Virus Excretion

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Hume Field - One of the best experts on this subject based on the ideXlab platform.

  • Physiological stress and Hendra Virus in flying-foxes (Pteropus spp.), Australia.
    PLOS ONE, 2017
    Co-Authors: Lee Mcmichael, Craig S Smith, Daniel Edson, Joanne Meers, Ina Smith, David G. Mayer, Steven R. Kopp, Hume Field
    Abstract:

    Pteropid bats (flying-foxes) are the natural reservoir of Hendra Virus, an emergent paramyxoVirus responsible for fatal infection in horses and humans in Australia. Pteropus alecto (the Black flying-fox) and the paraphyletic P. conspicillatus (the Spectacled flying-fox) appear to be the primary reservoir hosts. Previous studies have suggested that physiological and ecological factors may underpin infection dynamics in flying-foxes, and subsequent spillover to horses and in turn humans. We sought to examine temporal trends in urinary cortisol concentration in wild Australian flying-fox populations, to elucidate the putative relationship between Hendra Virus infection and physiological stress. Pooled and individual urine samples were non-invasively collected from under roosting flying-foxes at two latitudinally disparate regions in the eastern Australian state of Queensland. Hendra Virus detection, and (in individual urine samples) sex and species determination were PCR-based. Urinary cortisol measurement used a validated enzyme immunoassay. We found no direct correlation between increased urinary cortisol and Hendra Virus Excretion, but our findings do suggest a biologically plausible association between low winter temperatures and elevated cortisol levels in P. alecto in the lower latitude Southeast Queensland roosts. We hypothesize an indirect association between low winter temperatures and increased Hendra Virus infection and Excretion, mediated by the physiological cost of thermoregulation. Our findings and our approach are directly relevant to elaboration of the disease ecology of Nipah Virus and other emerging henipaViruses in bats. More broadly, they inform investigation of emerging disease infection dynamics across the wildlife/livestock/human interface.

  • RESEARCH ARTICLE Routes of Hendra Virus Excretion in Naturally-Infected Flying-Foxes: Implications for Viral Transmission and
    2016
    Co-Authors: Spillover Risk, Daniel Edson, Lee Mcmichael, Hume Field, Alice Broos, Deb Melville, A Vidgen, Lauren Goldspink, Joanna Kristoffersen, Carol De Jong
    Abstract:

    Pteropid bats or flying-foxes (Chiroptera: Pteropodidae) are the natural host of Hendra Virus (HeV) which sporadically causes fatal disease in horses and humans in eastern Australia. While there is strong evidence that urine is an important infectious medium that likely drives bat to bat transmission and bat to horse transmission, there is uncertainty about the relative importance of alternative routes of Excretion such as nasal and oral secretions, and faeces. Identifying the potential routes of HeV Excretion in flying-foxes is important to effectively mit-igate equine exposure risk at the bat-horse interface, and in determining transmission rates in host-pathogen models. The aim of this study was to identify the major routes of HeV Excretion in naturally infected flying-foxes, and secondarily, to identify between-species var-iation in Excretion prevalence. A total of 2840 flying-foxes from three of the four Australian mainland species (Pteropus alecto, P. poliocephalus and P. scapulatus) were captured and sampled at multiple roost locations in the eastern states of Queensland and New South Wales between 2012 and 2014. A range of biological samples (urine and serum, and uro-genital, nasal, oral and rectal swabs) were collected from anaesthetized bats, and tested fo

  • hendra Virus infection dynamics in australian fruit bats
    PLOS ONE, 2011
    Co-Authors: Hume Field, Ina Smith, Alice Broos, Carol De Jong, Deb Melville, Craig Smith, Yu Hsin Nina Kung, Amanda Mclaughlin
    Abstract:

