浅析鸭坦布苏病毒病及其防制

鸭坦布苏病毒（Duck Tembusu virus）属于黄病毒科（Flaviviridae）、黄病毒属（Flavivirus）、恩塔亚（Ntaya）病毒群。该病主要引起蛋鸭及种鸭发病,导致蛋鸭采食减少、产蛋率急剧降低甚至停产、种蛋受精率降低等。鸭坦布苏病毒除感染蛋鸭及种鸭外,还可引起樱桃谷肉鸭及北京鸭等多品种肉鸭发病,给中国养鸭业带来巨大经济损失。

PIC猪经口、鼻途径感染猪瘟石门毒株及兔化弱毒株后病毒的组织嗜性及动态分布规律研究

猪瘟（classical swine fever,CSF）是由猪瘟病毒（classical swine fever virus,CSFV）引起的一种高度接触性、症状差异极大的传染病〔1〕。病原属黄病毒科（Flaviviridae）瘟病毒属（Pestivirus）成员,只有一个血清型〔1〕。瘟病毒属（Pestivirus）是一群小的、有囊膜的、正链单股RNA病毒,其基因组大小约12.5kb,编码1个大的单一开放读码框架（ORF）,

A study on pathogenicity of hepatitis G virus

AIM To study the pathogenicity of hepatitis G virus (HGV) and observe the genesis and pathological process of hepatitis G.METHODS HGV-RNA in serum was detected by RT-PCR assay. The immunohistochemical assays of liver tissue were performed with HGV monocoloned antibody (McAb)expressed from the region of HGV NS5 nucleic acid sequence. The clinical and pathological data of 52 patients with hepatitis G were discussed. In animal experiment,the Chinese Rhesus monkeys were infected with the serum of a patient with HGV infection. And the dynamic changes in serology and liver histology of animals were observed.RESULTS One hundred and fifty-four patients with HGVRNA positive were selected from 1552 patients with various kinds of hepatitis. Of 154 patients with HGV infection, 52 were infected with HGV only, which accounted for 33.8% (52/154) and 102 with positive HGVRNA were super-infected with other hepatitis viruses,which accounted for 66.2% (102/154). The clinical and pathological observation showed that the acute and chronic hepatitis could be induced by HGV. The slight abnormality of transaminases ALT and AST in serum of monkeys lasted nearly 12 months and histological results showed a series of pathological changes.CONCLUSION HGV is a hepatotropic virus and has pathogenicty.

TT virus and hepatitis G virus infections in Korean blood donors and patients with chronic liver disease

AIM:To determine the prevalences of TTV and HGV infections among blood donors and patients with chronic liver disease in Korea,to investigate the association of TTV and HGV infections with blood transfusion,and to assess the correlation between TTV and HGV viremia and hepatic damage. METHODS:A total of 391 serum samples were examined in this study.Samples were obtained from healthy blood donors(n=110),hepatitis B surface antigen(HBsAg)-positive donors(n=112),anti-hepatitis C virus(anti-HCV)-positive donors(n=69),patients with type B chronic liver disease (n=81),and patients with type C chronic liver disease(n=19). Trv DNA was detected using the hemi-nested PCR.HGV RNA was tested using RT-PCR.A history of blood transfusion and serum levels of alanine aminotransferase(ALT)and aspartate aminotransferase(AST)were also determined. RESULTS:TTV DNA was detected in 8.2%of healthy blood donors,16.1%of HBsAg-positive donors,20.3%of anti- HCV-positive donors,21.0%of patients with type B chronic liver disease,and 21.1%of patients with type C chronic liver disease.HGV RNA was detected in 1.8%of healthy blood donors,1.8%of HBsAg-positive donors,17.4%of anti-HCV-positive donors,13.6%of patients with type B chronic liver disease,and 10.5%of patients with type C chronic liver disease.The prevalence of TTV and HGV infections in HBV- or HCV-positive donors and patients was significantly higher than in healthy blood donors(P<0.05), except for the detection rate of HGV in HBsAg-positive donors which was the same as for healthy donors.There was a history of transfusion in 66.7%of TTV DNA-positive patients and 76.9%of HGV RNA-positive patients(P<0.05).No significant increase in serum ALT and AST was detected in the TTV or HGV-positive donors and patients. CONCLUSION:TTV and HGV infections are more frequently found in donors and patients infected with HBV or HCV than in healthy blood donors.However,there is no significant association between TTV or HGV infections and liver injury.

Immunogenicity of HGV NS5 protein expressed from Sf9 insect cells

INTRODUCTIONAlthough reliable assays for the detection ofhepatitis C virus and E virus became available, still10% 20% hepatitis are not caused byhepatitis A-E virus[1-3]. In 1996, two research groups isolatedthis agent independently and almost simultaneouslyand named hepatitis G virus and GB virus C,respectively[4-7].

