Archives of virology. Supplementum最新文献

{"title":"Zoonotic viruses of wildlife: hither from yon.","authors":"J E Childs","doi":"10.1007/978-3-7091-0572-6_1","DOIUrl":"https://doi.org/10.1007/978-3-7091-0572-6_1","url":null,"abstract":"<p><p>The emergence of zoonotic viruses maintained by wildlife reservoir hosts is poorly understood. Recent discoveries of Hendra (HENV) and Nipah (NIPV) viruses in Australasia and the emergence of epidemic West Nile virus (WNV) in the United States have added urgency to the study of cross-species transmission. The processes by which zoonotic viruses are transmitted and infect other species are examined as four transitions. Two of these, inter-species contact and cross-species virus transmission (spillover), are essential and sufficient to cause epidemic emergence. Sustained transmission and virus adaptation within the spillover host are transitions not required for virus emergence, but determine the magnitude and scope of subsequent disease outbreaks. Ecologic, anthropogenic, and evolutionary factors modify the probability that viruses complete or move through transitions. As surveillance for wildlife diseases is rare and often outbreak-driven, targeted studies are required to elucidate the means by which important zoonotic viruses are maintained and spillover occurs.</p>","PeriodicalId":77010,"journal":{"name":"Archives of virology. Supplementum","volume":" 18","pages":"1-11"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24497565","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of surveillance in polio eradication and identification of emerging viral encephalitis.","authors":"E De Gourville,&nbsp;W R Dowdle","doi":"10.1007/978-3-7091-0572-6_2","DOIUrl":"https://doi.org/10.1007/978-3-7091-0572-6_2","url":null,"abstract":"<p><p>In 1988, when the World Health Assembly resolved to eradicate paralytic poliomyelitis, polio was endemic in 125 countries on 5 continents with an estimated 350,000 cases annually. By 2002, the number of countries was reduced to 7 and the number of cases by greater than 99%. Instrumental in this extraordinary progress is the timely detection and investigation of all cases of acute flaccid paralysis and the examination of stool samples in an accredited WHO Global Network laboratory. The Network consists of 124 National Poliovirus Laboratories, 15 Regional Reference Laboratories, and 7 Global Specialized Laboratories. Network Laboratories are held accountable to rigid performance standards for quality and timeliness in testing more than 60,000 stool samples annually. The Network is a hierarchical system in which polioviruses are isolated and identified in National Laboratories, differentiated as to wild or vaccine origin in Regional Reference Laboratories, and sequenced in Specialized Laboratories. Findings are promptly relayed to Regional and national program managers for immunization strategic planning, monitoring surveillance quality, and assessing eradication progress. Lessons from the Polio Laboratory Network demonstrate the value of a central coordinating body, an effective communication infrastructure, and full partnerships with peer epidemiology and medical sectors. Post-eradication polio surveillance will continue for many years. The Network legacy for other public health initiatives is access to an existing laboratory infrastructure and human resources with the proven ability to achieve technology transfer and quality laboratory performance even in resource-poor countries.</p>","PeriodicalId":77010,"journal":{"name":"Archives of virology. Supplementum","volume":" 18","pages":"13-20"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24497566","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Henipaviruses: recent observations on regulation of transcription and the nature of the cell receptor.","authors":"B T Eaton,&nbsp;P J Wright,&nbsp;L F Wang,&nbsp;O Sergeyev,&nbsp;W P Michalski,&nbsp;K N Bossart,&nbsp;C C Broder","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Hendra virus (HENV) and Nipah virus (NIPV) are classified in the new genus Henipavirus, within the subfamily Paramyxovirinae, family Paramyxoviridae. The genetic and biological characteristics that differentiate henipaviruses from other members of the subfamily are summarized. Although they do not display neuraminidase and hemagglutination activities and in