The Experts below are selected from a list of 87 Experts worldwide ranked by ideXlab platform

J. L. Hubbard - One of the best experts on this subject based on the ideXlab platform.

  • Enzyme immunoassay for detection of antibodies against eastern equine encephalomyelitis Virus in sentinel chickens.
    Journal of clinical microbiology, 1991
    Co-Authors: J.g. Olson, T W Scott, L.h. Lorenz, J. L. Hubbard
    Abstract:

    We developed an enzyme immunoassay (EIA) for the detection of immunoglobulin M (IgM) and IgG subclass antibodies directed against eastern equine encephalomyelitis (EEE) Virus in chickens. The assays were compared with the serum plaque reduction neutralization test (PRNT) and the hemagglutination inhibition (HI) test for ability to detect antibodies against EEE Virus in laboratory-infected birds. No cross-reactivity was detected in serum from chickens inoculated with St. Louis encephalitis or Highlands J Virus. The interval after infection when EEE Virus-specific antibodies were first detected by IgM and IgG EIAs was found to be similar to that determined by the PRNT and HI tests: 2 to 4 days. The IgG EIA, PRNT, and HI test detected antibodies to EEE Virus for at least 27 to 30 days after inoculation. In contrast, serum from five of seven chickens did not contain detectable IgM 30 days after infection. Similarly, in all three naturally infected sentinel chickens from Maryland, IgM class antibody was undetectable 1 to 5 weeks after IgM was initially detected. EIAs provide simple and rapid alternatives to traditional tests for monitoring EEE Virus infections in sentinel chicken flocks. Moreover, the IgM EIA provides a means to separate recently infected chickens from those infected greater than or equal to 1 month earlier.

Andrew B. Allison - One of the best experts on this subject based on the ideXlab platform.

  • evolutionary genetics and vector adaptation of recombinant Viruses of the western equine encephalitis antigenic complex provides new insights into alphaVirus diversity and host switching
    Virology, 2015
    Co-Authors: Andrew B. Allison, David E Stallknecht, Edward C. Holmes
    Abstract:

    Western equine encephalitis Virus (WEEV), Highlands J Virus (HJV), and Fort Morgan Virus (FMV) are the sole representatives of the WEE antigenic complex of the genus AlphaVirus, family Togaviridae, that are endemic to North America. All three Viruses have their ancestry in a recombination event involving eastern equine encephalitis Virus (EEEV) and a Sindbis (SIN)-like Virus that gave rise to a chimeric alphaVirus that subsequently diversified into the present-day WEEV, HJV, and FMV. Here, we present a comparative analysis of the genetic, ecological, and evolutionary relationships among these recombinant-origin Viruses, including the description of a nsP4 polymerase mutation in FMV that allows it to circumvent the host range barrier to Asian tiger mosquito cells, a vector species that is normally refractory to infection. Notably, we also provide evidence that the recombination event that gave rise to these three WEEV antigenic complex Viruses may have occurred in North America.

  • Genomic sequencing of Highlands J Virus: A comparison to western and eastern equine encephalitis Viruses
    Virus Research, 2009
    Co-Authors: Andrew B. Allison, David E Stallknecht
    Abstract:

    Abstract Highlands J Virus (HJV) is a member of the genus AlphaVirus , family Togaviridae . HJV is the sole representative of the western equine encephalitis (WEE) serocomplex found in the eastern United States, and circulates in nature in an apparently identical transmission cycle as eastern equine encephalitis Virus (EEEV). North American representatives of the WEE serocomplex [HJV, WEE Virus (WEEV), and Fort Morgan Virus (FMV)] are believed to be derived from a recombination event involving EEEV and a Sindbis (SIN)-like Virus, such that the nonstructural polyprotein, the capsid, and the terminal end of the 3′ UTR are derived from EEEV, while the surface glycoproteins (E1 and E2) and small peptides (E3 and 6K) encoded in the subgenomic RNA are derived from the SIN-like Virus. In this report, the complete nucleotide sequence of HJV is described, along with a comparative analysis of the HJV nonstructural polyprotein to WEEV and EEEV.

J.g. Olson - One of the best experts on this subject based on the ideXlab platform.

