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Mechanisms of control of porcine rep...

Xiao, Zhengguo.

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Mechanisms of control of porcine reproductive and respiratory syndrome virus (PRRSV) infection in pigs.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Mechanisms of control of porcine reproductive and respiratory syndrome virus (PRRSV) infection in pigs./
Author:	Xiao, Zhengguo.
Description:	169 p.
Notes:	Source: Dissertation Abstracts International, Volume: 65-02, Section: B, page: 0603.
Contained By:	Dissertation Abstracts International65-02B.
Subject:	Biology, Veterinary Science. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3121851
ISBN:	049669202X

Mechanisms of control of porcine reproductive and respiratory syndrome virus (PRRSV) infection in pigs.
Xiao, Zhengguo.

Mechanisms of control of porcine reproductive and respiratory syndrome virus (PRRSV) infection in pigs. - 169 p.

Source: Dissertation Abstracts International, Volume: 65-02, Section: B, page: 0603.

Thesis (Ph.D.)--University of Minnesota, 2004.

Porcine reproductive and respiratory syndrome virus (PRRSV) infection of pigs causes prolonged acute infection and viral persistence in lymphoid tissues for months. The T cell immune response was found to be weak and transient, subsiding after about one month. Antibody production to viral nucleocapsid is strong; however, antibody production to viral surface glycoprotein is delayed. Virus is distributed widely in lung and secondary lymphoid tissues including lymph nodes and spleen in acute infection, In contrast, the virus persists mainly in tonsils and selected lymph nodes, with at least 1000 times less virus than in acute infection. Interestingly, the PRRSV-specific T cell distribution was unrelated to viral load in secondary lymphoid tissues, with near to nil in tonsils. Dendritic cells (DC) derived from lung and bone marrow macrophages were highly permissive to PRRSV infection, and DCs were lysed soon after infection. Although expression of MHC II molecules and CD80/86 were not down regulated in the infected DCs, their function, assessed by allogeneic reaction, is impaired. In addition, PBMC and macrophages were different in permissiveness to PRRSV in vitro from that in vivo; PBMC, bone marrow and spleen macrophages were much better in supporting PRRSV reproduction, suggesting other factors are involved in PRRSV reproductions in vivo which influence the permissiveness of macrophages themselves. Furthermore, in vitro PRRSV infection of macrophages demonstrated no difference in infectivity of macrophages from four different tissues from control or infected pigs during either acute or persistent infection, which is completely different from the in vivo situation. Interestingly, the amount of residual virus in alveolar macrophages is extremely low, and they did not show significant replication when the cells were cultured in vitro. Expression of the viral receptor, sialoadhesin, is not related to differences in infectivity either in vivo or in vitro. However, despite the dysfunction of cellular and humoral responses, viral acute infection and persistence are eventually resolved, indicating some host defense mechanisms are effective. I hypothesize that cycles of macrophage lysis and replenishment cause a loss of permissive macrophages, leading to the reduction of PRRSV production, and eventually elimination of PRRSV throughout the body.

ISBN: 049669202XSubjects--Topical Terms:

1021733
Biology, Veterinary Science.

Mechanisms of control of porcine reproductive and respiratory syndrome virus (PRRSV) infection in pigs.
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520 $a Porcine reproductive and respiratory syndrome virus (PRRSV) infection of pigs causes prolonged acute infection and viral persistence in lymphoid tissues for months. The T cell immune response was found to be weak and transient, subsiding after about one month. Antibody production to viral nucleocapsid is strong; however, antibody production to viral surface glycoprotein is delayed. Virus is distributed widely in lung and secondary lymphoid tissues including lymph nodes and spleen in acute infection, In contrast, the virus persists mainly in tonsils and selected lymph nodes, with at least 1000 times less virus than in acute infection. Interestingly, the PRRSV-specific T cell distribution was unrelated to viral load in secondary lymphoid tissues, with near to nil in tonsils. Dendritic cells (DC) derived from lung and bone marrow macrophages were highly permissive to PRRSV infection, and DCs were lysed soon after infection. Although expression of MHC II molecules and CD80/86 were not down regulated in the infected DCs, their function, assessed by allogeneic reaction, is impaired. In addition, PBMC and macrophages were different in permissiveness to PRRSV in vitro from that in vivo; PBMC, bone marrow and spleen macrophages were much better in supporting PRRSV reproduction, suggesting other factors are involved in PRRSV reproductions in vivo which influence the permissiveness of macrophages themselves. Furthermore, in vitro PRRSV infection of macrophages demonstrated no difference in infectivity of macrophages from four different tissues from control or infected pigs during either acute or persistent infection, which is completely different from the in vivo situation. Interestingly, the amount of residual virus in alveolar macrophages is extremely low, and they did not show significant replication when the cells were cultured in vitro. Expression of the viral receptor, sialoadhesin, is not related to differences in infectivity either in vivo or in vitro. However, despite the dysfunction of cellular and humoral responses, viral acute infection and persistence are eventually resolved, indicating some host defense mechanisms are effective. I hypothesize that cycles of macrophage lysis and replenishment cause a loss of permissive macrophages, leading to the reduction of PRRSV production, and eventually elimination of PRRSV throughout the body.
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