Archives of virology. Supplementum最新文献

Filoviruses. A compendium of 40 years of epidemiological, clinical, and laboratory studies. 丝状病毒。40年流行病学、临床和实验室研究的汇编。

Archives of virology. Supplementum Pub Date : 2008-01-01

Jens H Kuhn

引用次数: 0

Regulation of rodent-borne viruses in the natural host: implications for human disease. 鼠传病毒在自然宿主中的调控:对人类疾病的影响。

Archives of virology. Supplementum Pub Date : 2005-01-01 DOI: 10.1007/3-211-29981-5_5

J N Mills

{"title":"Regulation of rodent-borne viruses in the natural host: implications for human disease.","authors":"J N Mills","doi":"10.1007/3-211-29981-5_5","DOIUrl":"https://doi.org/10.1007/3-211-29981-5_5","url":null,"abstract":"Prevalence and transmission rates of rodent-borne viruses within host populations vary in time and space and among host-virus systems. Improving our understanding of the causes of these variations will lead to a better understanding of changes in disease risk to humans. The regulators of prevalence and transmission can be categorized into five major classes: (1) Environmental regulators such as weather and food supply affect transmission rates through their effect on reproductive success and population densities. (2) Anthropogenic factors, such as disturbance, may lead to ecosystem simplification and decreased diversity. These changes favor opportunistic species, which may serve as reservoirs for zoonotic viruses. (3) Genetic factors influence susceptibility of mice to infection or capacity for chronic shedding and may be related to population cycling. (4) Behavioral factors, such as fighting, increase risk of transmission of some viruses and result in different patterns of infection between male and female mice. Communal nesting may result in overwinter transmission in colder climates. (5) Physiologic factors control host response to infection and length of time the host remains infectious. Risk prediction is difficult because these regulators are numerous and often interact, and the relative importance of each varies according to the host species, season, year, and geographic location.","PeriodicalId":77010,"journal":{"name":"Archives of virology. Supplementum","volume":" 19","pages":"45-57"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/3-211-29981-5_5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25751863","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}

引用次数: 90

Virus perpetuation in populations: biological variables that determine persistence or eradication. 病毒在人群中的延续:决定持续或根除的生物变量。

Archives of virology. Supplementum Pub Date : 2005-01-01 DOI: 10.1007/3-211-29981-5_2

N Nathanson

{"title":"Virus perpetuation in populations: biological variables that determine persistence or eradication.","authors":"N Nathanson","doi":"10.1007/3-211-29981-5_2","DOIUrl":"https://doi.org/10.1007/3-211-29981-5_2","url":null,"abstract":"In this review, I use the term \"perpetuation\" for persistence of a virus in a population, since this is a different phenomenon from persistence of a virus in an infected host. Important variables that influence perpetuation differ in small (<1000 individuals) and large (>10,000) populations: in small populations, two important variables are persistence in individuals, and turnover of the population, while in large populations important variables are transmissibility, generation time, and seasonality. In small populations, viruses such as poliovirus that cause acute infections cannot readily be perpetuated, in contrast to viruses such as hepatitis B virus, that cause persistent infections. However, small animal populations can turnover significantly each year, permitting the perpetuation of some viruses that cause acute infections. Large populations of humans are necessary for the perpetuation of acute viruses; for instance, measles required a population of 500,000 for perpetuation in the pre-measles vaccine era. Furthermore, if an acute virus, such as poliovirus, exhibits marked seasonality in large populations, then it may disappear during the seasonal trough, even in the presence of a large number of susceptible persons. Eradication is the converse of perpetuation and can be used as a definitive approach to the control of a viral disease, as in the instance of smallpox. Therefore, the requirements for perpetuation have significant implications for practical public health goals.","PeriodicalId":77010,"journal":{"name":"Archives of virology. Supplementum","volume":" 19","pages":"3-15"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/3-211-29981-5_2","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25751860","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 12

Host range, amplification and arboviral disease emergence. 宿主范围、扩增和虫媒病毒病的出现。

Archives of virology. Supplementum Pub Date : 2005-01-01 DOI: 10.1007/3-211-29981-5_4