  • Enzyme immunoassay for detection of antibodies against eastern equine encephalomyelitis Virus in sentinel chickens.
    Journal of clinical microbiology, 1991
    Co-Authors: J.g. Olson, T W Scott, L.h. Lorenz, J. L. Hubbard
    Abstract:

    We developed an enzyme immunoassay (EIA) for the detection of immunoglobulin M (IgM) and IgG subclass antibodies directed against eastern equine encephalomyelitis (EEE) Virus in chickens. The assays were compared with the serum plaque reduction neutralization test (PRNT) and the hemagglutination inhibition (HI) test for ability to detect antibodies against EEE Virus in laboratory-infected birds. No cross-reactivity was detected in serum from chickens inoculated with St. Louis encephalitis or Highlands J Virus. The interval after infection when EEE Virus-specific antibodies were first detected by IgM and IgG EIAs was found to be similar to that determined by the PRNT and HI tests: 2 to 4 days. The IgG EIA, PRNT, and HI test detected antibodies to EEE Virus for at least 27 to 30 days after inoculation. In contrast, serum from five of seven chickens did not contain detectable IgM 30 days after infection. Similarly, in all three naturally infected sentinel chickens from Maryland, IgM class antibody was undetectable 1 to 5 weeks after IgM was initially detected. EIAs provide simple and rapid alternatives to traditional tests for monitoring EEE Virus infections in sentinel chicken flocks. Moreover, the IgM EIA provides a means to separate recently infected chickens from those infected greater than or equal to 1 month earlier.

David E Stallknecht - One of the best experts on this subject based on the ideXlab platform.

  • evolutionary genetics and vector adaptation of recombinant Viruses of the western equine encephalitis antigenic complex provides new insights into alphaVirus diversity and host switching
    Virology, 2015
    Co-Authors: Andrew B. Allison, David E Stallknecht, Edward C. Holmes
    Abstract:

    Western equine encephalitis Virus (WEEV), Highlands J Virus (HJV), and Fort Morgan Virus (FMV) are the sole representatives of the WEE antigenic complex of the genus AlphaVirus, family Togaviridae, that are endemic to North America. All three Viruses have their ancestry in a recombination event involving eastern equine encephalitis Virus (EEEV) and a Sindbis (SIN)-like Virus that gave rise to a chimeric alphaVirus that subsequently diversified into the present-day WEEV, HJV, and FMV. Here, we present a comparative analysis of the genetic, ecological, and evolutionary relationships among these recombinant-origin Viruses, including the description of a nsP4 polymerase mutation in FMV that allows it to circumvent the host range barrier to Asian tiger mosquito cells, a vector species that is normally refractory to infection. Notably, we also provide evidence that the recombination event that gave rise to these three WEEV antigenic complex Viruses may have occurred in North America.

  • Genomic sequencing of Highlands J Virus: A comparison to western and eastern equine encephalitis Viruses
    Virus Research, 2009
    Co-Authors: Andrew B. Allison, David E Stallknecht
    Abstract:

    Abstract Highlands J Virus (HJV) is a member of the genus AlphaVirus , family Togaviridae . HJV is the sole representative of the western equine encephalitis (WEE) serocomplex found in the eastern United States, and circulates in nature in an apparently identical transmission cycle as eastern equine encephalitis Virus (EEEV). North American representatives of the WEE serocomplex [HJV, WEE Virus (WEEV), and Fort Morgan Virus (FMV)] are believed to be derived from a recombination event involving EEEV and a Sindbis (SIN)-like Virus, such that the nonstructural polyprotein, the capsid, and the terminal end of the 3′ UTR are derived from EEEV, while the surface glycoproteins (E1 and E2) and small peptides (E3 and 6K) encoded in the subgenomic RNA are derived from the SIN-like Virus. In this report, the complete nucleotide sequence of HJV is described, along with a comparative analysis of the HJV nonstructural polyprotein to WEEV and EEEV.

J S Guy - One of the best experts on this subject based on the ideXlab platform.

  • Experimental transmission of eastern equine encephalitis Virus and Highlands J Virus via semen of infected tom turkeys
    Avian Dis, 1995
    Co-Authors: J S Guy, H J Barnes, T D Siopes, L G Smith, W H Emory
    Abstract:

    Tom turkeys were experimentally inoculated with eastern equine encephalitis (EEE) Virus or Highlands J (HJ) Virus; semen was examined for presence of Virus and ability to transmit infection by artificial insemination. Mild depression and inappetence were observed in tom turkeys inoculated with either EEE Virus or HJ Virus. Toms were viremic on days 1-2 postinoculation (PI), and Virus was shed in semen on days 1-5 PI. Semen collected from EEE-Virus-inoculated or HJ-Virus-inoculated toms on days 1-2 PI and inseminated into turkey breeder hens transmitted the infection. EEE Virus was detected in one of 10 hens after insemination with semen from EEE-Virus-inoculated toms, and HJ Virus was detected in three of 10 hens after insemination with semen from HJ-Virus-inoculated toms. These results indicate that semen is a potential vehicle for transmission of EEE Virus and HJ Virus.