    Hendra Virus is a recently emerged zoonotic agent in Australia. Since first described in 1994, the Virus has spilled from its wildlife reservoir (pteropid fruit bats, or ‘flying foxes’) on multiple occasions causing equine and human fatalities. We undertook a three-year longitudinal study to detect Virus in the urine of free-living flying foxes (a putative route of Excretion) to investigate Hendra Virus infection dynamics. Pooled urine samples collected off plastic sheets placed beneath roosting flying foxes were screened for Hendra Virus genome by quantitative RT-PCR, using a set of primers and probe derived from the matrix protein gene. A total of 1672 pooled urine samples from 67 sampling events was collected and tested between 1 July 2008 and 30 June 2011, with 25% of sampling events and 2.5% of urine samples yielding detections. The proportion of positive samples was statistically associated with year and location. The findings indicate that Hendra Virus Excretion occurs periodically rather than continuously, and in geographically disparate flying fox populations in the state of Queensland. The lack of any detection in the Northern Territory suggests prevalence may vary across the range of flying foxes in Australia. Finally, our findings suggest that flying foxes can excrete Virus at any time of year, and that the apparent seasonal clustering of Hendra Virus incidents in horses and associated humans (70% have occurred June to October) reflects factors other than the presence of Virus. Identification of these factors will strengthen risk minimization strategies for horses and ultimately humans.

Ina Smith - One of the best experts on this subject based on the ideXlab platform.

  • Physiological stress and Hendra Virus in flying-foxes (Pteropus spp.), Australia.
    PLOS ONE, 2017
    Co-Authors: Lee Mcmichael, Craig S Smith, Daniel Edson, Joanne Meers, Ina Smith, David G. Mayer, Steven R. Kopp, Hume Field
    Abstract:

    Pteropid bats (flying-foxes) are the natural reservoir of Hendra Virus, an emergent paramyxoVirus responsible for fatal infection in horses and humans in Australia. Pteropus alecto (the Black flying-fox) and the paraphyletic P. conspicillatus (the Spectacled flying-fox) appear to be the primary reservoir hosts. Previous studies have suggested that physiological and ecological factors may underpin infection dynamics in flying-foxes, and subsequent spillover to horses and in turn humans. We sought to examine temporal trends in urinary cortisol concentration in wild Australian flying-fox populations, to elucidate the putative relationship between Hendra Virus infection and physiological stress. Pooled and individual urine samples were non-invasively collected from under roosting flying-foxes at two latitudinally disparate regions in the eastern Australian state of Queensland. Hendra Virus detection, and (in individual urine samples) sex and species determination were PCR-based. Urinary cortisol measurement used a validated enzyme immunoassay. We found no direct correlation between increased urinary cortisol and Hendra Virus Excretion, but our findings do suggest a biologically plausible association between low winter temperatures and elevated cortisol levels in P. alecto in the lower latitude Southeast Queensland roosts. We hypothesize an indirect association between low winter temperatures and increased Hendra Virus infection and Excretion, mediated by the physiological cost of thermoregulation. Our findings and our approach are directly relevant to elaboration of the disease ecology of Nipah Virus and other emerging henipaViruses in bats. More broadly, they inform investigation of emerging disease infection dynamics across the wildlife/livestock/human interface.

  • ecological dynamics of emerging bat Virus spillover
    Proceedings of The Royal Society B: Biological Sciences, 2015
    Co-Authors: Ina Smith, Raina K Plowright, Peggy Eby, Peter J Hudson, David A Westcott, W L Bryden, Deborah Middleton, Peter A Reid, Rosemary Mcfarlane
    Abstract:

    Viruses that originate in bats may be the most notorious emerging zoonoses that spill over from wildlife into domestic animals and humans. Understanding how these infections filter through ecological systems to cause disease in humans is of profound importance to public health. Transmission of Viruses from bats to humans requires a hierarchy of enabling conditions that connect the distribution of reservoir hosts, viral infection within these hosts, and exposure and susceptibility of recipient hosts. For many emerging bat Viruses, spillover also requires viral shedding from bats, and survival of the Virus in the environment. Focusing on Hendra Virus, but also addressing Nipah Virus, Ebola Virus, Marburg Virus and coronaViruses, we delineate this cross-species spillover dynamic from the within-host processes that drive Virus Excretion to land-use changes that increase interaction among species. We describe how land-use changes may affect co-occurrence and contact between bats and recipient hosts. Two hypotheses may explain temporal and spatial pulses of Virus shedding in bat populations: episodic shedding from persistently infected bats or transient epidemics that occur as Virus is transmitted among bat populations. Management of livestock also may affect the probability of exposure and disease. Interventions to decrease the probability of Virus spillover can be implemented at multiple levels from targeting the reservoir host to managing recipient host exposure and susceptibility.

