21 research outputs found

    High Rates of Detection of Clade 2.3.4.4 Highly Pathogenic Avian Influenza H5 Viruses in Wild Birds in the Pacific Northwest During the Winter of 2014–15

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    SUMMARY. In 2014, clade 2.3.4.4 H5N8 highly pathogenic avian influenza (HPAI) viruses spread across the Republic of Korea and ultimately were reported in China, Japan, Russia, and Europe. Mortality associated with a reassortant HPAI H5N2 virus was detected in poultry farms in western Canada at the end of November. The same strain (with identical genetic structure) was then detected in free-living wild birds that had died prior to December 8, 2014, of unrelated causes in Whatcom County, Washington, U. S. A., in an area contiguous with the index Canadian location. A gyrfalcon (Falco rusticolus) that had hunted and fed on an American wigeon (Anas americana) on December 6, 2014, in the same area, and died 2 days later, tested positive for the Eurasian-origin HPAI H5N8. Subsequently, an active surveillance program using hunter-harvested waterfowl in Washington and Oregon detected 10 HPAI H5 viruses, of three different subtypes (four H5N2, three H5N8, and three H5N1) with four segments in common (HA, PB2, NP, and MA). In addition, a mortality-based passive surveillance program detected 18 HPAI (14 H5N2 and four H5N8) cases from Idaho, Kansas, Oregon, Minnesota, Montana, Washington, and Wisconsin. Comparatively, mortality-based passive surveillance appears to have detected these HPAI infections at a higher rate than active surveillance during the period following initial introduction into the United States. RESUMEN. Altas tasas de detección del virus de influenza aviar altamente patógeno H5 clado 2.3.4.4 en aves silvestres en la parte noroeste del Pacífico durante el invierno 2014-15. En 2014, los virus de influenza aviar altamente patógenos H5N8 clado 2.3.4.4 se diseminaron a través de la República de Corea y posteriormente, se reportaron en China, Japón, Rusia y Europa. Se detectó mortalidad asociada con un virus reacomodado altamente patógeno de influenza aviar H5N2 en granjas avícolas en el oeste de Canadá a finales de noviembre. Se detectó entonces la misma cepa (con estructura genética idéntica) en aves silvestres de vida libre que habían muerto antes del 8 de diciembre del 2014 por causas no relacionadas en el Condado de Whatcom, Washington, en los Estados Unidos, en una zona contigua con la ubicación del caso índice en Canadá. Un halcón gerifalte (Falco rusticolus) que había cazado y se había alimentado de un silbón americano (Anas americana) el 6 de diciembre del 2014, en la misma zona, y que murió dos días después, resultó positivo a la presencia del virus de alta patogenicidad de origen euroasiático H5N8. Posteriormente, un programa de vigilancia activa basado en el muestreo de aves acuáticas cazadas y recolectadas en Washington y Oregón detectó diez virus de influenza aviar altamente patógena H5 de tres subtipos diferentes (cuatro del subtipo H5N2, tres del subtipo H5N8 y tres subtipo H5N1) con cuatro segmentos en común (HA, PB2, NP, y MA ). Además, mediante un programa de vigilancia pasiva basado en el muestreo de aves muertas se detectaron 18 virus de influenza aviar de alta patogenicidad (catorce subtipo H5N2 y cuatro H5N8) en Idaho, Kansas, Oregón, Minnesota, Montana, Washington y Wisconsin. Comparativamente, la vigilancia pasiva basada en la mortalidad parece haber detectado estas infecciones del virus de influenza de alta patogenicidad en un porcentaje mayor en comparación con la vigilancia activa durante este período después de la introducción inicial en los Estados Unidos

    Novel Eurasian Highly Pathogenic Avian Influenza A H5 Viruses in Wild Birds, Washington, USA, 2014

