The classification and nomenclature of viruses. Summary of results of meetings of the International Committee on Taxonomy of Viruses in Madrid, September 1975.
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Bacteriophages↗
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The classification and nomenclature of viruses. Summary of results of meetings of the International Committee on Taxonomy of Viruses in Madrid, September 1975.
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Bacteriophages↗
The classification and nomenclature of viruses. Summary of results of meetings of the International Committee on Taxonomy of Viruses in The Hague, September 1978.
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Societies, Scientific↗
The classification and nomenclature of viruses. Summary of results of meetings of the International Committee on Taxonomy of Viruses in Madrid, September 1975.
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Terminology as Topic↗
The classification and nomenclature of viruses: summary of results of meetings of the International Committee on Taxonomy of Viruses in Edmonton, Canada 1987.
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Plant Viruses↗
Genetics and pathogenicity of negative strand viruses. Abstracts of papers presented at the 7th International Meeting on Negative Strand Viruses. Dinard, France, 18-23 September 1988.
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Animals↗
The biology of negative strand viruses. Abstracts of papers presented at the 6th International Meeting on Negative Strand Viruses. Cambridge, 15-20 September 1985.
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RNA Viruses↗
International importation of measles virus--United States, 1993-2001.
To determine trends in international importations of measles, data from the National Notifiable Diseases Surveillance System were analyzed. Of the 2632 measles cases reported between 1993 and 2001, 449 cases (17%) were internationally imported. An additional 186 cases (7%) resulted from spread of measles virus from these imported cases, and 388 cases (15%) had virological evidence of importation. The number of imported cases averaged 50 per year (range, 26-79 cases). The proportion of cases imported increased from an average of 14% in 1993-1996 to an average of 35% in 1997-2001. Imported measles cases were acquired in 63 countries, with 6 countries (Japan, Germany, China, the Philippines, Italy, and the United Kingdom) accounting for 44% of all imported cases. Further reduction of measles in the United States requires international cooperation and improved global surveillance and control of measles.
Adolescent↗
Studies on pathogenesis following single and double infection with viral hemorrhagic septicemia virus and infectious hematopoietic necrosis virus in rainbow trout (Oncorhynchus mykiss).
Rainbow trout (Oncorhynchus mykiss) were bath challenged with viral hemorrhagic septicemia (VHS) virus or infectious hematopoietic necrosis (IHN) virus or with both viruses simultaneously. The viral distribution and development of histologic lesions were examined using immunohistochemistry, while virus titer in kidney was determined by viral titration in cell culture. Single infections with VHS virus and IHN virus showed similar distributions of virus in internal organs. The early identification of virus in gill epithelium, 1 and 2 days postinfection (PI) for VHS virus and IHN virus, respectively, indicates that this organ is the point of entry for both viruses. The detection of VHS virus at 1 day PI and 3 days PI for IHN virus is indicative of kidney and spleen being the target organs for these viruses. A simultaneous infection of VHS virus and IHN virus resulted in both viruses establishing an infection. Further double infection did not result in a statistically significant lower titer of both viruses in kidney but a more restricted distribution of IHN virus in internal organs compared with the single infected group. The most striking finding is that, for IHN virus, virus was not detected in the brain in situ in the double-infected group. This study provides support for the conclusion that simultaneous infection with two piscine rhabdoviruses in a susceptible host results in some degree of interaction at the cell level, leading to a reduced systemic distribution of IHN virus.
Animals↗
The international reference preparation of influenza virus haemagglutinin (type A).
This paper describes the international collaborative assay that led to the establishment in 1967 of the International Reference Preparation of Influenza Virus Haemagglutinin (Type A) and the studies completed during the following years on the use of the preparation for evaluating the haemagglutinin content of 46 influenza virus vaccines in terms of international units. The WHO Expert Committee on Biological Standardization (1967) defined the International Unit as 0,09361 mg of the International Reference Preparation.Altogether 14 laboratories in 12 countries took part in one or both studies, using a total of 24 methods (HA titrations and, in a few cases CCA titrations). Major differences in the HA titres were found between laboratories, while the potencies (the haemagglutinin content values) relative to the International Reference Preparation were free from most of these differences. Haemagglutination titres varied over a range factor up to 50, while the corresponding relative "potencies" varied with a factor of only 2. The CCA method used in a few laboratories gave results close to the lowest haemagglutination titres and showed relatively small variations between laboratories. The analyses of variance disclosed differences in the variation within laboratories, but for the majority of the laboratories the variation allowed an overall estimate of a standard error.The calculation of haemagglutinin content (in IU) from relative potencies is described. Advice is given on the selection, preparation, and titration of a local reference vaccine with a view to expressing its haemagglutinin content in international units.The test results with 46 local vaccines are also given. The deviations of the relative potencies from the average per vaccine showed a distribution with eight major discrepancies instead of the expected one. The background for these cases is discussed.
