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Inhibition of feline immunodeficiency virus (FIV) replication by CD8(+) T lymphocytes.
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
Inhibition of feline immunodeficiency virus (FIV) replication by CD8(+) T lymphocytes./
作者:
Jeng, Chian-Ren.
出版者:
Ann Arbor : ProQuest Dissertations & Theses, : 1994,
面頁冊數:
167 p.
附註:
Source: Dissertations Abstracts International, Volume: 55-12, Section: B.
Contained By:
Dissertations Abstracts International55-12B.
標題:
Veterinary services. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=9417641
ISBN:
9798635251515
Inhibition of feline immunodeficiency virus (FIV) replication by CD8(+) T lymphocytes.
Jeng, Chian-Ren.
Inhibition of feline immunodeficiency virus (FIV) replication by CD8(+) T lymphocytes.
- Ann Arbor : ProQuest Dissertations & Theses, 1994 - 167 p.
Source: Dissertations Abstracts International, Volume: 55-12, Section: B.
Thesis (Ph.D.)--North Carolina State University, 1994.
This item must not be added to any third party search indexes.
To determine if FIV infected cats have a CD8$\\sp+$ T suppressor (Ts) cell that can inhibit virus replication in vitro, virus expression in CD8$\\sp+$ cell-depleted PBMC or unfractionated PBMC was compared in 6 naturally and 24 experimentally FIV infected cats at difference stages of infection. FIV was more readily isolated from CD8$\\sp+$ cell-depleted PBMC than unfractionated PBMC in FIV infected cats. FIV was also more readily expressed in monocyte-derived macrophages than in unfractionated PBMC in FIV infected cats. Addition of supernatant from CD8$\\sp+$ cell culture restored the inhibition of viral expression in CD8$\\sp+$ cell-depleted PBMC. These results corresponded to the pattern of inhibition of viral expression by CD8$\\sp+$ T cell and CD8$\\sp+$ T cell supernatant in FCD4-E cell infected in vitro with FIV. The presence of Ts activity in cats was associated with the stage of infection; it did not occur in FIV uninfected cats or acutely infected cats, but appeared in some of the chronically infected cats. Ts activity was inversely correlated with the number of CD8$\\sp+$ cells, but not CD4$\\sp+$ cell number or CD4:CD8 ratio. There was no correlation between the proviral burden in PBMC and the presence of Ts activity. There were clear differences in the level of viral expression, as determined by reverse transcriptase (RT) activity and indirect immunofluorescence assay (IFA) for viral antigen between CD8$\\sp+$ cell-depleted PBMC and unfractionated PBMC in Ts positive cats but not Ts negative cats. The level of FIV mRNA detected by in situ hybridization was very low in cell preparation in both Ts positive and Ts negative cats. The cytokine profiles in PBMC of Ts positive cats and Ts negative cats were also characterized by performing RT-PCR for the following cytokines: TNF-$\\alpha$, IFN-$\\alpha$, IFN-$\\Gamma$, IL-2, IL-4, IL-6 and IL-10. There were no specific cytokine profiles that correlated with the presence of Ts activity; however, there was a trend toward higher frequency of IFN-$\\alpha$ expression in Ts positive cats compared to Ts negative cats. There was no measurable IFN activity in aliquots of supernatant from CD8$\\sp+$ T cell cultures in an IFN bioassay. These results suggest that an anti-FIV CD8$\\sp+$ T suppressor cell is present in some cats chronically infected with FIV and that a soluble factor other than those examined may play a role in this inhibition. (Abstract shortened by UMI.).
ISBN: 9798635251515Subjects--Topical Terms:
3433982
Veterinary services.
Subjects--Index Terms:
CD8$\\sp+$
Inhibition of feline immunodeficiency virus (FIV) replication by CD8(+) T lymphocytes.
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Advisor: Tompkins, Wayne A. F.
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Thesis (Ph.D.)--North Carolina State University, 1994.
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To determine if FIV infected cats have a CD8$\\sp+$ T suppressor (Ts) cell that can inhibit virus replication in vitro, virus expression in CD8$\\sp+$ cell-depleted PBMC or unfractionated PBMC was compared in 6 naturally and 24 experimentally FIV infected cats at difference stages of infection. FIV was more readily isolated from CD8$\\sp+$ cell-depleted PBMC than unfractionated PBMC in FIV infected cats. FIV was also more readily expressed in monocyte-derived macrophages than in unfractionated PBMC in FIV infected cats. Addition of supernatant from CD8$\\sp+$ cell culture restored the inhibition of viral expression in CD8$\\sp+$ cell-depleted PBMC. These results corresponded to the pattern of inhibition of viral expression by CD8$\\sp+$ T cell and CD8$\\sp+$ T cell supernatant in FCD4-E cell infected in vitro with FIV. The presence of Ts activity in cats was associated with the stage of infection; it did not occur in FIV uninfected cats or acutely infected cats, but appeared in some of the chronically infected cats. Ts activity was inversely correlated with the number of CD8$\\sp+$ cells, but not CD4$\\sp+$ cell number or CD4:CD8 ratio. There was no correlation between the proviral burden in PBMC and the presence of Ts activity. There were clear differences in the level of viral expression, as determined by reverse transcriptase (RT) activity and indirect immunofluorescence assay (IFA) for viral antigen between CD8$\\sp+$ cell-depleted PBMC and unfractionated PBMC in Ts positive cats but not Ts negative cats. The level of FIV mRNA detected by in situ hybridization was very low in cell preparation in both Ts positive and Ts negative cats. The cytokine profiles in PBMC of Ts positive cats and Ts negative cats were also characterized by performing RT-PCR for the following cytokines: TNF-$\\alpha$, IFN-$\\alpha$, IFN-$\\Gamma$, IL-2, IL-4, IL-6 and IL-10. There were no specific cytokine profiles that correlated with the presence of Ts activity; however, there was a trend toward higher frequency of IFN-$\\alpha$ expression in Ts positive cats compared to Ts negative cats. There was no measurable IFN activity in aliquots of supernatant from CD8$\\sp+$ T cell cultures in an IFN bioassay. These results suggest that an anti-FIV CD8$\\sp+$ T suppressor cell is present in some cats chronically infected with FIV and that a soluble factor other than those examined may play a role in this inhibition. (Abstract shortened by UMI.).
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