  • hendra Virus infection dynamics in australian fruit bats
    PLOS ONE, 2011
    Co-Authors: Hume Field, Ina Smith, Alice Broos, Carol De Jong, Deb Melville, Craig Smith, Yu Hsin Nina Kung, Amanda Mclaughlin
    Abstract:

    Hendra Virus is a recently emerged zoonotic agent in Australia. Since first described in 1994, the Virus has spilled from its wildlife reservoir (pteropid fruit bats, or ‘flying foxes’) on multiple occasions causing equine and human fatalities. We undertook a three-year longitudinal study to detect Virus in the urine of free-living flying foxes (a putative route of Excretion) to investigate Hendra Virus infection dynamics. Pooled urine samples collected off plastic sheets placed beneath roosting flying foxes were screened for Hendra Virus genome by quantitative RT-PCR, using a set of primers and probe derived from the matrix protein gene. A total of 1672 pooled urine samples from 67 sampling events was collected and tested between 1 July 2008 and 30 June 2011, with 25% of sampling events and 2.5% of urine samples yielding detections. The proportion of positive samples was statistically associated with year and location. The findings indicate that Hendra Virus Excretion occurs periodically rather than continuously, and in geographically disparate flying fox populations in the state of Queensland. The lack of any detection in the Northern Territory suggests prevalence may vary across the range of flying foxes in Australia. Finally, our findings suggest that flying foxes can excrete Virus at any time of year, and that the apparent seasonal clustering of Hendra Virus incidents in horses and associated humans (70% have occurred June to October) reflects factors other than the presence of Virus. Identification of these factors will strengthen risk minimization strategies for horses and ultimately humans.

Thijs Kuiken - One of the best experts on this subject based on the ideXlab platform.

  • pathogenicity and tissue tropism of currently circulating highly pathogenic avian influenza a Virus h5n1 clade 2 3 2 in tufted ducks aythya fuligula
    Veterinary Microbiology, 2015
    Co-Authors: Marco W. G. Van De Bildt, Caroline Brojer, Geert Van Amerongen, Peter Van Run, Albert D M E Osterhaus, Dolores Gavierwiden, Thijs Kuiken
    Abstract:

    Reports describing the isolation of highly pathogenic avian influenza (HPAI) Virus (H5N1) clade 2.3.2 in feces from apparently healthy wild birds and the seemingly lower pathogenicity of this clade compared to clade 2.2 in several experimentally infected species, caused concern that the new clade might be maintained in the wild bird population. To investigate whether the pathogenicity of a clade 2.3.2 Virus was lower than that of clades previously occurring in free-living wild birds in Europe, four tufted ducks were inoculated with influenza A/duck/HongKong/1091/2011 (H5N1) clade 2.3.2 Virus. The ducks were monitored and sampled for Virus Excretion daily during 4 days, followed by pathologic, immunohistochemical, and virological investigations. The Virus produced severe disease as evidenced by clinical signs, presence of marked lesions and abundant viral antigen in several tissues, especially the central nervous system. The study shows that HPAI-H5N1 Virus clade 2.3.2 is highly pathogenic for tufted ducks and thus, they are unlikely to maintain this clade in the free-living population or serve as long-distance vectors.

  • pathogenesis of infection with 2009 pandemic h1n1 influenza Virus in isogenic guinea pigs after intranasal or intratracheal inoculation
    American Journal of Pathology, 2015
    Co-Authors: Lidewij Wiersma, Geert Van Amerongen, Peter Van Run, Thijs Kuiken, Stella Vogelzangvan E Trierum, Nella J Nieuwkoop, Mechtild Ladwig, Stefanie Banneke, Hubert Schaefer, Ron A. M. Fouchier
    Abstract:

