Effect of Cell Maturation on the Susceptibility of Peripheral Blood Monocytes of Healthy Porcine Circovirus Type II-Carrier Pigs to PCV2 Infection

• Main Authors: Ying-Jun Lai, 賴盈君
• Other Authors: 龐飛
• Format: Others
• Language: zh-TW
• Published: 2008
• Online Access: http://ndltd.ncl.edu.tw/handle/40635561386091846217

碩士 === 國立臺灣大學 === 獸醫學研究所 === 96 === Porcine circovirus type 2 (PCV2) is the primary causative agent of postweaning multisystemic wasting syndrome (PMWS). At present, monocyte/macrophage lineage cells are considered as one of the major target cells; however, no evidence of PCV2 replication has been demonstrated in these cells in vitro. Our previous studies have led to the speculation that PCV2 once enters porcine alveolar macrophages (PAMs) by either passive endocytosis or phagocytosis may start intranuclear translocation and proliferation following lipopolysaccharide (LPS) stimulation. Tissue macrophages are derived from blood monocytes. Cell differentiation may induce some factors which may enhance viral infection and replication, such as receptors or transcription factors, and cell activation may up- or down-regulate the expression of these factors. Thus, the objective of the study was to evaluate the effect of cell differentiation with or without LPS stimulation on the susceptibility of peripheral blood monocytes (PBMs) to PCV2 infection. The results showed that a small amount of PCV2 antigens could be translocated from the cytoplasm into nucleus followed by viral replication with time in PBMs collected from healthy PCV2-carrier pigs after long term in vitro culture. Stimulation with appropriate concentration of LPS could promote earlier intranuclear translocation of PCV2 antigens and proliferation of PCV2 in PBMs. Moreover, the susceptibility of PBMs to PCV2 increased as PBMs transformed into macrophages with or without LPS stimulation; however, LPS stimulation seemed to induce a relatively quicker but insignificant maturation in PBMs. It is speculated that LPS may activate cells and promote intranuclear translocation of PCV2 earlier through some specific signal transduction pathways, and the actual mechanism of cell differentiation in promoting PCV2 replication needs to be further elucidated.