515 research outputs found

    Genetic diversity of Brazilian isolates of feline immunodeficiency virus

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    We isolated Feline immunodeficiency virus (FIV) from three adult domestic cats, originating from two open shelters in Brazil. Viruses were isolated from PBMC following co-cultivation with the feline T-lymphoblastoid cell line MYA-1. All amplified env gene products were cloned directly into pGL8MYA. The nucleic acid sequences of seven clones were determined and then compared with those of previously described isolates. The sequences of all of the Brazilian virus clones were distinct and phylogenetic analysis revealed that all belong to subtype B. Three variants isolated from one cat and two variants were isolated from each of the two other cats, indicating that intrahost diversity has the potential to pose problems for the treatment and diagnosis of FIV infection

    ŠŸŃ€Š¾Š±Š»ŠµŠ¼Š° Š²Š·Š°Ń”Š¼Š¾Š·Š²ā€™ŃŠ·Šŗу Š³Ń€Š¾Š¼Š°Š“яŠ½ŃŃŒŠŗŠ¾Š³Š¾ сусŠæіŠ»ŃŒŃŃ‚Š²Š° і Š“ŠµŃ€Š¶Š°Š²Š½Š¾Ń— Š±ŃŽŃ€Š¾ŠŗрŠ°Ń‚Ń–Ń— Š² Š£ŠŗрŠ°Ń—Š½Ń–: Š“ŠµŃŠŗі сучŠ°ŃŠ½Ń– Š°ŃŠæŠµŠŗтŠø істŠ¾Ń€Ń–Š¾Š³Ń€Š°Ń„Ń–Ń— Š“Š¾ŃŠ»Ń–Š“Š¶ŠµŠ½Š½Ń

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    Š Š¾Š·Š³Š»ŃŠ“Š°Ń”Ń‚ŃŒŃŃ Š²Š·Š°Ń”Š¼Š¾Š“ія Š³Ń€Š¾Š¼Š°Š“яŠ½ŃŃŒŠŗŠ¾Š³Š¾ сусŠæіŠ»ŃŒŃŃ‚Š²Š° і Š“ŠµŃ€Š¶Š°Š²Š½Š¾Ń— Š±ŃŽŃ€Š¾ŠŗрŠ°Ń‚Ń–Ń—. Š—Ń€Š¾Š±Š»ŠµŠ½Š¾ Š²ŠøсŠ½Š¾Š²Š¾Šŗ, щŠ¾ ŠæŠ¾Š·Šøції уŠŗрŠ°Ń—Š½ŃŃŒŠŗŠøх Š“Š¾ŃŠ»Ń–Š“Š½ŠøŠŗіŠ² Š²Ń–Š“ŠæŠ¾Š²Ń–Š“Š°ŃŽŃ‚ŃŒ Š½Š°ŠæрŠ°Ń†ŃŽŠ²Š°Š½Š½ŃŠ¼ Š·Š°Ń…Ń–Š“Š½Š¾Ń— Š½Š°ŃƒŠŗŠ¾Š²Š¾Ń— трŠ°Š“Šøції стŠ¾ŃŠ¾Š²Š½Š¾ тŠµŠ¾Ń€ŠµŃ‚ŠøчŠ½Šøх, Š° тŠ°ŠŗŠ¾Š¶ ŠæрŠ°ŠŗтŠøчŠ½Šøх сŠæŠ¾ŃŠ¾Š±Ń–Š² Š·Š°Š±ŠµŠ·ŠæŠµŃ‡ŠµŠ½Š½Ń Š²Š·Š°Ń”Š¼Š¾Š“ії іŠ½ŃŃ‚ŠøтутіŠ² Š³Ń€Š¾Š¼Š°Š“яŠ½ŃŃŒŠŗŠ¾Š³Š¾ сусŠæіŠ»ŃŒŃŃ‚Š²Š° і Š“ŠµŃ€Š¶Š°Š²Š½Š¾Š³Š¾ Š°ŠæŠ°Ń€Š°Ń‚Ńƒ.In this article the interrelation between civil society and state bureaucracy is analysed. The conclusion is made that the views of the Ukrainian scientists correlate with the western traditional scientific opinion concerning theoretical and practical ways of ensuring interaction between the civil society institutions and state apparatus