    To elucidate the pathogenesis and transmission of influenza Virus, the ferret model is typically used. To investigate protective immune responses, the use of inbred mouse strains has proven invaluable. Here, we describe a study with isogenic guinea pigs, which would uniquely combine the advantages of the mouse and ferret models for influenza Virus infection. Strain 2 isogenic guinea pigs were inoculated with H1N1pdm09 influenza Virus A/Netherlands/602/09 by the intranasal or intratracheal route. Viral replication kinetics were assessed by determining Virus titers in nasal swabs and respiratory tissues, which were also used to assess histopathologic changes and the number of infected cells. In all guinea pigs, Virus titers peaked in nasal secretions at day 2 after inoculation. Intranasal inoculation resulted in higher Virus Excretion via the nose and higher Virus titers in the nasal turbinates than intratracheal inoculation. After intranasal inoculation, infectious Virus was recovered only from nasal epithelium; after intratracheal inoculation, it was recovered also from trachea, lung, and cerebrum. Histopathologic changes corresponded with Virus antigen distribution, being largely limited to nasal epithelium for intranasally infected guinea pigs and more widespread in the respiratory tract for intratracheally infected guinea pigs. In summary, isogenic guinea pigs show promise as a model to investigate the role of humoral and cell-mediated immunities to influenza and their effect on Virus transmission.

  • highly pathogenic avian influenza Virus h7n7 isolated from a fatal human case causes respiratory disease in cats but does not spread systemically
    American Journal of Pathology, 2010
    Co-Authors: Debby Van Riel, Geert Van Amerongen, Albert D M E Osterhaus, Guus F Rimmelzwaan, Thijs Kuiken
    Abstract:

    Highly pathogenic avian influenza Viruses (HPAIV) of the H5 and H7 subtypes primarily infect poultry but are occasionally transmitted to humans and other mammalian species, often causing severe disease. Previously we have shown that HPAIV H5N1 causes severe systemic disease in cats. In this study, we investigated whether HPAIV H7N7 isolated from a fatal human case is also able to cause disease in cats. Additionally, we compared the cell tropism of both Viruses by immunohistochemistry and Virus histochemistry. Three domestic cats were inoculated intratracheally with HPAIV H7N7. Virus Excretion was restricted to the pharynx. At necropsy, 7 days post inoculation, lesions were restricted to the respiratory tract in all cats. Lesions consisted of diffuse alveolar damage and colocalized with Virus antigen expression in type II pneumocytes and nonciliated bronchiolar cells. The attachment patterns of HPAIV H7N7 and H5N1 were similar: both Viruses attached to nonciliated bronchiolar epithelial cells, type II pneumocytes, as well as alveolar macrophages. These data show for the first time that a non-H5 HPAIV is able to infect and cause respiratory disease in cats. The failure of HPAIV H7N7 to spread beyond the respiratory tract was not explained by differences in cell tropism compared to HPAIV H5N1. These findings suggest that HPAIV H5N1 possesses other characteristics that allow it to cause systemic disease in both humans and cats.

Ron A. M. Fouchier - One of the best experts on this subject based on the ideXlab platform.

  • Wild ducks excrete highly pathogenic avian influenza Virus H5N8 (2014–2015) without clinical or pathological evidence of disease
    2019
    Co-Authors: Judith M A Van Den Brand, Theo M Bestebroer, Josanne H. Verhagen, Edwin Veldhuis J. B. Kroeze, Marco W. G. Van De Bildt, Rogier Bodewes, Sander Herfst, Mathilde Richard, Pascal Lexmond, Ron A. M. Fouchier
    Abstract:

    Highly pathogenic avian influenza (HPAI) is essentially a poultry disease. Wild birds have traditionally not been involved in its spread, but the epidemiology of HPAI has changed in recent years. After its emergence in southeastern Asia in 1996, H5 HPAI Virus of the Goose/Guangdong lineage has evolved into several sub-lineages, some of which have spread over thousands of kilometers via long-distance migration of wild waterbirds. In order to determine whether the Virus is adapting to wild waterbirds, we experimentally inoculated the HPAI H5N8 Virus clade 2.3.4.4 group A from 2014 into four key waterbird species—Eurasian wigeon (Anas penelope), common teal (Anas crecca), mallard (Anas platyrhynchos), and common pochard (Aythya ferina)—and compared Virus Excretion and disease severity with historical data of the HPAI H5N1 Virus infection from 2005 in the same four species. Our results showed that Excretion was highest in Eurasian wigeons for the 2014 Virus, whereas Excretion was highest in common pochards and mallards for the 2005 Virus. The 2014 Virus infection was subclinical in all four waterbird species, while the 2005 Virus caused clinical disease and pathological changes in over 50% of the common pochards. In chickens, the 2014 Virus infection caused systemic disease and high mortality, similar to the 2005 Virus. In conclusion, the evidence was strongest for Eurasian wigeons as long-distance vectors for HPAI H5N8 Virus from 2014. The implications of the switch in species-specific Virus Excretion and decreased disease severity may be that the HPAI H5 Virus more easily spreads in the wild-waterbird population.