that regard resemble viruses in the genus Morbillivirus, several recent observations highlight similarities between henipaviruses and respiroviruses (genus Respirovirus) in structure and replication strategy. First, three-dimensional modeling studies suggest that the external globular head domain of the HENV G protein resembles that of respiroviruses rather than morbilliviruses. Second, the pattern of transcriptional attenuation in HENV-infected cells resembles that observed with Sendai virus, a respirovirus, and differs from that found in cells infected with measles virus, a morbillivirus. Henipaviruses have a broad host range in vitro and in vivo, indicating wide distribution of cellular receptor molecules. The extensive host range has been confirmed in a quantitative in vitro cell-fusion assay using recombinant vaccinia viruses expressing the attachment and fusion proteins of HENV and NIPV. Cell lines of diverse origin and which are permissive in the in vitro cell fusion assay have been identified and the pattern of relative susceptibilities is the same for both HENV and NIPV, implying that both viruses use the same cell receptor. Protease treatment of permissive cells destroys their ability to fuse with cells expressing viral envelope glycoproteins. Virus overlay protein binding assay (VOPBA) and radio-immune precipitation assays confirm that both HENV and NIPV bind to membrane proteins in the 35-50 kD range. Treatment of cell membrane proteins with N-glycosidase eliminates HeV binding activity in VOPBA whereas treatment with neuraminidase has no effect on binding. Thus preliminary evidence suggests that NIPV and HENV bind to the same glycoprotein receptor via a non-sialic acid-dependant mechanism.</p>","PeriodicalId":77010,"journal":{"name":"Archives of virology. Supplementum","volume":" 18","pages":"122-31"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24498168","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The entry machinery of flaviviruses.","authors":"F X Heinz,&nbsp;K Stiasny,&nbsp;S L Allison","doi":"10.1007/978-3-7091-0572-6_11","DOIUrl":"https://doi.org/10.1007/978-3-7091-0572-6_11","url":null,"abstract":"<p><p>We have been using the flavivirus tick-borne encephalitis virus (TBEV) as a model system for investigating the molecular mechanisms underlying the membrane fusion process mediated by a class II viral fusion protein, the flavivirus envelope protein E. In the mature virion this protein exists as a metastable dimer that dissociates at the acidic pH in endosomes and is converted into a more stable trimeric conformation. The dimer dissociation step liberates an internal fusion peptide that interacts with the target endosomal membrane, and then further conformational changes are believed to drive membrane fusion. Although flavivirus fusion appears to be a more facile and efficient process than that of alphaviruses, which also possess a class II viral fusion protein, the fusion mechanism in both viral systems involves structurally related interactions with lipids, specifically the 3beta-hydroxyl group at C3 of cholesterol. The class II viral fusion machineries are structurally different from those involving class I viral fusion proteins, such as those found in orthomyxoviruses, paramyxoviruses, retroviruses, and filoviruses, but have certain similarities in common with bacterial pore-forming proteins.</p>","PeriodicalId":77010,"journal":{"name":"Archives of virology. Supplementum","volume":" 18","pages":"133-7"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24498169","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulation of apoptosis by viruses that infect insects.","authors":"P M Irusta,&nbsp;E Lamos,&nbsp;H L Galonek,&nbsp;M A Vander Maten,&nbsp;M C H Boersma,&nbsp;Y B Chen,&nbsp;J M Hardwick","doi":"10.1007/978-3-7091-0572-6_15","DOIUrl":"https://doi.org/10.1007/978-3-7091-0572-6_15","url":null,"abstract":"<p><p>Orthobunyviruses and alphaviruses cause encephalitis, neuronal apoptosis and mortality in mammals, but fail to kill the mosquitoes that transmit these viruses. Therefore, host cell factors, as well as viral factors, regulate the outcome of infection. Drosophila Reaper is a pro-death factor in the Drosophila nervous system during development but homologues were not previously known to exist outside flies. Recent discovery of a Reaper protein encoded by orthobunyaviruses provides interesting insight into the mechanisms by which viruses modulate the death pathway in both vertebrate and invertebrate hosts.