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    The novel Eurasian lineage clade 2.3.4.4 highly pathogenic avian influenza (HPAI) A(H5N8) virus (http://www.who.int/influenza/gisrs_laboratory/h5_nomenclature_clade2344/en/) spread rapidly and globally during 2014, substantially affecting poultry populations. The first outbreaks were reported during January 2014 in chickens and domestic ducks in South Korea and subsequently in China and Japan (1–4), reaching Germany, the Netherlands, and the United Kingdom by November 2014 and Italy in early December 2014 (5). Also in November 2014, a novel HPAI H5N2 virus was reported in outbreaks on chicken and turkey farms in Fraser Valley, British Columbia, Canada (5). This H5N2 influenza virus is a reassortant that contains the Eurasian clade 2.3.4.4 H5 plus 4 other Eurasian genes (polymerase acidic protein subunit, matrix protein, polymerase basic protein subunit [PB] 2, nonstructural protein) and 3 North American wild bird lineage genes (neuraminidase [NA], nucleoprotein, PB1) (5). Taiwan has recently reported novel reassortants of the H5 clade 2.3.4.4 with other Eurasian viruses (H5N2, H5N3)

    Possibility for reverse zoonotic transmission of SARS-CoV-2 to free-ranging wildlife: a case study of bats

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    The COVID-19 pandemic highlights the substantial public health, economic, and societal consequences of virus spillover from a wildlife reservoir. Widespread human transmission of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) also presents a new set of challenges when considering viral spillover from people to naïve wildlife and other animal populations. The establishment of new wildlife reservoirs for SARS-CoV-2 would further complicate public health control measures and could lead to wildlife health and conservation impacts. Given the likely bat origin of SARS-CoV-2 and related beta-coronaviruses (β-CoVs), free-ranging bats are a key group of concern for spillover from humans back to wildlife. Here, we review the diversity and natural host range of β-CoVs in bats and examine the risk of humans inadvertently infecting free-ranging bats with SARS-CoV-2. Our review of the global distribution and host range of β-CoV evolutionary lineages suggests that 40+ species of temperate-zone North American bats could be immunologically naïve and susceptible to infection by SARS-CoV-2. We highlight an urgent need to proactively connect the wellbeing of human and wildlife health during the current pandemic and to implement new tools to continue wildlife research while avoiding potentially severe health and conservation impacts of SARS-CoV-2 "spilling back" into free-ranging bat populations

    Possibility for reverse zoonotic transmission of SARS-CoV-2 to free-ranging wildlife: a case study of bats

    Get PDF
    The COVID-19 pandemic highlights the substantial public health, economic, and societal consequences of virus spillover from a wildlife reservoir. Widespread human transmission of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) also presents a new set of challenges when considering viral spillover from people to naïve wildlife and other animal populations. The establishment of new wildlife reservoirs for SARS-CoV-2 would further complicate public health control measures and could lead to wildlife health and conservation impacts. Given the likely bat origin of SARS-CoV-2 and related beta-coronaviruses (β-CoVs), free-ranging bats are a key group of concern for spillover from humans back to wildlife. Here, we review the diversity and natural host range of β-CoVs in bats and examine the risk of humans inadvertently infecting free-ranging bats with SARS-CoV-2. Our review of the global distribution and host range of β-CoV evolutionary lineages suggests that 40+ species of temperate-zone North American bats could be immunologically naïve and susceptible to infection by SARS-CoV-2. We highlight an urgent need to proactively connect the wellbeing of human and wildlife health during the current pandemic and to implement new tools to continue wildlife research while avoiding potentially severe health and conservation impacts of SARS-CoV-2 "spilling back" into free-ranging bat populations

    CD24 Is Not Required for Tumor Initiation and Growth in Murine Breast and Prostate Cancer Models

