hashimoto et al., 2005; Kato & Hashimoto, 2008). The new deletion unit, LD3-5-1, was constructed and combined with Δ16aK using the ‘ApR-415S Sm system’ to construct Δ17aK. First, the DNA fragments for the ampicillin-resistant (ApR) deletion units were constructed by two rounds of PCR (Hashimoto et al., 2005). The DNA fragments were introduced into Δ16aK and the ApR recombinants, and DNA sequencing confirmed the presence of the deletion unit.

These observations support the application of gyrB analyses for differentiating and identification of the species of Stenotrophomonas. Furthermore, these results lend support to the notion that many strains identified as S. maltophilia, often on the basis of limited or inadequate data, in fact represent distinct species. Further investigations of gyrB variation within the ‘S. maltophilia complex’, as well as among all the species of the genus, will be necessary to evaluate the full potential of this

taxonomic and identification tool. However, the low gyrB similarities between some strains with very high 16S rRNA gene sequence similarities offer a caveat to relying too heavily upon 16S rRNA gene sequence analyses for identifications, not only among selleck screening library strains of S. maltophilia, but also between different species of the Stenotrophomonas genus. This study was supported by funding from The Health & Medical Care Committee of the Regional Executive Board, Region Västra Götaland, Sweden (Project Nos. ALFGBG-3238, ALFGBG 11574, VGREG-30781 and VGFOU-72241). “
“Indole is most commonly known as a diagnostic marker and a malodorous chemorepellent. selleck More recently, it has been recognized that

indole also functions as an extracellular signaling molecule that controls bacterial physiology and virulence. The gene (tnaA) for tryptophanase, which produces indole, ammonia, and pyruvate via β-elimination of l-tryptophan, was cloned from Prevotella intermedia ATCC 25611 and recombinant TnaA was purified and enzymatically characterized. Analysis by reverse transcriptase-mediated PCR showed that the gene was not cotranscribed with flanking genes in P. intermedia. The results of gel-filtration chromatography suggested that P. intermedia TnaA forms homodimers, unlike other reported TnaA proteins. Alectinib clinical trial Recombinant TnaA exhibited a Km of 0.23 ± 0.01 mM and kcat of 0.45

± 0.01 s−1. Of 22 Prevotella species tested, detectable levels of indole were present in the culture supernatants of six, including P. intermedia. Southern hybridization showed that tnaA-positive signals were present in the genomic DNA from the six indole-producing strains, but not the other 16 strains tested. The indole-producing strains, with the exception of Prevotella micans, formed a phylogenetic cluster based on trees constructed using 16S rRNA gene sequences, which suggested that tnaA in P. micans might have been transferred from other Prevotella species relatively recently. Strains of the genus Prevotella are strictly anaerobic, non-spore-forming, gram-negative, moderately saccharolytic, bile-sensitive rods that are frequently recovered as members of the polymicrobial flora, including in humans, of the oral, intestinal, and urogenital tracts (Shah & Collins, 1990).

This adaptation to host cells is reflected in the genome of L. pneumophila, which encodes for an abundance of eukaryotic-like proteins (Cazalet et al., 2004). Lcl is predicted to encode a 49.6 kDa protein with GXY collagen-like repeats. Enzymatic assays were performed to confirm the collagen-like structure. Lcl and rat tail collagen type I reacted in the same way on collagenase and trypsin incubation (data not shown). Furthermore, the GXY repeats were encoded by the VNTR region and a change in the number of repeat units had an influence on the number of GXY repeats

and consequently on the collagen-like protein structure. Some of the Legionella eukaryotic-like proteins have already proven their role in virulence and show that these eukaryotic-like proteins Palbociclib mw are putative candidates to play a role in the L. pneumophila pathogenesis (Cazalet et al., 2004). Therefore, the study of eukaryotic-like proteins, such as Lcl, is important to define

