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BackgroundMouse hepatitis virus (MHV) A59 is a highly infectious pathogen and starts in the respiratory tract and progresses to systemic infection in laboratory mice. The complement system is an important part of the host immune response to viral infection. It is not clear the role of the classical complement pathway in MHV infection.ObjectivesThe purpose of this study was to determine the importance of the classical pathway in coronavirus pathogenesis by comparing C1qa KO mice and wild-type mice.MethodsWe generated a C1qa KO mouse using CRISPR/Cas9 technology and compared the susceptibility to MHV A59 infection between C1qa KO and wild-type mice. Histopathological and immunohistochemical changes, viral loads, and chemokine expressions in both mice were measured.ResultsMHV A59-infected C1qa KO mice showed severe histopathological changes, such as hepatocellular necrosis and interstitial pneumonia, compared to MHV A59-infected wild-type mice. Virus copy numbers in the olfactory bulb, liver, and lungs of C1qa KO mice were significantly higher than those of wild-type mice. The increase in viral copy numbers in C1qa KO mice was consistent with the histopathologic changes in organs. These results indicate that C1qa deficiency enhances susceptibility to MHV A59 systemic infection in mice. In addition, this enhanced susceptibility effect is associated with dramatic elevations in spleen IFN-γ, MIP-1 α, and MCP-1 in C1qa KO mice.ConclusionsThese data suggest that C1qa deficiency enhances susceptibility to MHV A59 systemic infection, and activation of the classical complement pathway may be important for protecting the host against MHV A59 infection.  相似文献   
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This study was conducted to investigate the effects of dietary propolis supplementation on growth performance, immune responses, disease resistance and body composition of juvenile eel, Anguilla japonica, in order to evaluate its bioavailability as a feed additive for this species. A total of 540 fish averaging 7.7?±?0.22?g (mean?±?SD) were randomly distributed into 18 tanks in groups of 30, and each tank was then randomly assigned to one of three replicates of six diets containing 0 (P0), 0.25 (P0.25), 0.5 (P0.5), 1.0 (P1), 2.0 (P2) and 4.0 (P4) % dietary propolis. At the end of 12?weeks of feeding trial, weight gain (WG), specific growth rate (SGR), feed efficiency (FE) and protein efficiency ratio (PER) of fish fed P0.5 diet were significantly higher than those of fish fed P0, P1, P2 and P4 diets (P?<?0.05). These parameters were 148.9%, 0.72% day?1, 94.4% and 2.9, respectively for fish fed P0.5 diet. Serum lysozyme activity of fish fed P0.5 (105.7 units mL?1) and P1 (106.0 units mL?1) diets were significantly higher than those of fish fed P0, P0.25, P2 and P4 diets. Mucus lysozyme activity of fish fed P1 (8.4 units 10?cm?2) diet was significantly higher than those of fish fed P0, P2 and P4 diets. Results indicated that the optimum dietary propolis supplementation levels could be 0.25?C0.5% for optimum growth and feed efficiency, and 0.5?C1% for enhanced immune responses and disease resistance in eel, A. japonica. This study may suggest that the dietary propolis level for the optimum immune responses could be higher than the level for the optimum growth of eel.  相似文献   
3.
Journal of Crop Science and Biotechnology - In this study, the effect of light on the regulation of flavonoid production in young barley leaves (YBLs) was investigated. YBLs following germination...  相似文献   
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A 2 × 3 factorial design was used to reevaluate the dietary protein requirements and to determine the optimum dietary protein to energy (P/E) ratios in Japanese eel, Anguilla japonica, reared in the recirculating system. For each of two experiments, six experimental diets (45P16, 45P17, 45P19, 50P16, 50P17, and 50P19) were formulated and prepared to contain two protein levels (45 and 50%) and three energy levels (16, 17, and 19 kJ/g diet) at each protein level. In the first experiment, glass eel of initial weight 0.1 ± 0.02 g (mean ± SD) were used, while the second experiment was conducted with juvenile eel of initial weight 15.0 ± 3 g (mean ± SD). The first and second experimental periods were 6 and 16 wk for the glass and juvenile eel, respectively. At the end of the first experiment, there were no protein, energy, and their interaction effects. Also, there were no significant differences in weight gain (WG), specific growth rate (SGR), feed efficiency (FE), and protein efficiency ratio (PER) for glass Japanese eel fed all diets. Although there were no significant differences in growth parameters of glass eel fed all experimental diets, these parameters were higher for fish fed 50P16 than for fish fed the other diets. For the second experiment, there were significant protein effects on WG, SGR, and PER (P < 0.05). However, there were neither significant energy effects nor protein and energy interaction effects on WG, SGR, FE, and PER. Fish fed 45P19 had a higher WG, SGR, and PER than did fish fed 45P16, 50P16, and 50P19 (P < 0.05). However, there were no significant differences in growth parameters among fish fed 45P16, 45P17, 50P16, 50P17, and 50P19 and among those fed 45P17, 45P19, and 50P17. These results may indicate that the optimum dietary protein requirement and the P/E ratio could be 44.3% and 24.1 mg protein/kJ (45P19), respectively, in juvenile Japanese eel, based on WG, SGR, and PER.  相似文献   
5.
Viperin is an interferon-inducible protein that is directly induced in cells by human cytomegalovirus (HCMV) infection. Why HCMV would induce viperin, which has antiviral activity, is unknown. We show that HCMV-induced viperin disrupts cellular metabolism to enhance the infectious process. Viperin interaction with the viral protein vMIA resulted in viperin relocalization from the endoplasmic reticulum to the mitochondria. There, viperin interacted with the mitochondrial trifunctional protein that mediates β-oxidation of fatty acids to generate adenosine triphosphate (ATP). This interaction with viperin, but not with a mutant lacking the viperin iron-sulfur cluster-binding motif, reduced cellular ATP generation, which resulted in actin cytoskeleton disruption and enhancement of infection. This function of viperin, which was previously attributed to vMIA, suggests that HCMV has coopted viperin to facilitate the infectious process.  相似文献   
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