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    CD24 is a small, heavily glycosylated, GPI-linked membrane protein, whose expression has been associated with the tumorigenesis and progression of several types of cancer. Here, we studied the expression of CD24 in tumors of MMTV-PyMT, Apc1572/T+ and TRAMP genetic mouse models that spontaneously develop mammary or prostate carcinoma, respectively. We found that CD24 is expressed during tumor development in all three models. In MMTV-PyMT and Apc1572T/+ breast tumors, CD24 was strongly but heterogeneously expressed during early tumorigenesis, but decreased in more advanced stages, and accordingly was increased in poorly differentiated lesions compared with well differentiated lesions. In prostate tumors developing in TRAMP mice, CD24 expression was strong within hyperplastic lesions in comparison with non-hyperplastic regions, and heterogeneous CD24 expression was maintained in advanced prostate carcinomas. To investigate whether CD24 plays a functional role in tumorigenesis in these models, we crossed CD24 deficient mice with MMTV-PyMT, Apc1572T/+ and TRAMP mice, and assessed the influence of CD24 deficiency on tumor onset and tumor burden. We found that mice negative or positive for CD24 did not significantly differ in terms of tumor initiation and burden in the genetic tumor models tested, with the exception of Apc1572T/+ mice, in which lack of CD24 reduced the mammary tumor burden slightly but significantly. Together, our data suggest that while CD24 is distinctively expressed during the early development of murine mammary and prostate tumors, it is not essential for the formation of tumors developing in MMTV-PyMT, Apc1572T/+ and TRAMP mice

    Consensus guidelines for the use and interpretation of angiogenesis assays

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    The formation of new blood vessels, or angiogenesis, is a complex process that plays important roles in growth and development, tissue and organ regeneration, as well as numerous pathological conditions. Angiogenesis undergoes multiple discrete steps that can be individually evaluated and quantified by a large number of bioassays. These independent assessments hold advantages but also have limitations. This article describes in vivo, ex vivo, and in vitro bioassays that are available for the evaluation of angiogenesis and highlights critical aspects that are relevant for their execution and proper interpretation. As such, this collaborative work is the first edition of consensus guidelines on angiogenesis bioassays to serve for current and future reference

    Pre-EMTing metastasis? Recapitulation of morphogenetic processes in cancer.

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    EMT (epithelial-mesenchymal transition) is a morphogenetic process in which cells loose their epithelial characteristics and gain mesenchymal properties during embryogenesis. Similar processes regulated by similar pathways are recapitulated during tumour progression, endowing cells with invasive properties, thereby contributing to the formation of metastases. In this review, we outline key features of EMT and discuss the evidence for its involvement in the dissemination of tumours. Finally we review the recent literature concerning the mechanisms that regulate EMT in the tumour context, with a particular focus on breast cancer.info:eu-repo/semantics/publishe

    CD24 is expressed during MMTV-PyMT mammary tumorigenesis.

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    <p>To determine the expression of CD24 during tumorigenesis, female MMTV-PyMT mice were sacrificed at a variety of ages, and their mammary glands were cut into sections and stained with antibodies specific for CD24. After counterstaining with hematoxylin, the sections of 12 animals were photographed and analysed. Representative sections are shown. Scale bars indicate 100 μm. (A) Hyperplastic preneoplastic lesions and small adenomas that are either stained strongly or negative for CD24. (B) Isotype control stained serial section corresponding to A. (C) Different degrees of CD24 staining within one and the same neoplastic lesion. (D) A histopathologic analysis was performed and the intensity of the CD24 staining was evaluated. Score:—no staining; + moderate staining; ++ strong staining. A two-sided Fisher´s exact test was performed to test the null hypothesis "staining intensity is independent of histopathologic appearance". The null hypothesis was rejected based on a calculated p-value of 0.00035 (3x3 contingency table). Scoring was categorized into CD24 negative ("-") or CD24 positive ("+" or "++"), and two-sided Fisher´s exact tests and 2x2 contingency tables were used to perform pairwise comparisons of (i) "invasive well differentiated" vs. "invasive poorly differentiated" (p = 0.21), (ii) "preinvasive" vs. "invasive well differentiated" (p = 0.45) and (iii) "preinvasive" vs. "invasive poorly differentiated" (p = 0.015). (E) More advanced tumor showing weak and diffuse staining. <b>F:</b> More advanced tumor negative for CD24.</p
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