    ABCD : Update of the 2009 guidelines on prevention and management of feline infectious diseases

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    In this article, the ABCD guidelines published in the JFMS Special Issue of July 2009 (Volume 11, Issue 7, pages 527-620) are updated by including previously unavailable and novel information. For a better picture, the reader is advised to consult that issue before focusing on the novel features

    Influenza virus infections in cats

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    In the past, cats were considered resistant to influenza. Today, we know that they are susceptible to some influenza A viruses (IAVs) originating in other species. Usually, the outcome is only subclinical infection or a mild fever. However, outbreaks of feline disease caused by canine H3N2 IAV with fever, tachypnoea, sneezing, coughing, dyspnoea and lethargy are occasionally noted in shelters. In one such outbreak, the morbidity rate was 100% and the mortality rate was 40%. Recently, avian H7N2 IAV infection occurred in cats in some shelters in the USA, inducing mostly mild respiratory disease. Furthermore, cats are susceptible to experimental infection with the human H3N2 IAV that caused the pandemic in 1968. Several studies indicated that cats worldwide could be infected by H1N1 IAV during the subsequent human pandemic in 2009. In one shelter, severe cases with fatalities were noted. Finally, the highly pathogenic avian H5N1 IAV can induce a severe, fatal disease in cats, and can spread via cat-to-cat contact. In this review, the Advisory Board on Cat Diseases (ABCD), a scientifically independent board of experts in feline medicine from 11 European countries, summarises current data regarding the aetiology, epidemiology, pathogenesis, clinical picture, diagnostics, and control of feline IAV infections, as well as the zoonotic risks

    Anthropogenic infection of cats during the 2020 covid-19 pandemic

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    COVID-19 is a severe acute respiratory syndrome (SARS) caused by a new coronavirus (CoV), SARS-CoV-2, which is closely related to SARS-CoV that jumped the animalā€“human species bar-rier and caused a disease outbreak in 2003. SARS-CoV-2 is a betacoronavirus that was first described in 2019, unrelated to the commonly occurring feline coronavirus (FCoV) that is an alphacoronavirus associated with feline infectious peritonitis (FIP). SARS-CoV-2 is highly contagious and has spread globally within a few months, resulting in the current pandemic. Felids have been shown to be susceptible to SARS-CoV-2 infection. Particularly in the Western world, many people live in very close contact with their pet cats, and natural infections of cats in COVID-19-positive households have been described in several countries. In this review, the European Advisory Board on Cat Diseases (ABCD), a scientifically independent board of experts in feline medicine from 11 European Countries, discusses the current status of SARS-CoV infections in cats. The review examines the host range of SARS-CoV-2 and human-to-animal transmissions, including infections in domestic and non-domestic felids, as well as mink-to-human/-cat transmission. It summarises current data on SARS-CoV-2 prevalence in domestic cats and the results of experimental infections of cats and provides expert opinions on the clinical relevance and prevention of SARS-CoV-2 infection in cats

    The role of the chemokine receptor CXCR4 in infection with feline immunodeficiency virus

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    Infection with feline immunodeficiency virus (FIV) leads to the development of a disease state similar to AIDS in man. Recent studies have identified the chemokine receptor CXCR4 as the major receptor for cell culture-adapted strains of FIV, suggesting that FIV and human immunodeficiency virus (HIV) share a common mechanism of infection involving an interaction between the virus and a member of the seven transmembrane domain superfamily of molecules. This article reviews the evidence for the involvement of chemokine receptors in FIV infection and contrasts these findings with similar studies on the primate lentiviruses HIV and SIV (simian immunodeficiency virus)