</p>","PeriodicalId":77010,"journal":{"name":"Archives of virology. Supplementum","volume":" 18","pages":"171-8"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24498697","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recombinant canarypoxvirus vaccine carrying the prM/E genes of West Nile virus protects horses against a West Nile virus-mosquito challenge.","authors":"J M Minke,&nbsp;L Siger,&nbsp;K Karaca,&nbsp;L Austgen,&nbsp;P Gordy,&nbsp;R Bowen,&nbsp;R W Renshaw,&nbsp;S Loosmore,&nbsp;J C Audonnet,&nbsp;B Nordgren","doi":"10.1007/978-3-7091-0572-6_20","DOIUrl":"https://doi.org/10.1007/978-3-7091-0572-6_20","url":null,"abstract":"<p><p>An ALVAC (canarypoxvirus)-based recombinant (vCP2017) expressing the prM and E genes derived from a 1999 New York isolate of West Nile virus (WNV) was constructed and assessed for its protective efficacy in horses in two different experiments. In the first trial, a dose titration study was conducted to evaluate both serum neutralising antibody responses to WNV and duration of immunity. In the second trial the onset of protection was determined. Twenty-eight adult horses received two doses of vCP2017 administered intramuscularly at 5-week intervals and sixteen horses comprised age-matched non-vaccinated controls. Individual sera were taken periodically and tested for neutralising antibodies against WNV. Horses were challenged by allowing WNV-infected Aedes albopictus mosquitoes to feed on them two weeks (second trial) or one year (first trial) after the second vaccination. After challenge, horses were monitored for clinical signs of disease, and blood samples were collected for detection of WNV viremia and antibody. In both trials, all vaccinated horses developed neutralising antibodies against WNV. None of the vaccinated or control horses developed clinical signs of WNV disease upon challenge. None of the nine horses challenged 2 weeks after primary vaccination and only one of the ten vaccinated horses challenged 1 year after vaccination developed detectable viremia after challenge, whereas more than 80% of the controls became infected. Results from these studies demonstrated that a primary course of two doses of vCP2017 provides both antibody response and an early immunity in horses against WNV viremia.</p>","PeriodicalId":77010,"journal":{"name":"Archives of virology. Supplementum","volume":" 18","pages":"221-30"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/978-3-7091-0572-6_20","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24498014","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic determinants of Venezuelan equine encephalitis emergence.","authors":"S C Weaver,&nbsp;M Anishchenko,&nbsp;R Bowen,&nbsp;A C Brault,&nbsp;J G Estrada-Franco,&nbsp;Z Fernandez,&nbsp;I Greene,&nbsp;D Ortiz,&nbsp;S Paessler,&nbsp;A M Powers","doi":"10.1007/978-3-7091-0572-6_5","DOIUrl":"https://doi.org/10.1007/978-3-7091-0572-6_5","url":null,"abstract":"<p><p>Following a period of inactivity from 1973-1991, Venezuelan equine encephalitis (VEE) reemerged during the past decade in South America and Mexico. Experimental studies of VEE virus (VEEV) infection of horses with virus strains isolated during these outbreaks have revealed considerable variation in the ability of equine-virulent, epizootic strains to exploit horses as efficient amplification hosts. Subtype IC strains from recent outbreaks in Venezuela and Colombia amplify efficiently in equines, with a correlation between maximum viremia titers and the extent of the outbreak from which the virus strain was isolated. Studies of enzootic VEEV strains that are believed to represent progenitors of the epizootic subtypes support the hypothesis that adaptation to efficient replication in equines is a major determinant of emergence and the ability of VEEV to spread geographically. Correlations between the ability of enzootic and epizootic VEEV strains to infect abundant, equiphilic mosquitoes, and the location and extent of these outbreaks, also suggest that specific adaptation to Ochlerotatus taeniorhynchus mosquitoes is a determinant of some but not all emergence events. Genetic studies imply that mutations in the E2 envelope glycoprotein gene are major determinants of adaptation to both equines and mosquito vectors.