Objective To investigate the variability of human cytomegalovirus （HCMV） UL138 open reading frame （ORF） in clinical strains. Methods HCMV UL138 ORF was amplified by polymerase chain reaction （PCR） and PCR amplif...Objective To investigate the variability of human cytomegalovirus （HCMV） UL138 open reading frame （ORF） in clinical strains. Methods HCMV UL138 ORF was amplified by polymerase chain reaction （PCR） and PCR amplification products were sequenced directly, and the data were analyzed in 19 clinical strains. Results LIL138 ORF in all 30 clinical strains was amplified successfully. Compared with that of Toledo strain, the nucleotide and amino acid sequence identifies of LIL138 ORF in all strains were 97.41% to 99.41% and 98.24% to 99.42%, respectively. All of the nucleofide mutations were substitutions. The spatial structure and post-translational modification sites of HL138 encoded proteins were conserved. The result of phylogenetic tree showed that HCMV HL138 sequence variations were not definitely related with different clinical symptoms. Conclusion HCMV UL138 ORF in clinical strains is high conservation, which might be helpful for UL138 encoded protein to play a role in latent infection of HCMV.展开更多
Several case reports deal with the relationship between hepatitis C virus （HCV） infection and pulmonary or he- patic sarcoidosis. Most publications describe interferon m-induced sarcoidosis. However, HCV infection p...Several case reports deal with the relationship between hepatitis C virus （HCV） infection and pulmonary or he- patic sarcoidosis. Most publications describe interferon m-induced sarcoidosis. However, HCV infection per se is also suggested to cause sarcoqdosis. The present case report describes a case of biopsy-verified lung and liver sarcoidosis and HCV infection, and the out- come of antiviral therapy. In March 2009, a 25-year-old man presented with moderately elevated liver enzymes without any clinical symptoms. The patient was posi- tive for HCV antibodies and HCV RNA of genotype lb. Four months later the patient became dyspnoic and pulmonary sarcoidosis was diagnosed by lung biopsy and radiography. A short course of corticosteroid treat- ment relieved symptoms. Three months later, liver biopsy showed noncaseating granulomas consisting of epithelioid histiocytes and giant cells with a small amount of peripheral lymphocyte infiltration, without any signs of fibrosis. Chronic HCV infection with co- existence of pulmonary and hepatic sarcoidosis was diagnosed. Antiviral therapy with peginterferon ~ and ribavirin at standard doses was started, which lasted 48 wk, and sustained viral response was achieved. A second liver biopsy showed disappearance of granulo- mas and chest radiography revealed normalization of mediastinal and perihilar glands. The hypothesis that HCV infection perse may have triggered systemic sar- coidosis was proposed. Successful treatment of HCV infection led to continuous remission of pulmonary and hepatic sarcoidosis. Further studies are required to un- derstand the relationship between systemic sarcoidosis and HCV infection.展开更多
基金Supported by the National Natural Science Foundation of China (30801254)
文摘Objective To investigate the variability of human cytomegalovirus （HCMV） UL138 open reading frame （ORF） in clinical strains. Methods HCMV UL138 ORF was amplified by polymerase chain reaction （PCR） and PCR amplification products were sequenced directly, and the data were analyzed in 19 clinical strains. Results LIL138 ORF in all 30 clinical strains was amplified successfully. Compared with that of Toledo strain, the nucleotide and amino acid sequence identifies of LIL138 ORF in all strains were 97.41% to 99.41% and 98.24% to 99.42%, respectively. All of the nucleofide mutations were substitutions. The spatial structure and post-translational modification sites of HL138 encoded proteins were conserved. The result of phylogenetic tree showed that HCMV HL138 sequence variations were not definitely related with different clinical symptoms. Conclusion HCMV UL138 ORF in clinical strains is high conservation, which might be helpful for UL138 encoded protein to play a role in latent infection of HCMV.
基金Supported by A grant from the Estonian Science Foundation,No.7650a grant from the University of Tartu,No. SF0180081s07
文摘Several case reports deal with the relationship between hepatitis C virus （HCV） infection and pulmonary or he- patic sarcoidosis. Most publications describe interferon m-induced sarcoidosis. However, HCV infection per se is also suggested to cause sarcoqdosis. The present case report describes a case of biopsy-verified lung and liver sarcoidosis and HCV infection, and the out- come of antiviral therapy. In March 2009, a 25-year-old man presented with moderately elevated liver enzymes without any clinical symptoms. The patient was posi- tive for HCV antibodies and HCV RNA of genotype lb. Four months later the patient became dyspnoic and pulmonary sarcoidosis was diagnosed by lung biopsy and radiography. A short course of corticosteroid treat- ment relieved symptoms. Three months later, liver biopsy showed noncaseating granulomas consisting of epithelioid histiocytes and giant cells with a small amount of peripheral lymphocyte infiltration, without any signs of fibrosis. Chronic HCV infection with co- existence of pulmonary and hepatic sarcoidosis was diagnosed. Antiviral therapy with peginterferon ~ and ribavirin at standard doses was started, which lasted 48 wk, and sustained viral response was achieved. A second liver biopsy showed disappearance of granulo- mas and chest radiography revealed normalization of mediastinal and perihilar glands. The hypothesis that HCV infection perse may have triggered systemic sar- coidosis was proposed. Successful treatment of HCV infection led to continuous remission of pulmonary and hepatic sarcoidosis. Further studies are required to un- derstand the relationship between systemic sarcoidosis and HCV infection.
