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At least 199 records · Page 11Linked to original sources
PubMed1988

Differential ability of B cells specific for external vs. internal influenza virus proteins to respond to help from influenza virus-specific T-cell clones in vivo.

When a helper T-cell (TH) clone specific for the hemagglutinin, neuraminidase, matrix protein, or nucleoprotein of influenza strain A/PR/8/34 is adoptively transferred to athymic mice 1 day after virus infection the anti-viral antibody response of the mouse is enhanced. This response is directed predominantly to the hemagglutinin and requires associative T-cell-B-cell interactions. Delaying transfer of the TH clone has three consequences: (i) the onset of the anti-hemagglutinin antibody response is delayed; (ii) the titer of the anti-hemagglutinin response is reduced; and (iii) the titer of the antibody in the response against the internal proteins, matrix protein and nucleoprotein, is enhanced upon transfer of matrix protein- or nucleoprotein-specific, but not hemagglutinin- or neuraminidase-specific, TH clones. Thus, there is a hierarchy of help: B cells recognizing viral surface components, hemagglutinin or neuraminidase, can receive help from TH clones specific for any of the major structural viral proteins. In contrast, B cells responding to internal viral components, matrix protein or nucleoprotein, are restricted to receiving help almost exclusively from TH clones with the same protein specificity. These observations suggest that, upon B-cell surface immunoglobulin-antigen interaction and uptake of intact virus, B cells specific for viral surface proteins process and present all major structural viral antigens, enabling the B cells to interact with TH clones specific for any virion protein. B cells recognizing internal viral components, which may be accessible to interaction with B-cell immunoglobulin receptors mainly as free proteins, would present only the protein for which they are specific and, thereby, receive help only from the TH clones of the same protein specificity.

Animals↗
PubMed1985

Structure of viral DNA in a rat cell line transformed by the cloned EcoRI-C fragment of adenovirus 12.

A DNA segment carrying viral DNA was cloned from a rat cell line transformed by the cloned EcoRI-C fragment (0 to 16.4 map units) of human adenovirus type 12(Ad12), and the viral sequence in the clone was analysed. The cloned segment contained the region from nucleotide positions 118 to 3520 of the Ad12 genome in the middle. No unique structure was found at the viral and non-viral DNA junctions. When examined the transforming activity, the conserved viral sequence was able to transform rat 3Y1 cells efficiently. Southern blotting analysis of the viral sequence in five re-transformed cell lines showed that the viral sequence was inserted at different sites of cellular DNA. These results indicate that (I) the Ad12 DNA moiety from the enhancer-promoter region of the E1A gene to the end of the E1B gene contains enough information for efficient transformation of the rat cell, and (II) integration of the viral sequence at unique cellular sites is not prerequisite for transformation.

Adenoviruses, Human↗
PubMed1998

The structural protein ODV-EC27 of Autographa californica nucleopolyhedrovirus is a multifunctional viral cyclin.

Two major characteristics of baculovirus infection are arrest of the host cell at G2/M phase of the cell cycle with continuing viral DNA replication. We show that Autographa californica nucleopolyhedrovirus (AcMNPV) encodes for a multifunctional cyclin that may partially explain the molecular basis of these important characteristics of AcMNPV (baculovirus) infection. Amino acids 80-110 of the viral structural protein ODV-EC27 (-EC27) demonstrate 25-30% similarity with cellular cyclins within the cyclin box. Immunoprecipitation results using antibodies to -EC27 show that -EC27 can associate with either cdc2 or cdk6 resulting in active kinase complexes that can phosphorylate histone H1 and retinoblastoma protein in vitro. The cdk6-EC27 complex also associates with proliferating cell nuclear antigen (PCNA) and we demonstrate that PCNA is a structural protein of both the budded virus and the occlusion-derived virus. These results suggest that -EC27 can function as a multifunctional cyclin: when associated with cdc2, it exhibits cyclin B-like activity; when associated with cdk6, the complex possesses cyclin D-like activity and binds PCNA. The possible roles of such a multifunctional cyclin during the life cycle of baculovirus are discussed, along with potential implications relative to the expression of functionally authentic recombinant proteins by using baculovirus-infected cells.

Amino Acid Sequence↗
PubMed2002

Viral ion channels: structure and function.

Viral ion channels are short auxiliary membrane proteins with a length of ca. 100 amino acids. They are found in enveloped viruses from influenza A, influenza B and influenza C (Orthomyxoviridae), and the human immunodeficiency virus type 1 (HIV-1, Retroviridae). The channels are called M2 (influenza A), NB (influenza B), CM2 (influenza C) and Vpu (HIV-1). Recently, in Paramecium bursaria chlorella virus (PBCV-1, Phycodnaviridae), a K+ selective ion channel has been discovered. The viral channels form homo oligomers to allow an ion flux and represent miniaturised systems. Proton conductivity of M2 is established; NB, Vpu and the potassium channel from PBC-1 conduct ions; for CM2 ion conductivity is still under proof. This review summarises the current knowledge of these short viral membrane proteins. Their discovery is outlined and experimental evidence for their structure and function is discussed. Studies using computational methods are presented as well as investigations of drug-protein interactions.

Amino Acid Sequence↗
PubMedDate not supplied

Class I and class II viral fusion protein structures reveal similar principles in membrane fusion.