Agglutination Tests↗
Nucleotide sequence of an aberrant glycoprotein mRNA synthesized by the internal deletion mutant of vesicular stomatitis virus.
The transcriptionally active internal deletion mutant (DI-LT) of vesicular stomatitis virus synthesizes an abnormal mRNA (G*) containing a transcript of the remnant polymerase gene covalently linked to the 3' end of the glycoprotein message (R.C. Herman and R.A. Lazzarini, J. Virol. 40:78-86, 1981). A complementary DNA copy of the 3' end of the G* transcript was molecularly cloned and then chemically sequenced. The results showed that the deletion removed the last 54 nucleotides of the normal glycoprotein gene, the intergenic dinucleotide, and all but the last 258 nucleotides of the polymerase gene. The sequence of DI-LT at the deletion site was compared to that of the transcriptionally inactive DI-LT2 particle.
Animals↗
Studies of a myxovirus recovered from patients with infectious hepatitis. II. Fine structure and electron microscopic demonstration of intracytoplasmic internal component and viral filament formation.
WB virus has been shown to have a fine structure which is characteristic of members of the mumps-NDV-parainfluenza group of viruses. Viral internal component has been demonstrated within the cytoplasm of infected cells. The incorporation of internal component into virus filaments at the cell surface has also been demonstrated. The evidence presented suggests that virus filament formation occurs by a process of invagination of the cell membrane about the coiled strands of internal component lying beneath the membrane.
Hepatitis A↗
Consensus proposals for a unified system of nomenclature of hepatitis C virus genotypes.
International standardization and coordination of the nomenclature of variants of hepatitis C virus (HCV) is increasingly needed as more is discovered about the scale of HCV-related liver disease and important biological and antigenic differences that exist between variants. A group of scientists expert in the field of HCV genetic variability, and those involved in development of HCV sequence databases, the Hepatitis Virus Database (Japan), euHCVdb (France), and Los Alamos (United States), met to re-examine the status of HCV genotype nomenclature, resolve conflicting genotype or subtype names among described variants of HCV, and draw up revised criteria for the assignment of new genotypes as they are discovered in the future. A comprehensive listing of all currently classified variants of HCV incorporates a number of agreed genotype and subtype name re-assignments to create consistency in nomenclature. The paper also contains consensus proposals for the classification of new variants into genotypes and subtypes, which recognizes and incorporates new knowledge of HCV genetic diversity and epidemiology. A proposal was made that HCV variants be classified into 6 genotypes (representing the 6 genetic groups defined by phylogenetic analysis). Subtype name assignment will be either confirmed or provisional, depending on the availability of complete or partial nucleotide sequence data, or remain unassigned where fewer than 3 examples of a new subtype have been described. In conclusion, these proposals provide the framework by which the HCV databases store and provide access to data on HCV, which will internationally coordinate the assignment of new genotypes and subtypes in the future.
Genotype↗
Artificial defective interfering RNAs derived from RNA 2 of beet necrotic yellow vein virus.
Long internal deletions were introduced into cloned cDNA of beet necrotic yellow vein virus RNAs 1-4 and transcripts containing the deletions were tested for their ability to inhibit replication of viral RNA in Chenopodium quinoa protoplasts and plants. No inhibition was observed with the deletion mutants based on RNAs 1, 3 and 4 but the RNA 2 deletion mutants all provoked a dramatic inhibition of synthesis of viral RNAs 1 and 2.
Blotting, Northern↗
Composition of the helical internal components of influenza virus as revealed by immunogold labeling/electron microscopy.
The composition of the large helical internal components of influenza virus was investigated by immunogold labeling/electron microscopy with antibodies to the nucleoprotein (NP), matrix protein (M), and polymerase complex (PB1, PB2, and PA) of the virus. The morphologically intact helices, obtained by air-drying of the virions on the electron microscope grid, showed little or no labeling with any of the above antibodies. However, partial to full degradation of the helix by proteinase K (2 ng/ml) prior to immunogold labeling made the helices accessible to all three antibodies. The results are consistent with a model that the helix represents a polymer of M protein enclosing or containing the influenza ribonucleoprotein(s).