  • pathogenesis of infection with 2009 pandemic h1n1 influenza Virus in isogenic guinea pigs after intranasal or intratracheal inoculation
    American Journal of Pathology, 2015
    Co-Authors: Lidewij Wiersma, Geert Van Amerongen, Peter Van Run, Thijs Kuiken, Stella Vogelzangvan E Trierum, Nella J Nieuwkoop, Mechtild Ladwig, Stefanie Banneke, Hubert Schaefer, Ron A. M. Fouchier
    Abstract:

    To elucidate the pathogenesis and transmission of influenza Virus, the ferret model is typically used. To investigate protective immune responses, the use of inbred mouse strains has proven invaluable. Here, we describe a study with isogenic guinea pigs, which would uniquely combine the advantages of the mouse and ferret models for influenza Virus infection. Strain 2 isogenic guinea pigs were inoculated with H1N1pdm09 influenza Virus A/Netherlands/602/09 by the intranasal or intratracheal route. Viral replication kinetics were assessed by determining Virus titers in nasal swabs and respiratory tissues, which were also used to assess histopathologic changes and the number of infected cells. In all guinea pigs, Virus titers peaked in nasal secretions at day 2 after inoculation. Intranasal inoculation resulted in higher Virus Excretion via the nose and higher Virus titers in the nasal turbinates than intratracheal inoculation. After intranasal inoculation, infectious Virus was recovered only from nasal epithelium; after intratracheal inoculation, it was recovered also from trachea, lung, and cerebrum. Histopathologic changes corresponded with Virus antigen distribution, being largely limited to nasal epithelium for intranasally infected guinea pigs and more widespread in the respiratory tract for intratracheally infected guinea pigs. In summary, isogenic guinea pigs show promise as a model to investigate the role of humoral and cell-mediated immunities to influenza and their effect on Virus transmission.

Jeffrey S Hall - One of the best experts on this subject based on the ideXlab platform.

  • experimental challenge of a north american bat species big brown bat eptesicus fuscus with sars cov 2
    Transboundary and Emerging Diseases, 2021
    Co-Authors: Jeffrey S Hall, Sean W Nashold, Susan Knowles, Ariel Elizabeth Leon, Tonie E Rocke, Saskia Annatina Keller, Mariano Carossino, Udeni B R Balasuriya, Erik K Hofmeister
    Abstract:

    The recently emerged novel coronaVirus, SARS-CoV-2, is phylogenetically related to bat coronaViruses (CoVs), specifically SARS-related CoVs from the Eurasian bat family Rhinolophidae. As this human pandemic Virus has spread across the world, the potential impacts of SARS-CoV-2 on native North American bat populations are unknown, as is the ability of North American bats to serve as reservoirs or intermediate hosts able to transmit the Virus to humans or to other animal species. To help determine the impacts of the pandemic Virus on North American bat populations, we experimentally challenged big brown bats (Eptesicus fuscus) with SARS-CoV-2 under BSL-3 conditions. We inoculated the bats both oropharyngeally and nasally, and over the ensuing three weeks we measured infectivity, pathology, Virus concentrations in tissues, oral and rectal Virus Excretion, Virus transmission, and clinical signs of disease. We found no evidence of SARS-CoV-2 infection in any examined bat, including no viral Excretion, no transmission, no detectable Virus in tissues, and no signs of disease or pathology. Based on our findings it appears that big brown bats are resistant to infection with the SARS-CoV-2. The potential susceptibility of other North American bat species to SARS-CoV-2 remains to be investigated.