S C Weaver

{"title":"Host range, amplification and arboviral disease emergence.","authors":"S C Weaver","doi":"10.1007/3-211-29981-5_4","DOIUrl":"https://doi.org/10.1007/3-211-29981-5_4","url":null,"abstract":"Etiologic agents of arboviral diseases are primarily zoonotic pathogens that are maintained in nature in cycles involving arthropod transmission among a variety of susceptible reservoir hosts. In the simplest form of human exposure, spillover occurs from the enzootic cycle when humans enter zoonotic foci and/or enzootic amplification increases circulation near humans. Examples include Eastern (EEEV) and Western equine encephalitis viruses (WEEV), as well as West Nile (WNV), St. Louis encephalitis (SLEV) and Yellow fever viruses. Spillover can involve direct transmission to humans by primary enzootic vectors (e.g. WNV, SLEV and WEEV) and/or bridge vectors with more catholic feeding preferences that include humans (e.g. EEEV). Some viruses, such as Rift Valley fever, Japanese encephalitis and Venezuelan equine encephalitis viruses (VEEV) undergo secondary amplification involving replication in livestock animals, resulting in greater levels of spillover to humans in rural settings. In the case of VEEV, secondary amplification involves equines and requires adaptive mutations in enzootic strains that allow for efficient viremia production. Two of the most important human arboviral pathogens, Yellow fever and dengue viruses (DENV), have gone one step further and adopted humans as their amplification hosts, allowing for urban disease. The ancestral forms of DENV, sylvatic viruses transmitted among nonhuman primate reservoir hosts by arboreal mosquitoes, adapted to efficiently infect the urban mosquito vectors Aedes aegypti and Ae. albopictus during the past few thousand years as civilizations arose. Comparative studies of the sylvatic and urban forms of DENV may elucidate the evolution of arboviral virulence and the prospects for DENV eradication should effective vaccines be implemented.","PeriodicalId":77010,"journal":{"name":"Archives of virology. Supplementum","volume":" 19","pages":"33-44"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/3-211-29981-5_4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25754431","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}

引用次数: 111

The virulence of the 1918 pandemic influenza virus: unraveling the enigma. 1918年大流行性流感病毒的毒力:解开谜团。

Archives of virology. Supplementum Pub Date : 2005-01-01 DOI: 10.1007/3-211-29981-5_9

J K Taubenberger

{"title":"The virulence of the 1918 pandemic influenza virus: unraveling the enigma.","authors":"J K Taubenberger","doi":"10.1007/3-211-29981-5_9","DOIUrl":"https://doi.org/10.1007/3-211-29981-5_9","url":null,"abstract":"The 1918 influenza pandemic caused acute illness in 25-30% of the world's population and resulted in the death of up to 40 million people. Using lung tissue of 1918 influenza victims, the complete genomic sequence of the 1918 influenza virus is being deduced. Neither the 1918 hemagglutinin nor neuraminidase genes possess mutations known to increase tissue tropicity that account for virulence of other influenza virus strains, such as A/WSN/33 or the highly pathogenic avian influenza H5 or H7 viruses. Using reverse genetics approaches, influenza virus constructs containing the 1918 hemagglutinin and neuraminidase on an A/WSN/33 virus background were lethal in mice. The genotypic basis of this virulence has not yet been elucidated. The complete sequence of the non-structural (NS) gene segment of the 1918 virus was deduced and also tested to determine the validity of the hypothesis that enhanced virulence in 1918 could have been due to type I interferon inhibition by the NS1 protein. Results from these experiments suggest that in human cells the 1918 NS1 is a very effective interferon antagonist. Sequence analysis of the 1918 influenza virus is allowing us to test hypotheses as to the origin and virulence of this strain. This information should help elucidate how pandemic influenza virus strains emerge and what genetic features contribute to virulence in humans.","PeriodicalId":77010,"journal":{"name":"Archives of virology. Supplementum","volume":" 19","pages":"101-15"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/3-211-29981-5_9","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25751740","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}

引用次数: 35

Population dynamics of RNA viruses: the essential contribution of mutant spectra. RNA病毒的种群动态:突变谱的基本贡献。

Archives of virology. Supplementum Pub Date : 2005-01-01 DOI: 10.1007/3-211-29981-5_6

E Domingo, C Gonzalez-Lopez, N Pariente, A Airaksinen, C Escarmís

引用次数: 19

Ehrlichia under our noses and no one notices. 埃利希菌就在我们眼皮底下，却没人注意到。

Archives of virology. Supplementum Pub Date : 2005-01-01 DOI: 10.1007/3-211-29981-5_12

