Virus Survival

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Nicholas J. C. King - One of the best experts on this subject based on the ideXlab platform.

  • A theoretical model of the West Nile Virus Survival data
    BMC Immunology, 2017
    Co-Authors: James K. Peterson, Alison M. Kesson, Nicholas J. C. King
    Abstract:

    Background In this work, we develop a theoretical model that explains the Survival data in West Nile Virus infection. Results We build a model based on three cell populations in an infected host; the collateral damage cells, the infected dividing cell, and the infected non-dividing cells. T cell-mediated lysis of each of these populations is dependent on the level of MHC-1 upregulation, which is different in the two infected cell populations, interferon-gamma and free Virus levels. Conclusions The model allows us to plot a measure of host health versus time for a range of initial viral doses and from that infer the dependence of minimal health versus viral dose. This inferred functional relationship between the minimal host health and viral dose is very similar to the data that has been collected for WNV Survival curves under experimental conditions.

  • A theoretical model of the West Nile Virus Survival data.
    BMC Immunology, 2017
    Co-Authors: James K. Peterson, Alison M. Kesson, Nicholas J. C. King
    Abstract:

    In this work, we develop a theoretical model that explains the Survival data in West Nile Virus infection. We build a model based on three cell populations in an infected host; the collateral damage cells, the infected dividing cell, and the infected non-dividing cells. T cell-mediated lysis of each of these populations is dependent on the level of MHC-1 upregulation, which is different in the two infected cell populations, interferon-gamma and free Virus levels. The model allows us to plot a measure of host health versus time for a range of initial viral doses and from that infer the dependence of minimal health versus viral dose. This inferred functional relationship between the minimal host health and viral dose is very similar to the data that has been collected for WNV Survival curves under experimental conditions.

James K. Peterson - One of the best experts on this subject based on the ideXlab platform.

  • A theoretical model of the West Nile Virus Survival data
    BMC Immunology, 2017
    Co-Authors: James K. Peterson, Alison M. Kesson, Nicholas J. C. King
    Abstract:

    Background In this work, we develop a theoretical model that explains the Survival data in West Nile Virus infection. Results We build a model based on three cell populations in an infected host; the collateral damage cells, the infected dividing cell, and the infected non-dividing cells. T cell-mediated lysis of each of these populations is dependent on the level of MHC-1 upregulation, which is different in the two infected cell populations, interferon-gamma and free Virus levels. Conclusions The model allows us to plot a measure of host health versus time for a range of initial viral doses and from that infer the dependence of minimal health versus viral dose. This inferred functional relationship between the minimal host health and viral dose is very similar to the data that has been collected for WNV Survival curves under experimental conditions.

  • A theoretical model of the West Nile Virus Survival data.
    BMC Immunology, 2017
    Co-Authors: James K. Peterson, Alison M. Kesson, Nicholas J. C. King
    Abstract:

    In this work, we develop a theoretical model that explains the Survival data in West Nile Virus infection. We build a model based on three cell populations in an infected host; the collateral damage cells, the infected dividing cell, and the infected non-dividing cells. T cell-mediated lysis of each of these populations is dependent on the level of MHC-1 upregulation, which is different in the two infected cell populations, interferon-gamma and free Virus levels. The model allows us to plot a measure of host health versus time for a range of initial viral doses and from that infer the dependence of minimal health versus viral dose. This inferred functional relationship between the minimal host health and viral dose is very similar to the data that has been collected for WNV Survival curves under experimental conditions.

Alison M. Kesson - One of the best experts on this subject based on the ideXlab platform.

  • A theoretical model of the West Nile Virus Survival data
    BMC Immunology, 2017
    Co-Authors: James K. Peterson, Alison M. Kesson, Nicholas J. C. King
    Abstract:

    Background In this work, we develop a theoretical model that explains the Survival data in West Nile Virus infection. Results We build a model based on three cell populations in an infected host; the collateral damage cells, the infected dividing cell, and the infected non-dividing cells. T cell-mediated lysis of each of these populations is dependent on the level of MHC-1 upregulation, which is different in the two infected cell populations, interferon-gamma and free Virus levels. Conclusions The model allows us to plot a measure of host health versus time for a range of initial viral doses and from that infer the dependence of minimal health versus viral dose. This inferred functional relationship between the minimal host health and viral dose is very similar to the data that has been collected for WNV Survival curves under experimental conditions.

