The model of porcine reproductive and respiratory syndrome (PRRS) infection with porcine reproductive and respiratory syndrome virus Sichuan strain (PRRSV-SC1) in piglets was established in order to provide data for the pathopoiesis of PRRSV-SC1.The objective of the present study focused on the ultra structural pathological changes and the apoptosis in the infected tissues of piglets which were infected artificially with (PRRSV-SC1). The ultrastructural changes of piglets, the morphogenesis and distribution of PRRSV, and the morphology of apoptotic cells were observed and analysed using electron microscopic techniques. The pathomorphology of piglets and the apoptotic cells were observed and detected by microscopy, and the latter was quantitative using the TUNEL method (termina deoxy nucleotibyl transferase(TdT) -mediated dUTP-biotin nick end labelling).Microscopic lesions of lung and lymph node in the PRRSV-inoculated groups are visible. The investigation showed that microscopic lung lesions were similar in type of interstitial pneumonia but varied in severity and timing of onset. At the early stage of the infection, the lesions were characterized by acute interstitial pneumonia, the blood capillary of alveolar wall engorged and hemorrhaged, interalveolar septum. At the late stage of the infection, interalveolar septum thickened, alveolar space shrank, endothelial cells of membrana mucosa in bronchiole were hyperplasic, and there are amounts of alveolar exudates and necrotic in the lumens of bronchiole. Debris septal infiltration with mononuclear cells around bronchiole could be observed, and mechanocytes and collagenous fibril proliferated. Alveolar epithelial cells decreased, swelled and shed from the interalveolar septum.Microscopic lymph node lesions were lymphatic nodule swelled. The lymphocytes, macrophages and reticulocytes proliferated.The distribution of PRRSV observed using electron microscopy, and the investigation showed that a few typical porcine reproductive and respiratory syndrome virus (PRRSV) were observed in the lung, uterus, liver, hilar lymph node, tonsils and spleen. The nucleo-capsids have peplos, were globularlike, measured 40-65nm in diameter could be found in cytoplasm. The virions attached the membrane by budding from cellular membrane and there were vacuoles in the cytoplasm, and mature viruses aggregated in the vacuoles. The virions budded from cytoplasmic membrane and scattered in the extracellular space. The ultrastructural changes appeared in systema respiratorium and genitale. and the mostserious changes were in immunological organs and organum respiratorium. The investigation showed that various kinds of organellae were the lesion membrane structure obviously in the ultrastructural changes, especially in the mononuclear phagocytes system. The cytochondriome and rough endoplasmic reticulum (RER) changed severely. Most of the cells were necrotic, including swollen mitochondria, dilated endoplasmic reticulum, clumped or iysed chromatin. During the replication of PRRSV, some lymphocytes in tissues were apoptotic.The morphological changes of the apoptotic cells of lungs and uteruses were observed and analyzed using electron microscopic techniques after piglets had been infected by porcine reproductive and respiratory syndrome virus (PRRSV) infection. The investigation showed that the typical apoptosis of lungs and uterus were induced by PRRSV, and the apoptosis mostly occurred in the lungs’macrophages and alveolar epithelial cells and the uteruses’ endometrial cells and endometrial glandular cells. The studies also indicated that the apoptosis induced by PRRSV had typical morphogenesis with the different days-post-infection (DPI). The nucleus condensed and the cytoplasm was full of proliferated plastosome. Plastosome in the cytoplasm was hyperplasic; the smooth endoplasmic reticulum (SER) was cacuoled, there were particles dropped from the rough endoplasmic reticulum (RER). The cytoplasm was full of proliferated organelles. The cells shrank, separated from other cells, and then drop out from the nucleus and condensed; the chromatin appeared massive-like.The apoptosis induced by the viruses were detected by TUNEL, and the index numbers of the apoptosis were different with the different infection stage. At the early stage, only few apoptotic cells could be detected, apoptosis cells could be found 8 hours post infection; 30 hours post infection obvious apoptotic cells could be found and the numbers of the apoptosis cells came to a peak; 7 days post infection the numbers went down gradually. 42 days post infection, still few apoptotic cells could be detected, the apoptosis locations were mostly the target organs like the lungs, the uteruses and the lymph nodes. The distribution of apoptosis were alveolar epithelial cells, epithelial cells of bronchus, lung alveolus macrophage, monocytes in interalveolar septum, epithelial cells of endometria and uterine gland.