D H Walker

{"title":"Ehrlichia under our noses and no one notices.","authors":"D H Walker","doi":"10.1007/3-211-29981-5_12","DOIUrl":"https://doi.org/10.1007/3-211-29981-5_12","url":null,"abstract":"Ehrlichia chaffeensis, an obligately intracellular bacterium, resides within a cytoplasmic vacuole in macrophages, establishes persistent infection in natural hosts such as white-tailed deer and canids, and is transmitted transstadially and during feeding by ticks, particularly Amblyomma americanum. Ehrlichial cell walls contain glycoproteins and a family of divergent 28 kDa proteins, but no peptidoglycan or lipopolysaccharide. The dense-cored ultrastructural form preferentially expresses certain glycoproteins, including a multiple repeat unit-containing adhesin. Ehrlichiae attach to L-selectin and E-selectin, inhibit phagolysosomal fusion, apoptosis, and JAK/STAT activation, and downregulate IL-12, IL-15, IL-18, TLR2 and 3, and CD14. Mouse models implicate overproduction of TNF-alpha by antigen-specific CD8 T lymphocytes in pathogenesis and strong type 1 CD4 and CD8 T lymphocyte responses, synergistic activities of IFN-gamma and TNF-alpha, and IgG2a antibodies in immunity. Human monocytotropic ehrlichiosis (HME) manifests as a flu-like illness that progresses in severity to resemble toxic shock-like syndrome, with meningoencephalitis or adult respiratory distress syndrome in some patients, and requires hospitalization in half. In immunocompromised patients, HME acts as an overwhelming opportunistic infection. In one family physician's practice, active surveillance for three years revealed an incidence of 1000 cases per million population. Diagnosis employs serology or polymerase chain reaction, which are not utilized sufficiently to establish the true impact of this emerging virus-like illness.","PeriodicalId":77010,"journal":{"name":"Archives of virology. Supplementum","volume":" 19","pages":"147-56"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/3-211-29981-5_12","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25754434","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}

引用次数: 27

Emerging infectious diseases: the public's view of the problem and what should be expected from the public health community. 新出现的传染病：公众对这一问题的看法以及对公共卫生界的期望。

Archives of virology. Supplementum Pub Date : 2005-01-01 DOI: 10.1007/3-211-29981-5_17

J M Hughes

引用次数: 0

Pathogenesis of Rift Valley fever virus in mosquitoes--tracheal conduits & the basal lamina as an extra-cellular barrier. 裂谷热病毒在蚊子中的发病机制——气管导管和作为细胞外屏障的基底层。

Archives of virology. Supplementum Pub Date : 2005-01-01 DOI: 10.1007/3-211-29981-5_8

W S Romoser, M J Turell, K Lerdthusnee, M Neira, D Dohm, G Ludwig, L Wasieloski

{"title":"Pathogenesis of Rift Valley fever virus in mosquitoes--tracheal conduits & the basal lamina as an extra-cellular barrier.","authors":"W S Romoser, M J Turell, K Lerdthusnee, M Neira, D Dohm, G Ludwig, L Wasieloski","doi":"10.1007/3-211-29981-5_8","DOIUrl":"https://doi.org/10.1007/3-211-29981-5_8","url":null,"abstract":"Knowledge of the fate of an arbovirus in a mosquito is fundamental to understanding the mosquito's competence to transmit the virus. When a competent mosquito ingests viremic vertebrate blood, virus infects midgut epithelial cells and replicates, then disseminates to other tissues, including salivary glands and/or ovaries. The virus is then transmitted to the next vertebrate host horizontally via bite and/or vertically to the mosquito's offspring. Not all mosquitoes that ingest virus become infected or, if infected, transmit virus. Several \"barriers\" to arbovirus passage, and ultimately transmission, have been identified in incompetent or partially competent mosquitoes, including, among others, gut escape barriers and salivary gland infection barriers. The extra-cellular basal lamina around the midgut epithelium and the basal lamina that surrounds the salivary glands may act as such barriers. Midgut basal lamina pore sizes are significantly smaller than arboviruses and ultrastructural evidence suggests that midgut tracheae and tracheoles may provide a means for viruses to circumvent this barrier. Further, immunocytochemical evidence indicates the existence of a salivary gland infection barrier in Anopheles stephensi. The basal lamina may prevent access to mosquito cell surface virus receptors and help explain why anopheline mosquitoes are relatively incompetent arbovirus transmitters when compared to culicines.","PeriodicalId":77010,"journal":{"name":"Archives of virology. Supplementum","volume":" 19","pages":"89-100"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/3-211-29981-5_8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25751738","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}

引用次数: 48

Structural biology of old world and new world alphaviruses. 旧世界和新世界甲病毒的结构生物学。

Archives of virology. Supplementum Pub Date : 2005-01-01 DOI: 10.1007/3-211-29981-5_14

A Paredes, S Weaver, S Watowich, W Chiu

引用次数: 14