the survival strategies of this intracellular parasite. Virulence factors are also often outer membrane proteins or secreted proteins and previous studies have already identified several outer membrane proteins of L. pneumophila that are involved in the adhesion Rapamycin order and invasion of host cells (Mintz et al., 1992; Chang et al., 2005; D’Auria et al., 2008). Different cellular fractions (the cytoplasm, inner membrane, outer membrane and supernatant) were tested for the presence of Lcl. Separation of the cellular fractions by SDS-PAGE, followed by immunodetection with Lcl-specific antibodies, revealed an immunoreactive band in the outer membrane protein fraction and the extracellular fraction (Fig. 1a). Proteins used as a control were present in the expected fractions (Fig. 1b–d). The results of the cellular fractionation demonstrated that Lcl is an outer membrane protein that can also be found in the extracellular fraction. This could be due to the fragmentation of Lcl, situated at the cell surface, into the

extracellular space, or Lcl could have an additional function as a secreted protein. Other work has also yielded conflicting results regarding the localization of Lcl (DebRoy et al., 2006; Galka et al., 2008; Khemiri et al., 2008), Isoconazole which is probably due to the different techniques used. As Lcl contains the characteristic C-terminal consensus AAVRAVRAF, with a hydrophilic amino acid only in position 3, the outer membrane localization is most likely. The VNTR region of lcl of all 108 strains was amplified by PCR (see Materials and methods). The resulting PCR fragments of different sizes led to the identification of 12 polymorphisms ranging from 7 to 19 repeats of 45 nt. The repeat distribution of lcl in the 108 strains is bimodal, with a preference for 8 or 13 and 14 repeats (Fig. 2a).

The WHO guidelines also recommend that premature modification from first-line to second-line treatment should be avoided, with the assumption that the provision of second-line drugs is in the public sector and the availability is usually limited. This may mean that clinicians are not willing to modify the regimen immediately in the presence of treatment failure if virological failure cannot be confirmed. The higher rate of modification after virological failure in TAHOD

than after immunological and clinical failure lends support to this interpretation. However, there remain a large see more proportion of patients (nearly 40%) who continue the same failing regimen 1 year after identification of virological failure, which

is probably a result of the limited treatment options available. We found that advanced disease stage (CDC category C), a lower CD4 cell count and a higher HIV viral load were associated with a higher rate of treatment modification after failure. This probably indicates that the clinicians in TAHOD clinics were prioritizing treatment options to those failed patients with more advanced immune deficiency as a result of limited resources. In a case note and questionnaire-based audit in the United Kingdom [14], after virological failure (defined as a viral load rebound from undetectable, not reaching an undetectable level, and/or an increase in viral load), change of therapy was found to occur in <4 months in 43% of patients, in 4–6 months in 20% of patients Target Selective Inhibitor Library price and in >6 months in 34% of patients. Of the patients with virological failure who had their treatment modified, 48% switched to three or more new drugs, 32% to two new drugs and 20% to one new drug. In another study from the United Kingdom, Collaborative HIV Cohort (CHIC) [15], only one-third of patients remained on a failing regimen for more than 6 months after virological rebound of >400 copies/mL, unless and the

proportions were 20% and 9% at 1 and 2 years after rebound, respectively. The rate of treatment modification after treatment failure in TAHOD patients is clearly slower than that seen in the United Kingdom, where routine HIV viral load tests and second-line treatment options are readily available. Treatment failure was only one of the reported reasons for modification of treatment after identification of failure. These clinical data provide an insight into clinical practice with regard to HIV treatment and care in the Asia and Pacific region. Adverse events were reported to be a major reason for treatment change after initiation, both in TAHOD [13,16] and in other cohorts [14]. This suggests that the TAHOD clinicians are aware of the adverse effects associated with cART and are ready to change treatment if toxicity is present.