Phylogeny of Culex theileri virus flavivirus in Spain, Myanmar, Portugal and Turkey

Objective: To study the genetic diversity of Culex theileri flavivirus and the spread of this virus among Spain, Portugal and Turkey.Methods: A database consisting of 55 sequences of the NS5/3'UTR region of Culex theileri flavivirus group downloaded from GenBank were aligned and manual edited with Bioedit.ModelT est v.3.7 was used to select the simplest evolutionary model that adequately fitted the sequence data.Maximum likelihood analysis was performed using MEGA7.The phylogenetic signal of the dataset was investigated by the likelihood mapping analysis.Results: The phylogenetic tree showed three clusters.Myanmar sequences clusterd together with Turkish sequences, Spain and Portugal strains grouped together and two Turkish sequences grouped separately.Selective pressure analysis showed a moderate percentage of sites(22.5%) under pervasive negative selection and only 1% under pervasive positive selection.The sites subject to selective pressure in CTFV RdRp NS5 fragments have been located onto the predicted three-dimensional structure.Conclusions: Phylogenetic and evolutionary analysis can be an important tool for understanding the evolutionary impact of the probable contemporary existence between nonpathogenic and pathogenic flaviviruses among these vectors.

Combatting Zika Virus through Enhancing RNAi

The outbreak and rapid spread of Zika virus (ZIKV) in the Western Hemisphere has imposed a global public health threat since 2015. ZIKV is a positive-sense single-stranded RNA virus (where the ‘positive-sense’ means that the viral RNA can be directly translated by the host cell into viral proteins) that belongs to the genus Flavivirus in the family Flaviviridae.

Phylogenetic analysis revealed the central roles of two African countries in the evolution and worldwide spread of Zika virus

Recent outbreaks of Zika virus （ZIKV） infections in Oceania＇s islands and the Americas were characterized by high numbers of cases and the spread of the virus to new areas. To better understand the origin of ZIKV, its epidemic history was reviewed. Although the available records and information are limited, two major genetic lineages of ZIKV were identified in previous studies. However, in this study, three lineages were identified based on a phylogenetic analysis of all virus sequences from GenBank, including those of the envelope protein （E） and non-structural protein 5 （NS5） coding regions. The spatial and temporal distributions of the three identified ZIKV lineages and the recombination events and mechanisms underlying their divergence and evolution were further elaborated. The potential migration pathway of ZIKV was also characterized. Our findings revealed the central roles of two African countries, Senegal and Cote d＇lvoire, in ZIKV evolution and genotypic divergence. Furthermore, our results suggested that the outbreaks in Asia and the Pacific islands originated from Africa. The results provide insights into the geographic origins of ZlKV outbreaks and the spread of the virus, and also contribute to a better understanding of ZlKV evolution, which is important for the prevention and control of ZlKV infections.

Zika virus and Zika fever

An emerging mosquito-borne arbovirus named Zika virus(ZIKV), of the family Flaviviridae and genus Flavivirus, is becoming a global health threat. ZIKV infection was long neglected due to its sporadic nature and mild symptoms. However, recently, with its rapid spread from Asia to the Americas, affecting more than 30 countries, accumulating evidences have demonstrated a close association between infant microcephaly and Zika infection in pregnant women. Here, we reviewed the virological, epidemiological, and clinical essentials of ZIKV infection.

Retromer localizes to autophagosomes during HCV replication

Dear Editor,Hepatitis C virus（HCV）is a positive-strand RNA virus that belongs to the genus Hepacivirus within the Flaviviridae family.HCV causes chronic liver diseases,and185 million people are infected（Messina et al.,2015）.Currently,there is no approved vaccine to prevent hepatitis C.HCV induces autophagy through elevating reactive oxygen species（ROS）levels via the unfolded protein response （UPR） or via direct interference with the autophagic pathway.

The emerging roles of retromer and sorting nexins in the life cycle of viruses

Retromer and sorting nexins(SNXs)transport cargoes from endosomes to the trans-Golgi network or plasma membrane.Recent studies have unveiled the emerging roles for retromer and SNXs in the life cycle of viruses,including members of Coronaviridae,Flaviviridae and Retroviridae.Key components of retromer/SNXs,such as Vps35,Vps26,SNX5 and SNX27,can affect multiple steps of the viral life cycle,including facilitating the entry of viruses into cells,participating in viral replication,and promoting the assembly of virions.Here we present a comprehensive updated review on the interplay between retromer/SNXs and virus,which will shed mechanistic insights into controlling virus infection.