  • avian influenza in shorebirds experimental infection of ruddy turnstones arenaria interpres with avian influenza Virus
    Influenza and Other Respiratory Viruses, 2013
    Co-Authors: Jeffrey S Hall, Christian J Franson, Joshua L Teslaa, Sean W Nashold, Scott Krauss, David E Stallknecht, Richard J Webby, Robert G Webster
    Abstract:

    Please cite this paper as: Hall et al. (2012) Avian influenza in shorebirds: experimental infection of ruddy turnstones (Arenaria interpres) with avian influenza Virus. Influenza and Other Respiratory Viruses DOI: 10.1111/j.1750-2659.2012.00358.x. Background  Low pathogenic avian influenza Viruses (LPAIV) have been reported in shorebirds, especially at Delaware Bay, USA, during spring migration. However, data on patterns of Virus Excretion, minimal infectious doses, and clinical outcome are lacking. The ruddy turnstone (Arenaria interpres) is the shorebird species with the highest prevalence of influenza Virus at Delaware Bay. Objectives  The primary objective of this study was to experimentally assess the patterns of influenza Virus Excretion, minimal infectious doses, and clinical outcome in ruddy turnstones. Methods  We experimentally challenged ruddy turnstones using a common LPAIV shorebird isolate, an LPAIV waterfowl isolate, or a highly pathogenic H5N1 avian influenza Virus. Cloacal and oral swabs and sera were analyzed from each bird. Results  Most ruddy turnstones had pre-existing antibodies to avian influenza Virus, and many were infected at the time of capture. The infectious doses for each challenge Virus were similar (103·6–104·16 EID50), regardless of exposure history. All infected birds excreted similar amounts of Virus and showed no clinical signs of disease or mortality. Influenza A-specific antibodies remained detectable for at least 2 months after inoculation. Conclusions  These results provide a reference for interpretation of surveillance data, modeling, and predicting the risks of avian influenza transmission and movement in these important hosts.

  • experimental challenge and pathology of highly pathogenic avian influenza Virus h5n1 in dunlin calidris alpina an intercontinental migrant shorebird species
    Influenza and Other Respiratory Viruses, 2011
    Co-Authors: Jeffrey S Hall, Robert E. Gill, Christian J Franson, Carol U Meteyer, Joshua L Teslaa, Sean W Nashold, Robert J Dusek
    Abstract:

    Please cite this paper as: Hall et al. (2011). Experimental challenge and pathology of highly pathogenic avian influenza Virus H5N1 in dunlin (Calidris alpina), an intercontinental migrant shorebird species. Influenza and Other Respiratory Viruses 5(5), 365–372. Background  Shorebirds (Charadriiformes) are considered one of the primary reservoirs of avian influenza. Because these species are highly migratory, there is concern that infected shorebirds may be a mechanism by which highly pathogenic avian influenza Virus (HPAIV) H5N1 could be introduced into North America from Asia. Large numbers of dunlin (Calidris alpina) migrate from wintering areas in central and eastern Asia, where HPAIV H5N1 is endemic, across the Bering Sea to breeding areas in Alaska. Low pathogenic avian influenza Virus has been previously detected in dunlin, and thus, dunlin represent a potential risk to transport HPAIV to North America. To date no experimental challenge studies have been performed in shorebirds. Methods  Wild dunlin were inoculated intranasally and intrachoanally various doses of HPAIV H5N1. The birds were monitored daily for Virus Excretion, disease signs, morbidity, and mortality. Results  The infectious dose of HPAIV H5N1 in dunlin was determined to be 101.7 EID50/100 μl and that the lethal dose was 101.83 EID50/100 μl. Clinical signs were consistent with neurotropic disease, and histochemical analyses revealed that infection was systemic with viral antigen and RNA most consistently found in brain tissues. Infected birds excreted relatively large amounts of Virus orally (104 EID50) and smaller amounts cloacally. Conclusions  Dunlin are highly susceptible to infection with HPAIV H5N1. They become infected after exposure to relatively small doses of the Virus and if they become infected, they are most likely to suffer mortality within 3–5 days. These results have important implications regarding the risks of transport and transmission of HPAIV H5N1 to North America by this species and raises questions for further investigation.