  • A theoretical model of the West Nile Virus Survival data.
    BMC Immunology, 2017
    Co-Authors: James K. Peterson, Alison M. Kesson, Nicholas J. C. King
    Abstract:

    In this work, we develop a theoretical model that explains the Survival data in West Nile Virus infection. We build a model based on three cell populations in an infected host; the collateral damage cells, the infected dividing cell, and the infected non-dividing cells. T cell-mediated lysis of each of these populations is dependent on the level of MHC-1 upregulation, which is different in the two infected cell populations, interferon-gamma and free Virus levels. The model allows us to plot a measure of host health versus time for a range of initial viral doses and from that infer the dependence of minimal health versus viral dose. This inferred functional relationship between the minimal host health and viral dose is very similar to the data that has been collected for WNV Survival curves under experimental conditions.

Kalmia E Kniel - One of the best experts on this subject based on the ideXlab platform.

  • NoroVirus Surrogate Survival on Spinach During Preharvest Growth
    Phytopathology, 2013
    Co-Authors: Kirsten A. Hirneisen, Kalmia E Kniel
    Abstract:

    ABSTRACT Produce can become contaminated with human viral pathogens in the field through soil, feces, or water used for irrigation; through application of manure, biosolids, pesticides, and fertilizers; and through dust, insects, and animals. The objective of this study was to assess the Survival and stability of human noroViruses and noroVirus surrogates (Murine noroVirus [MNV] and Tulane Virus [TV]) on foliar surfaces of spinach plants in preharvest growth conditions. Spinach plants were housed in a biocontrol chamber at optimal conditions for up to 7 days and infectivity was determined by plaque assay. Virus inoculation location had the largest impact on Virus Survival as Viruses present on adaxial leaf surfaces had lower decimal reduction time (D values) than Viruses present on abaxial leaf surfaces. Under certain conditions, spinach type impacted Virus Survival, with greater D values observed from Survival on semi-savoy spinach leaves. Additional UVA and UVB exposure to mimic sunlight affected Virus ...

  • Pre-harvest Viral Contamination of Crops Originating from Fecal Matter
    Food and Environmental Virology, 2010
    Co-Authors: Jie Wei, Kalmia E Kniel
    Abstract:

    Pre-harvest contamination of fresh produce and fruits is a possible route for viral transmission which should not be ignored. The contamination originates from Viruses shed in human or animal fecal materials which eventually reach crops through many steps and hurdles, including spread of Viruses into the agricultural environment through leakage of septic tanks/pipes or runoff from animal lagoons, Virus Survival during biosolids and manure treatment, Virus Survival and transport in soil and subsequent contamination of irrigation water, and Virus transmission to crops through irrigation water, etc. Initially, large quantities of Virus particles may be released from infected humans or animals, and then in the environment Viruses are gradually inactivated under various natural conditions (e.g., temperature, water activity, microbial activities, etc.) and only a tiny portion of Viruses may reach crops and cause the contamination. However, the fact that the infectious dose of some foodborne Viruses is as low as 10–100 particles makes the pre-harvest contamination still a threat to human health. In the USA, the Environmental Protection Agency (USEPA) and United States Department of Agriculture (USDA) regulations and guidances on proper treatment and usage of manure and biosolids for agricultural purpose may largely reduce the release of Viruses to the environment; however, pre-harvest viral contamination due to fecal matter is not completely avoidable. This review focuses on the current knowledge of pre-harvest viral contamination and describes the complex transmission process regarding the presence and Survival of Virus in soil and fecal material, the effect of different biosolids/manure treatment on Virus inactivation, the transmission of Virus from soil to water, the contamination of crops by irrigation water and Survival of Virus on crops.

Salma Abd El-sattar - One of the best experts on this subject based on the ideXlab platform.