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Immune dysfunction following infecti...

Cloud, Sandra Sue.

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Immune dysfunction following infection with chicken anemia virus and infectious bursal disease virus.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Immune dysfunction following infection with chicken anemia virus and infectious bursal disease virus./
作者:	Cloud, Sandra Sue.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 1993,
面頁冊數:	195 p.
附註:	Source: Dissertations Abstracts International, Volume: 55-06, Section: B.
Contained By:	Dissertations Abstracts International55-06B.
標題:	Animal diseases. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=9334016

Immune dysfunction following infection with chicken anemia virus and infectious bursal disease virus.
Cloud, Sandra Sue.

Immune dysfunction following infection with chicken anemia virus and infectious bursal disease virus. - Ann Arbor : ProQuest Dissertations & Theses, 1993 - 195 p.

Source: Dissertations Abstracts International, Volume: 55-06, Section: B.

Thesis (Ph.D.)--University of Delaware, 1993.

This item must not be sold to any third party vendors.

The potential effect of chicken anemia virus (CAV) alone or in combination with infectious bursal disease virus (IBDV) on the immature avian immune system was determined by measuring alterations in hematocrit values, lymphoid organ to body weight ratios and lymphoid cell concentrations at various time intervals post inoculation (PI). CAV inoculation of one-day-old susceptible chickens induced substantial but transient thymic atrophy, bursal atrophy, generalized lymphocytopenia, anemia, aplastic bone marrow and elevated ratios of T helper to cytotoxic T cell populations prior to recovery. T helper and cytotoxic T cells in the thymus, Ia expressing cells in the bursa and macrophage in spleen were specifically depressed following CAV inoculation. Severity of clinical signs, changes in lymphocyte populations or their ratios and the time required for recovery increased in birds simultaneously inoculated with CAV and IBDV. Functional abnormalities induced by CAV were assessed by measuring the in vivo response to heterologous live vaccine viruses administered during the acute phase of CAV infection (2 weeks PI). Immunological responses were evaluated based on production of specific antibody, protection against appropriate challenge virus and development of persistent vaccine reactions. The possible underlying mechanisms involved in the development of immune dysfunction following infection were investigated using in vitro lymphoproliferation assays. Mitogen stimulated splenic lymphocytes were tested for their ability to produce and/or secrete two different lymphokines, interleukin-2 (IL-2) and interferon (IFN). CAV infection was associated with the development of in vivo immune dysfunction based on decreased Newcastle disease virus antibody titers, increased incidence of persistent fowlpox vaccination lesions and enhanced protection against infectious laryngotracheitis challenge virus following vaccination during the acute phase of CAV infection. Splenic lymphocytes harvested from chickens during the acute phase were characterized by a depressed in vitro lymphoproliferation response to mitogens and decreased ability to produce and/or secrete IL-2 and IFN. Increases and decreases in specific lymphocyte subpopulations and/or their ability to produce the appropriate regulatory lymphokines following CAV infection in young chickens can partially explain the demonstrated in vivo immune dysfunction. Concomitant infection with IBDV enhanced the deregulation of immune responses induced by CAV alone.Subjects--Topical Terms:

3181862
Animal diseases.

Immune dysfunction following infection with chicken anemia virus and infectious bursal disease virus.
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520 $a The potential effect of chicken anemia virus (CAV) alone or in combination with infectious bursal disease virus (IBDV) on the immature avian immune system was determined by measuring alterations in hematocrit values, lymphoid organ to body weight ratios and lymphoid cell concentrations at various time intervals post inoculation (PI). CAV inoculation of one-day-old susceptible chickens induced substantial but transient thymic atrophy, bursal atrophy, generalized lymphocytopenia, anemia, aplastic bone marrow and elevated ratios of T helper to cytotoxic T cell populations prior to recovery. T helper and cytotoxic T cells in the thymus, Ia expressing cells in the bursa and macrophage in spleen were specifically depressed following CAV inoculation. Severity of clinical signs, changes in lymphocyte populations or their ratios and the time required for recovery increased in birds simultaneously inoculated with CAV and IBDV. Functional abnormalities induced by CAV were assessed by measuring the in vivo response to heterologous live vaccine viruses administered during the acute phase of CAV infection (2 weeks PI). Immunological responses were evaluated based on production of specific antibody, protection against appropriate challenge virus and development of persistent vaccine reactions. The possible underlying mechanisms involved in the development of immune dysfunction following infection were investigated using in vitro lymphoproliferation assays. Mitogen stimulated splenic lymphocytes were tested for their ability to produce and/or secrete two different lymphokines, interleukin-2 (IL-2) and interferon (IFN). CAV infection was associated with the development of in vivo immune dysfunction based on decreased Newcastle disease virus antibody titers, increased incidence of persistent fowlpox vaccination lesions and enhanced protection against infectious laryngotracheitis challenge virus following vaccination during the acute phase of CAV infection. Splenic lymphocytes harvested from chickens during the acute phase were characterized by a depressed in vitro lymphoproliferation response to mitogens and decreased ability to produce and/or secrete IL-2 and IFN. Increases and decreases in specific lymphocyte subpopulations and/or their ability to produce the appropriate regulatory lymphokines following CAV infection in young chickens can partially explain the demonstrated in vivo immune dysfunction. Concomitant infection with IBDV enhanced the deregulation of immune responses induced by CAV alone.
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