</p>","PeriodicalId":77010,"journal":{"name":"Archives of virology. Supplementum","volume":" 18","pages":"43-64"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24498163","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Emerging encephalitogenic viruses: lyssaviruses and henipaviruses transmitted by frugivorous bats.","authors":"J S Mackenzie,&nbsp;H E Field","doi":"10.1007/978-3-7091-0572-6_8","DOIUrl":"https://doi.org/10.1007/978-3-7091-0572-6_8","url":null,"abstract":"<p><p>Three newly recognized encephalitogenic zoonotic viruses spread from fruit bats of the genus Pteropus (order Chiroptera, suborder Megachiroptera) have been recognised over the past decade. These are: Hendra virus, formerly named equine morbillivirus, which was responsible for an outbreak of disease in horses and humans in Brisbane, Australia, in 1994; Australian bat lyssavirus, the cause of a severe acute encephalitis, in 1996; and Nipah virus, the cause of a major outbreak of encephalitis and pulmonary disease in domestic pigs and people in peninsula Malaysia in 1999. Hendra and Nipah viruses have been shown to be the first two members of a new genus, Henipavirus, in the family Paramyxoviridae, subfamily Paramyxovirinae, whereas Australian bat lyssavirus is closely related antigenically to classical rabies virus in the genus Lyssavirus, family Rhabdoviridae, although it can be distinguished on genetic grounds. Hendra and Nipah viruses have neurological and pneumonic tropisms. The first humans and equids with Hendra virus infections died from acute respiratory disease, whereas the second human patient died from an encephalitis. With Nipah virus, the predominant clinical syndrome in humans was encephalitic rather than respiratory, whereas in pigs, the infection was characterised by acute fever with respiratory involvement with or without neurological signs. Two human infections with Australian bat lyssavirus have been reported, the clinical signs of which were consistent with classical rabies infection and included a diffuse, non-suppurative encephalitis. Many important questions remain to be answered regarding modes of transmission, pathogenesis, and geographic range of these viruses.</p>","PeriodicalId":77010,"journal":{"name":"Archives of virology. Supplementum","volume":" 18","pages":"97-111"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24498166","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Subversive neuroinvasive strategy of rabies virus.","authors":"M Lafon","doi":"10.1007/978-3-7091-0572-6_13","DOIUrl":"https://doi.org/10.1007/978-3-7091-0572-6_13","url":null,"abstract":"<p><p>Rabies virus (RABV) is a pathogen well-adapted to the nervous system, where it infects the neurons. RABV is transmitted by the bite of an infected animal. It enters the nervous system via a motor neuron through the neuromuscular junction, or via a sensory nerve through nerve spindles. It then travels from one neuron to the next, along the spinal cord to the brain and the salivary glands. The virions are then excreted in the saliva of the animal and can be transmitted to another host by bite. Thus, preservation of the neuronal network integrity is crucial for the virus to be transmitted. Successful invasion of the nervous system by RABV seems to be the result of a subversive strategy based on the survival of infected neurons including protection against virus-mediated apoptosis and destruction of T cells that invade the CNS in response to infection.</p>","PeriodicalId":77010,"journal":{"name":"Archives of virology. Supplementum","volume":" 18","pages":"149-59"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/978-3-7091-0572-6_13","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24498695","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vaccination against cytomegalovirus.","authors":"S. Plotkin","doi":"10.1007/978-3-7091-6259-0_13","DOIUrl":"https://doi.org/10.1007/978-3-7091-6259-0_13","url":null,"abstract":"","PeriodicalId":77010,"journal":{"name":"Archives of virology. Supplementum","volume":"17 1","pages":"121-34"},"PeriodicalIF":0.0,"publicationDate":"2001-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/978-3-7091-6259-0_13","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"51396260","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}