Antibodies, Monoclonal↗
Initiation of vesicular stomatitis virus mutant polR1 transcription internally at the N gene in vitro.
The vesicular stomatitis virus (VSV) polymerase is thought to initiate transcription of its genome by first copying a small leader RNA complementary to the 3' end of the template. The polR VSV mutants, in contrast to wild-type virus, frequently read through the leader termination site during transcription in vitro. To shed light on polymerase termination and reinitiation events at the crucial leader-N gene junction, we employed RNase protection assays to precisely measure molar ratios of leader, N, and readthrough transcript accumulation in vitro. Wild-type virus synthesized essentially equimolar amounts of leader and N transcripts, but, unexpectedly, the polR1 mutant yielded about twice as much N mRNA as leader (ratio of 1.9 +/- 0.1). Primer extension assays ruled out an increase in abortive N transcript synthesis for polR1. Transcription entailed multiple rounds of synthesis, with transcript ratios remaining the same after 0.5 or 2 h of synthesis, ruling out a significant contribution from polymerases "pre-positioned" at the N gene. No significant degradation of either leader or N transcripts was observed after incubating purified products with virions. Our data lead us to conclude that transcription can initiate internally at the N gene, at least in the case of polR1 VSV. We propose, however, that productive internal initiation of transcription is a fundamental property of the VSV polymerase and that of related viruses. A model postulating two distinct polymerase complexes, one for leader synthesis and one for internal initiation, is presented.
Gene Expression Regulation, Viral↗
Dendritic cell-specific intercellular adhesion molecule 3-grabbing non-integrin (DC-SIGN)-mediated enhancement of dengue virus infection is independent of DC-SIGN internalization signals.
Dengue virus (DV) is a mosquito-borne flavivirus that causes hemorrhagic fever in humans. In the natural infection, DV is introduced into human skin by an infected mosquito vector where it is believed to target immature dendritic cells (DCs) and Langerhans cells (LCs). We found that DV productively infects DCs but not LCs. We show here that the interactions between DV E protein, the sole mannosylated glycoprotein present on DV particles, and the C-type lectin dendritic cell-specific intercellular adhesion molecule 3-grabbing non-integrin (DC-SIGN) are essential for DV infection of DCs. Binding of mannosylated N-glycans on DV E protein to DC-SIGN triggers a rapid and efficient internalization of the viral glycoprotein. However, we observed that endocytosis-defective DC-SIGN molecules allow efficient DV replication, indicating that DC-SIGN endocytosis is dispensable for the internalization step in DV entry. Together, these results argue in favor of a mechanism by which DC-SIGN enhances DV entry and infection in cis. We propose that DC-SIGN concentrates mosquito-derived DV particles at the cell surface to allow efficient interaction with an as yet unidentified entry factor that is ultimately responsible for DV internalization and pH-dependent fusion into DCs.
Base Sequence↗
Roles of the polypyrimidine tract and 3' noncoding region of hepatitis C virus RNA in the internal ribosome entry site-mediated translation.
Hepatitis C virus (HCV) genome contains a 3'noncoding region (3'NCR) consisting of a variable region, a polypyrimidine tract (polyU/UC) and the X region. To examine the roles of 3'NCR and polyU/UC tract in the internal ribosome entry site (IRES)-mediated translation process, a variety of 3'NCRs containing different lengths of polyU/UC tract were obtained from HCV infected patients and cloned respectively to the downstream of the firefly luciferase coding gene linked to HCV 5'NCR and 30 nucleotides of core gene (containing IRES element). The results of in vitro translation in rabbit reticulocyte lysate (RRL) and cell transfection assay in mammalian cells showed that the IRES-mediated translation efficiency could be enhanced by the full-length of 3'NCR of HCV RNA. However, contradictory results were observed when the role of polyU/UC tract in the IRES-mediated translation was studied. While the IRES-mediated translation efficiency was inhibited by the presence of polyU/UC tract in in vitro translation experiments, transfection of these expression cassettes into hepatic cell line showed that polyU/UC tract enhanced IRES-mediated translation efficiency in vivo. Cellular-fraction complement experiments showed that cellular factors were required for the enhancement by the polyU/UC tract. Further antibody blocking assay and UV cross-linking assay suggested the correlation of IRES-mediated translation with host factors, including the La protein. The data above also indicated that the modulations of the IRES-mediated translation by the HCV 3'NCR and the polyU/UC tract were in a length-independent manner.
3' Untranslated Regions↗