    Measuring the humoral immune response in cats exposed to feline leukaemia virus

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    Retroviruses belong to an important and diverse family of RNA viruses capable of causing neoplastic disease in their hosts. Feline leukaemia virus (FeLV) is a gammaretrovirus that infects domestic and wild cats, causing immunodeficiency, cytopenia and neoplasia in progressively infected cats. The outcome of FeLV infection is influenced by the host immune response; progressively infected cats demonstrate weaker immune responses compared to regressively infected cats. In this study, humoral immune responses were examined in 180 samples collected from 123 domestic cats that had been naturally exposed to FeLV, using a novel ELISA to measure antibodies recognizing the FeLV surface unit (SU) glycoprotein in plasma samples. A correlation was demonstrated between the strength of the humoral immune response to the SU protein and the outcome of exposure. Cats with regressive infection demonstrated higher antibody responses to the SU protein compared to cats belonging to other outcome groups, and samples from cats with regressive infection contained virus neutralising antibodies. These results demonstrate that an ELISA that assesses the humoral response to FeLV SU complements the use of viral diagnostic tests to define the outcome of exposure to FeLV. Together these tests could allow the rapid identification of regressively infected cats that are unlikely to develop FeLV-related disease

    Gastrointestinal dysfunction in patients and mice expressing the autism-associated R451C mutation in neuroligin-3

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    Gastrointestinal (GI) problems constitute an important comorbidity in many patients with autism. Multiple mutations in the neuroligin family of synaptic adhesion molecules are implicated in autism, however whether they are expressed and impact GI function via changes in the enteric nervous system is unknown. We report the GI symptoms of two brothers with autism and an R451C mutation in Nlgn3 encoding the synaptic adhesion protein, neuroligin-3. We confirm the presence of an array of synaptic genes in the murine GI tract and investigate the impact of impaired synaptic protein expression in mice carrying the human neuroligin-3 R451C missense mutation (NL3R451C ). Assessing in vivo gut dysfunction, we report faster small intestinal transit in NL3R451C compared to wild-type mice. Using an ex vivo colonic motility assay, we show increased sensitivity to GABAA receptor modulation in NL3R451C mice, a well-established Central Nervous System (CNS) feature associated with this mutation. We further show increased numbers of small intestine myenteric neurons in NL3R451C mice. Although we observed altered sensitivity to GABAA receptor modulators in the colon, there was no change in colonic neuronal numbers including the number of GABA-immunoreactive myenteric neurons. We further identified altered fecal microbial communities in NL3R451C mice. These results suggest that the R451C mutation affects small intestinal and colonic function and alter neuronal numbers in the small intestine as well as impact fecal microbes. Our findings identify a novel GI phenotype associated with the R451C mutation and highlight NL3R451C mice as a useful preclinical model of GI dysfunction in autism. LAY SUMMARY: People with autism commonly experience gastrointestinal problems, however the cause is unknown. We report gut symptoms in patients with the autism-associated R451C mutation encoding the neuroligin-3 protein. We show that many of the genes implicated in autism are expressed in mouse gut. The neuroligin-3 R451C mutation alters the enteric nervous system, causes gastrointestinal dysfunction, and disrupts gut microbe populations in mice. Gut dysfunction in autism could be due to mutations that affect neuronal communication.This work was supported by an Idea Development Award from the United States Department of Defenseā€™s Congressionally Directed Medical Research Programs (CDMRP) Autism Research Program (AR110134) to E.L.H.-Y. and J.C.B.; the Victorian Government through the Operational Infrastructure Scheme, National Health and Medical Research Council (NHMRC) project grants (APP566642 to J.C.B. and APP1047674 to E.L.H.-Y.) and the Royal Melbourne Hospital Neuroscience Foundation. E.L.H.-Y. also received an ARC Future Fellowship (FT160100126) and an RMIT Vice Chancellorā€™s Senior Research Fellowship which supported G.K.B. and S.H. T.S., P.U., and N.Y. were funded by grants RO1AI100914, P30-DK56338, and U01-AI24290 awards to Baylor College of Medicine funded from the National Institute of Allergy and Infectious Diseases and National Institute of Diabetes and Digestive and Kidney Diseases at the National Institutes of Health (T.C.S.)
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