Modulation of Phenotype and Function of Monocyte-derived Macrophages Following Infection with Classical Swine Fever Virus

碩士 === 國立中興大學 === 獸醫病理學研究所 === 91 === Classical swine fever (CSF) is an acute viral disease of swine. It causes severe impairment of immune modulation and results in persistent infection. CSF virus (CSFV) is a monocytotropic virus, whereas it can infect all the subpopulation of lymphocyte...

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Bibliographic Details
Main Authors: Shiao-Ching Chen, 陳筱青
Other Authors: Wei-Cheng Lee
Format: Others
Language:zh-TW
Published: 2003
Online Access:http://ndltd.ncl.edu.tw/handle/00231793521769796611
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Summary:碩士 === 國立中興大學 === 獸醫病理學研究所 === 91 === Classical swine fever (CSF) is an acute viral disease of swine. It causes severe impairment of immune modulation and results in persistent infection. CSF virus (CSFV) is a monocytotropic virus, whereas it can infect all the subpopulation of lymphocytes. CSFV can highly replicate in PAMs and not promote cell to death that suggest monocytic cells may play an important role in the persistent infection of CSFV. The aim of the study is to investigate the effect of CSFV infection on monocyte-derived macrophages (MDMs). MDMs generated from monocytes of PBMC were cultured by suspension or adherence for 4 days. The cells were infected with 0.5 MOI different strains of CSFV (ALD, s59, 94.4) for 3 days, and the expression of CSFV E2 antigen in MDMs were then detected. Further analysis the effect on expression of SLA I and SLA II molecules, phagocytosis and antigen presenting function of MDMs after CSFV infection was undertaken. The results showed that the suspensively cultured cells had smaller cell size, lower cytoplasmic granules and SLA expression compared with PAMs. The loss of the macrophage marker-SWC3 expression was also noted. The adherently cultured cells had similar cell morphology and phenotype to PAMs. It reveals the adherent condition is essential for MDMs culture. Therefore, the adherent culture system was used in following assay. Compared with PAMs, the replication of CSFV in MDMs were limited. CSFV infections delayed MDMs toward to death and down regulated the expression of SLA I and SLA II (p<0.05). However there were no significant difference in the function assays of phagocytosis and antigen presentation. Conclusively, CSFV replicated limitedly in MDMs, down regulated SLA molecule and extended the survival of MDMs, suggesting MDMs may play an important role in the persistent infection of CSFV.