The reported transmission of avian H9N2 influenza viruses to humans and the isolation of these viruses from Hong Kong poultry markets lend urgency to studies of their ecology and pathogenicity. We found that H9N2 viruses from North America differ from those of Asia. The North American viruses, which infect primarily domestic turkeys, replicated poorly in inoculated chickens. Phylogenetic analysis of the hemagglutinin and nucleoprotein genes indicated that the Asian H9N2 influenza viruses could be divided into three sublineages. Initial biological characterization of at least one virus from each lineage was done in animals. Early isolates of one lineage (A/Chicken/Beijing/1/94, H9N2) caused as high as 80% mortality rates in inoculated chickens, whereas all other strains were nonpathogenic. Sequence analysis showed that some isolates, including the pathogenic isolate, had one additional basic amino acid (A-R/K-S-S-R-) at the hemagglutinin cleavage site. Later isolates of the same lineage (A/Chicken/Hong Kong/G9/97, H9N2) that contains the PB1 and PB2 genes similar to Hong Kong/97 H5N1 viruses replicated in chickens, ducks, mice, and pigs but were pathogenic only in mice. A/Quail/Hong Kong/G1/97 (H9N2), from a second lineage that possesses the replicative complex similar to Hong Kong/97 H5N1 virus, replicated in chickens and ducks without producing disease signs, was pathogenic in mice, and spread to the brain without adaptation. Examples of the third Asian H9N2 sublineage (A/Chicken/Korea/323/96, Duck/Hong Kong/Y439/97) replicated in chickens, ducks, and mice without producing disease signs. The available evidence supports the notion of differences in pathogenicity of H9N2 viruses in the different lineages and suggests that viruses possessing genome segments similar to 1997 H5N1-like viruses are potentially pathogenic in mammals.
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Background The objective of this study was to determine the effects of supplementing Cu on growth performance, Cu metabolism and Cu-related enzyme activities of weanling pigs fed diets with two different Cu sources, and to estimate optimal Cu requirements and relative bioavailability from these two sources for pigs. Methods Weanling pigs were allocated to 14 treatments arranged factorially, including 6 added Cu levels (5, 10, 20, 40, 80, 160 mg/kg), and 2 mineral sources (tribasic Cu chloride, TBCC and copper proteinate, CuPro), as well as one negative control (0 mg/kg added Cu level) and one maximum allowed level treatment (200 mg/kg TBCC) for the entire 38-d experiment. Growth performance, mineral status and enzyme activities were measured at the end of this study. Results Increasing levels of Cu showed linear and quadratic responses (P < 0.01) for final BW, ADG and FCR regardless of the sources. Supplementation with TBCC (> 80 mg/kg) and CuPro (> 20 mg/kg) significantly decreased (P < 0.05) diarrhea incidence of weanling pigs. There were linear and quadratic increases (P < 0.01) in bile, hepatic, and intestinal Cu concentrations, fecal Cu contents, and plasma enzyme activities (alkaline phosphatase, ceruloplasmin, Cu, Zn-Superoxide dismutase (Cu/Zn SOD), and glutathione peroxidase), whereas plasma malondialdehyde decreased (P < 0.01) linearly and quadratically as dietary Cu level increased. Similarly, pigs fed CuPro absorbed and retained more Cu and excreted less Cu than those fed TBCC when supplemented 80 mg/kg and above. Optimal dietary Cu requirements for pigs from 28 to 66 d of age estimated based on fitted broken-line models (P < 0.05) of bile Cu, plasma Cu/Zn SOD and growth performance were 93–140 mg/kg from TBCC, and 63–98 mg/kg from CuPro accordingly. According to slope ratios from multiple linear regression, the bioavailability value of CuPro relative to TBCC (100%) was 156–263% (P < 0.01). Conclusion The findings indicated that Cu recommendation from current NRC (5–6 mg/kg) was not sufficient to meet the high requirement of weanling pigs. Cu from CuPro was significantly more bioavailable to weanling pigs than TBCC in stimulating growth and enzyme activities, decreasing diarrhea frequency and fecal Cu contents to the environment.
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