This species is particularly problematic due to the fact that it is ubiquitous in the dairy environment (Bramley & Dodd, 1984). Although the prevalence of mastitis with contagious pathogens has been reduced by improved milking hygiene, this has had little effect on environmental species (Leigh et al., 1999). Despite the severe economic

impact caused by the high prevalence of S. uberis in many well-managed dairy herds, virulence selleck screening library factors associated with pathogenesis are not well understood and constitute a major obstacle for the development of strategies to control this important mastitis pathogen (Oliver et al., 1998). Several putative virulence-associated genes of S. uberis have been described. Among these, resistance to phagocytosis conferred by a hyaluronic acid capsule (Ward et al., 2001), plasminogen activator proteins such as PauA (Rosey et al., 1999), PauB Cell Cycle inhibitor (Ward & Leigh, 2002) and SK (Johnsen et al., 1999), lactoferrin-binding proteins (Moshynskyy et al., 2003), adherence to and invasion of epithelial cells mediated by SUAM (Almeida et al., 2006), CAMP factor (Jiang et al., 1996), a surface dehydrogenase protein GapC (Pancholi et al., 1993) and Opp proteins involved in the active transport of solutes essential for growth in milk (Smith et al., 2002) have been found. As yet, nothing has

been reported about the occurrence of virulence-associated genes among S. uberis isolates from cattle with mastitis in Argentina, and about the possible distribution of virulence patterns at various dairy herds. The aim here was to examine 11 putative and known virulence-associated genes by PCR in 78 S. uberis strains isolated from cattle with bovine mastitis in Argentina. In addition, the distribution of virulence patterns at various herds was determined.

Although many studies relating the distribution of one or a few virulence-associated Urease genes have been reported, to our knowledge this is the first study that investigates the presence of a greater number of virulence determinants. Milk samples were obtained from 2359 milk-producing cows. Seventy-eight isolates were collected from udders of 78 cows with mastitis (>250 000 cells mL−1) from 21 dairy herds (I–XXI) between 2005 and 2006. One to 17 isolates were isolated from each herd. The size of the herds included in the study varied from 79 to 204 cows. The isolates included in this study are representative of those that cause bovine mastitis in Argentina as they were obtained from the four major dairy provinces (Buenos Aires, Córdoba, Entre Ríos and Santa Fé) located in the east-central region of Argentina. The shortest distance between herds was 24 miles, and the greatest distance between herds was 203 miles.

7 In comparison, the rates among US, Asian/Australian, and Japanese

travelers using chemoprophylaxis were 46.2%,6 41.7%,7 and 20.0%, respectively.10 Further investigation detected some confusion about the concepts of prevention and treatment. Some of the travelers seemed to be misled, as they were told that if any one in a group had a “presumed” case of malaria, the standby treatment doses had to be taken by the entire group for prevention of an outbreak. This reflects Cisplatin concentration that the general practitioners may lack training and knowledge of travel medicine. Some travelers thought that in case of illness visiting a physician would be better than self-treatment. This belief matched the high acceptance of malaria treatment in case of infection during the trip. In conclusion, over the last 10 years, Chinese outbound travel and export of labor services have grown dramatically. Our data indicate a profound lack of KAP with respect to prevention of malaria in at-risk travelers. There is an urgent need for public education in malaria prevention for this population; also it must become a common CHIR 99021 knowledge that pre-travel health consultations are essential. Additionally, professional training of medical providers in travel medicine must be intensified. Moreover, more research is needed to develop

effective measures to improve malaria prevention among Chinese international travelers. We thank Ms Assunta Marcolongo of IAMAT for her encouragement during the survey. We appreciate and thank all CIQ staff members at the international airports for their contributions. Data entry was performed by a working group at Guangdong International Travel Healthcare Center (GD ITHC). The authors state they have no conflicts of interest to declare. “
“Age distribution Celastrol of 4,986 cases of influenza A (H1N1) 2009 in Japan was analyzed. Cases with a travel history within 10 days preceding the illness onset were significantly

older than indigenous cases (p < 0.01) reflecting age-specific travel patterns. Border controls should account for the high frequency of infection among adults. The importance of age specificity in influenza A (H1N1) 2009 virus infection has been increasingly recognized. The infection is most frequently seen among those aged <20 years,1,2 and severe cases accumulate in young adults, reflecting the second highest frequency of infection in this group.3 While these patterns evoke the concept of age-related disease control policies, including school closures, and treatment and prevention in relation to preexisting immunity,4,5 the impact of human travel and age, and implications for preventing widespread pandemics have yet to be clarified.6 This article reports the age specificity of imported and indigenous cases in Japan. All confirmed cases of H1N1 2009 virus infection were mandatorily reported to the Japanese Government by the end of July 2009.