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Virus Diseases Commons™

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2014

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Articles 61 - 63 of 63

Full-Text Articles in Virus Diseases

Theories On Varicella Zoster Virus Reactivation Based On Shingles Patterns, Ralph Nussbaum Jan 2014

Theories On Varicella Zoster Virus Reactivation Based On Shingles Patterns, Ralph Nussbaum

The Science Journal of the Lander College of Arts and Sciences

Herpes zoster, a disease also known as shingles or as zoster, infects the sensory nerve ganglion and the peripheral nerve and its branches, resulting in pain to the affected dermatomes. Infection results from reactivation of the varicella-zoster virus, the same virus which causes varicella, or chickenpox. The varicella-zoster virus usually causes chickenpox to its host at an early age and then withdraws to the dorsal root ganglia where it enters a latency stage. The virus may reemerge at any time and infect its host with shingles. As shingles is most common in ages 50 and above, it is assumed that …

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Bovine Herpesvirus 1 Productive Infection Stimulates Inflammosome Formation And Caspase 1 Activity, Jianlin Wang, Jeffrey Alexander, Matthew S. Wiebe, Clinton J. Jones Jan 2014

Bovine Herpesvirus 1 Productive Infection Stimulates Inflammosome Formation And Caspase 1 Activity, Jianlin Wang, Jeffrey Alexander, Matthew S. Wiebe, Clinton J. Jones

Nebraska Center for Virology: Faculty Publications

Bovine herpesvirus 1 (BoHV-1), a significant viral pathogen of cattle, causes inflammation in affected tissue during acute infection. Consequently, we tested whether productively infected bovine cells stimulate inflammasome formation. Expression of two components required for inflammasome formation, the DNA sensor IFI16 (gamma-interferon-inducible protein 16) and NLRP3 (NOD-like receptor family, pyrin domain containing 3), were induced in bovine kidney cells by eight hours after infection. IFI16 was detected in punctate granules localized to the cytoplasm and nucleus. During productive infection, more than ten times more cells were caspase 1 positive, which is activated following inflammasome formation. Two caspase 1 inhibitors had …

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Using Quantitative Disease Dynamics As A Tool For Guiding Response To Avian Influenza In Poultry In The United States Of America, K. M. Pepin, E. Spackman, J. D. Brown, K. L. Pabilonia, Lindsey P. Garber, J. Todd Weaver, D. A. Kennedy, Kelly A. Patyk, K. P. Huyvaert, Ryan S. Miller, Alan B. Franklin, Kerri Pedersen, T. L. Bogich, P. Rohani, Susan A. Shriner, Colleen T. Webb, S. Riley Jan 2014

Using Quantitative Disease Dynamics As A Tool For Guiding Response To Avian Influenza In Poultry In The United States Of America, K. M. Pepin, E. Spackman, J. D. Brown, K. L. Pabilonia, Lindsey P. Garber, J. Todd Weaver, D. A. Kennedy, Kelly A. Patyk, K. P. Huyvaert, Ryan S. Miller, Alan B. Franklin, Kerri Pedersen, T. L. Bogich, P. Rohani, Susan A. Shriner, Colleen T. Webb, S. Riley

United States Department of Agriculture Wildlife Services: Staff Publications

Wild birds are the primary source of genetic diversity for influenza A viruses that eventually emerge in poultry and humans. Much progress has been made in the descriptive ecology of avian influenza viruses (AIVs), but contributions are less evident from quantitative studies (e.g., those including disease dynamic models). Transmission between host species, individuals and flocks has not been measured with sufficient accuracy to allow robust quantitative evaluation of alternate control protocols. We focused on the United States of America (USA) as a case study for determining the state of our quantitative knowledge of potential AIV emergence processes from wild hosts …

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