  • Decreased egg production in turkeys experimentally infected with eastern equine encephalitis Virus or Highlands J Virus
    Avian Dis, 1994
    Co-Authors: J S Guy, W H Emory, M D Ficken, H J Barnes, L G Smith, D P Wages
    Abstract:

    Turkey breeder hens were experimentally infected with strains of eastern equine encephalitis (EEE) Virus or Highlands J (HJ) Virus previously isolated from turkey hens experiencing decreased egg production. Depression and inappetance were observed on day 1 postexposure (PE) in hens inoculated with either EEE Virus or HJ Virus, and egg production fell in each Virus-inoculated group from approximately 75% to less than 20% within 2-3 days PE. Egg production remained depressed (less than 20%) for 15 days in EEE-Virus-inoculated hens and for 7 days in HJ-Virus-inoculated hens. EEE Virus and HJ Virus were recovered from various tissues on days 1-5 PE, and Virus was detected in eggs laid on days 2-5 PE. The findings of this study confirm that EEE Virus and HJ Virus are potential causes of decreased egg production in turkey breeder hens.

  • Experimental infection of young broiler chickens with eastern equine encephalitis Virus and Highlands J Virus.
    Avian diseases, 1994
    Co-Authors: J S Guy, H J Barnes, L G Smith
    Abstract:

    SUMMARY. Two-week-old broiler chickens were experimentally infected with either eastern equine encephalitis (EEE) Virus or Highland J (HJ) Virus. Mortality rates were 24/30 (80%) in EEE-Virus-inoculated chickens and 2/30 (7%) in HJ-Virus-inoculated chickens. Chickens inoculated with EEE Virus exhibited severe depression and somnolence on days 1-6 postexposure (PE), with 17/30 birds dying during this period. After day 6 PE, EEE-Virusinoculated chickens exhibited abdominal distention, depression, and growth retardation, and an additional seven chickens died. Pathologic changes in EEE-Virus-inoculated chickens dying on days 1-6 PE consisted of multifocal necrosis in the heart and liver, as well as lymphoid depletion and necrosis in the thymus, spleen, and bursa of Fabricius. Ascites, pericardial effusion, and right ventricular dilatation of the heart were the predominant lesions in chickens dying after day 6 PE. No clinical signs were observed in sham-inoculated controls or in most HJ-Virus-inoculated chickens. Ascites, pericardial effusion, and multifocal myocardial necrosis were observed in 2/30 HJ-Virus-inoculated chickens that died or were euthanatized after development of clinical signs. These findings indicate that both EEE Virus and HJ Virus are pathogenic for young chickens.

  • Experimental infection of young turkeys with eastern equine encephalitis Virus and Highlands J Virus
    Avian Dis, 1993
    Co-Authors: J S Guy, M D Ficken, D P Wages, H J Barnes, L G Smith
    Abstract:

    Depression, somnolence, and increased mortality were observed in 2-week-old turkeys inoculated intramuscularly with either eastern equine encephalitis (EEE) Virus or Highlands J (HJ) Virus. Mortality rates in EEE Virus- and HJ Virus-inoculated turkeys were 7/30 (23%) and 9/30 (27%), respectively; no sham-inoculated controls died. Both EEE Virus- and HJ Virus-inoculated turkeys developed viremia that lasted 2 days; peak mean titers were 5.5 and 3.2 log10 plaque-forming units per ml of blood, respectively. Pathologic changes in both EEE Virus- and HJ Virus-inoculated turkeys consisted primarily of multifocal necrosis in the heart, kidney, and pancreas, and lymphoid necrosis and depletion in the thymus, spleen, and bursa of Fabricius. The findings indicate that EEE Virus and HJ Virus are pathogenic for young turkeys.

  • High mortality of domestic turkeys associated with Highlands J Virus and eastern equine encephalitis Virus infections.
    Avian diseases, 1993
    Co-Authors: M D Ficken, J S Guy, D P Wages, J. A. Quinn, W H Emory
    Abstract:

    High mortality occurred in two flocks of commercial turkey hens placed in southern North Carolina in fall 1991. Daily mortality peaked at 3.19% in Flock 1 and 3.79% in Flock 2. Clinical signs included restlessness, somnolence, vocalization, and acute death. Gross lesions included atrophy of the bursa of Fabricius, thymus, and spleen, and watery intestinal contents. Microscopic changes included moderate to marked lymphocyte necrosis and depletion in the bursa, thymus, and spleen, widely scattered necrosis of pancreatic acinar cells, and mild villous atrophy and fusion in the JeJunum and ileum with cuboidal to low columnar epithelial cells covering the villous tips. In Flock 1, at 27 days of age, reoVirus and picornaVirus particles were detected in the feces. One week later, togaVirus-like particles were observed in fecal contents, and two of seven serum samples showed seroconversion to Highlands J Virus. Eleven days later, five of six serum samples were positive for antibodies against Highlands J Virus, with a fourfold increase in the geometric mean titer. In Flock 2, seroconversion to eastern equine encephalitis Virus was observed in four of 10 serum samples 11 days after the onset of clinical signs. Based on the above observations, it is suspected that these alphaViruses were the cause of the clinical syndrome.