Structural modifications of macrophages initiated by tick-borne encephalitis virus
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Poxviridae
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SUMMARY The xenotropic (X-tropic) mouse type C virus (MuLV) and its pseudotype of murine sarcoma virus (MSV) were inoculated into several fertilized developing Pekin duck eggs. The development of the duck embryos was substantially reduced in those receiving the X-tropic viruses compared to eggs inoculated only with tissue culture medium. Infectious virus was isolated from some of the adult animals; in others, evidence for integrated virus sequences in the tissues was noted. No specific pathology was found in the ducks that received X-tropic MuLV alone, but one duck developed multiple fibrosarcomas when inoculated at birth with the X-tropic virus pseudotype of MSV. Two ducks receiving X-tropic MuLV had signs of haematopoietic disorders. In addition, more virus-inoculated animals had evidence of hepatitis and encephalitis than control ducks. Antibody production to X-tropic MuLV was present in several ducks inoculated with virus either in embryo or at birth. Absence of antiviral antibodies was noted in those animals whose tissues contained replicating virus. These studies confirm the observations with X-tropic virus in tissue culture. They demonstrate in vivo that avian species are susceptible to infection by the mouse X-tropic virus and that their fibroblasts can be transformed by the X-tropic MuLV pseudotype of MSV.
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Newcastle Disease
Veterinary virology
Viral culture
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Newcastle Disease
Pestivirus
Heterologous
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Abstract The hemagglutinin (HA) protein of influenza virus mediates essential viral functions including the binding to host receptor and virus entry. It also has the antigenic sites required for virus neutralization by host antibodies. Here, we characterized an H3N2 triple reassortant (TR) influenza virus (A/turkey/Ohio/313053/04) with a mutation at the receptor binding domain (Asp190Ala) that occurred upon virus transmission from turkeys to pigs in an experimental infection study. The mutant virus replicated less efficiently than the parental virus in human, pig and turkey primary tracheal/bronchial epithelial cells, with more than 3-log 10 difference in virus titer at 72 hours post infection. In addition, the mutant virus demonstrated lower binding efficiency to plasma membrane preparations from all three cell types compared to the parental virus. Antisera raised against the parental virus reacted equally to both homologous and heterlogous viruses, however, antisera raised against the mutant virus showed 4-8 folds lower reactivity to the parental virus.
H5N1 genetic structure
Antibody-dependent enhancement
Veterinary virology
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SummarySpider monkeys and chimpanzees were given a series of three injections consisting of 17D yellow fever virus, followed by living West Nile virus, followed by a third injection which consisted of formalin-inactivated Russian spring-summer virus vaccine. On the basis of neutralizing antibody responses, the limitation of viremia, or both, developing when the animals were challenged with virulent viruses, these primates were judged to be protected to a considerable extent against Japanese B encephalitis, West Nile virus, St. Louis encephalitis, Murray Valley encephalitis virus, dengue types 1, 2, 3, and 4, two antigenic types of the Russian spring-summer virus complex, and Wesselsbron virus.An isolate of West Nile virus was passed a number of times in chick embryo tissue cultures and purified by the plaque technique. The progeny of two virus plaques, in a concentration of 106 mouse intracerebral lethal doses, did not produce encephalitis in intracerebrally inoculated rhesus monkeys. These attenuated viral preparations, on the basis of intracerebral titrations in mice, had at least 1,000 times the virus concentration that was necessary to produce encephalitis with the parent type. One of these attenuated isolates still produced homologous and heterologous neutralizing antibodies comparable to those of the parent strain. The data indicate that this attenuated West Nile virus did not revert to a more virulent form after alternate intracerebral passages in rhesus monkeys and suckling mice.The TP-21 strain of the Russian spring-summer virus complex was passed a number of times in chick embryo tissue cultures and purified by the plaque technique. The progeny from one of the virus plaques, in a concentration of approximately 300,000 mouse i.c. LD50, did not produce encephalitis when inoculated intracerebrally into rhesus monkeys. When this purified virus isolate of TP-21 was substituted for the formalin-inactivated Russian spring-summer vaccine in the triple vaccination procedure, considerable protection was noted in spider monkeys challenged with four members of the Russian spring-summer group of viruses.
Viremia
Flavivirus
Attenuated vaccine
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A virus (Peiping encephalitis virus) capable of producing encephalitis in Swiss mice and a monkey was isolated from a case of acute encephalitis. On the basis of animal pathogenicity and virus neutralization tests, the virus is considered to behave like the Japanese type B virus, but to be serologically distinguishable from the St. Louis encephalitis virus.
Veterinary virology
Encephalitis Viruses
Virus isolation
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Abstract T’Ho virus is a poorly characterized orthoflavivirus most closely related to Rocio virus and Ilheus virus, two orthoflaviviruses associated with human disease, suggesting that T’Ho virus could also be a human pathogen. The genome of T’Ho virus has been sequenced but an isolate has never been recovered, impeding its phenotypic characterization. In an attempt to generate recombinant T’Ho virus, the entire viral genome was synthesized as three overlapping DNA fragments, joined by Gibson assembly, and transfected into mosquito cells. Several cell culture passages were performed, but virus was not recovered. Subsequent experiments focused on the development of a chimeric orthoflavivirus that contains the premembrane and envelope protein genes of T’Ho virus in the genetic background of Zika virus. The chimeric virus replicated in mosquito (C6/36) and vertebrate (Vero) cells, demonstrating that the major structural glycoproteins of T’Ho virus permit entry into both cell types. The chimeric virus produced plaques in Vero cells that were significantly smaller than those produced by Zika virus. The chimeric virus can potentially be used as a surrogate diagnostic reagent in place of T’Ho virus in plaque reduction neutralization tests, allowing T’Ho virus to be considered in the differential diagnosis.
Vero cell
Zika Virus
Flavivirus
Recombinant virus
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S olberg , R. A., and J. G. B ald . (U. California, Los Angeles.) Cytoplasmic structure of healthy and TMV‐infected living cells. Amer. Jour. Bot. 49 (2) : 149–157. Illus. 1962.—Epidermal leaf hairs from tobacco‐mosaic‐virus‐infected (TMV) tobacco plants were examined with a high‐resolution, phase‐contrast microscope. The infected cells were at a stage, following virus multiplication, when many of them contained crystals and X‐bodies. Attention was concentrated on the background cytoplasm. Structural features were seen that do not usually appear in descriptions of normal cytoplasm. In the parietal cytoplasm of normal cells are relatively homogeneous regions and regions containing what may be interpreted as included portions of the vacuolar system (vesicles). There are also ridges on the vacuolar surface of the cytoplasm representing lines of flow. Thus, the cytoplasm has a varied and changeable topography. The description of normal cytoplasm, apart from such features, corroborates many observations of previous workers; but some of these are included to provide the necessary contrast with diseased cytoplasm. Cytoplasm infected with TMV exhibits increased density and viscosity. Vesicles become isolated, some of the membranous separations retract, cyclosis slows, and vesicles become less elongate as the forces of cyclosis are reduced. Lines of flow in the nonvesiculate cytoplasm may also retract. Typical virus crystals precipitate. X‐bodies form from regions of coagulated cytoplasm and include constituents of the chondriome. The relationship between the vesiculate nature of cytoplasm and the endoplasmic reticulum of electron microscopists is discussed. The presence of non‐aggregated, dispersed virus in cytoplasm is related to the microscopic symptoms of TMV infection.
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