Recent crystal structures of Flavivirus and Alphavirus fusion proteins (class II) confirm two major principles of protein machineries that mediate the merger of two opposing lipid bilayers. First, the fusion protein can bridge both membranes tethered by two membrane anchors. Second, refolding or domain rearrangement steps lead to the positioning of both anchors into close proximity at the same end of an elongated structure. Although these two steps are in principle sufficient to pull two opposing membranes together and initiate membrane fusion, accumulating evidence suggests that the process requires the concerted action of a number of fusion proteins at and outside the contact sites. This review will focus on the structures of viral class I and class II fusion proteins and their similarities in facilitating membrane fusion.

Animals↗
PubMed1994

Detection of equine arteritis virus following amplification of structural and nonstructural viral genes by reverse transcription-PCR.

A reverse transcription (RT)-PCR assay was developed for the detection of equine arteritis virus (EAV) in cell culture supernatant and in horse semen. Four different sets of oligonucleotide primers complementary to sequences located in the 3' end of the polymerase gene (open reading frame [ORF] 1b) and to sequences representing the entire ORFs 3, 4, and 7, which encode for nonstructural (ORFs 3 and 4) or viral nucleocapsid (ORF 7) proteins, were compared for their abilities to amplify the targeted EAV sequences by the RT-PCR procedure. The sensitivities of the RT-PCR for amplification of EAV sequences located in the 3' end of ORF 1b and ORF 4 were 2 median tissue culture infective doses (TCID50s) of viral particles in the EAV-infected cell culture supernatant for both ORFs and 20 and 200 TCID50s of viral particles, respectively, in virus-containing horse semen. The sensitivities were much lower when primers complementary to ORFs 3 and 7 were used in the RT-PCR, with a minimum detection limit of only 2 x 10(4) TCID50s of viral particles in virally infected cell culture supernatant, as determined by analyzing the resulting RT-PCR products on ethidium bromide-stained agarose gels. The specificities of the RT-PCR assays for all primer sets tested were confirmed when the amplified cDNA products of the expected size reacted positively with the corresponding virus-specific digoxigenin-labeled cDNA probes in the chemiluminescence assays. Although the sensitivity of the RT-PCR for amplification of ORF 3 and 7 sequences was lower, all sets or primers were capable of amplifying several cell culture-adapted EAV field isolates when the virus was present in high enough quanities in the test sample. When horse semen samples were analyzed for the presence of EAV by the RT-PCR with primers specific to the ORF 1b 3' end and ORF 4 sequences and by virus isolation in cell cultures, there was 100% concordance among the assays. The RT-PCR assay targeting the 3' end of ORF 1b and/or ORF 4 EAV RNA may be an alternative to conventional methods for the diagnosis of EAV infection in horses.

Animals↗
PubMed2000

Vaccinia virus envelope H3L protein binds to cell surface heparan sulfate and is important for intracellular mature virion morphogenesis and virus infection in vitro and in vivo.

An immunodominant antigen, p35, is expressed on the envelope of intracellular mature virions (IMV) of vaccinia virus. p35 is encoded by the viral late gene H3L, but its role in the virus life cycle is not known. This report demonstrates that soluble H3L protein binds to heparan sulfate on the cell surface and competes with the binding of vaccinia virus, indicating a role for H3L protein in IMV adsorption to mammalian cells. A mutant virus defective in expression of H3L (H3L(-)) was constructed; the mutant virus has a small plaque phenotype and 10-fold lower IMV and extracellular enveloped virion titers than the wild-type virus. Virion morphogenesis is severely blocked and intermediate viral structures such as viral factories and crescents accumulate in cells infected with the H3L(-) mutant virus. IMV from the H3L(-) mutant virus are somewhat altered and less infectious than wild-type virions. However, cells infected by the mutant virus form multinucleated syncytia after low pH treatment, suggesting that H3L protein is not required for cell fusion. Mice inoculated intranasally with wild-type virus show high mortality and severe weight loss, whereas mice infected with H3L(-) mutant virus survive and recover faster, indicating that inactivation of the H3L gene attenuates virus virulence in vivo. In summary, these data indicate that H3L protein mediates vaccinia virus adsorption to cell surface heparan sulfate and is important for vaccinia virus infection in vitro and in vivo. In addition, H3L protein plays a role in virion assembly.

Amino Acid Sequence↗
PubMed1984

Varicella-zoster virus-specific gp140: a highly immunogenic and disulfide-linked structural glycoprotein.

A 140,000-dalton disulfide-linked glycoprotein (gp140) specified by varicella-zoster virus (VZV) in infected cultured cells was identified and precipitated by two murine monoclonal antibodies (VZ-151 and VZ-158). When analyzed under reducing conditions by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, gp140 was cleaved predominantly into a 66,000 lower-molecular-weight product (gp66). This protein was classified as a viral structural component, since it was observed in the polypeptide profile of metrizamide gradient-purified enveloped virions. By immunofluorescence analyses with a monoclonal antibody probe, gp140 expression was documented to be highly conserved both within cultured cells inoculated with homologous (VZV-Oka) and heterologous (VZV-32) strains and in infected human tissues from chicken pox and zoster patients. That the glycoprotein was highly immunogenic was confirmed by the presence of high-titer anti-gp140 antibody in the sera of both hyperimmunized laboratory animals and naturally infected humans. Temporally, the humoral response to gp140 following primary VZV infection preceded that against the other viral glycoproteins. These studies describe, therefore, an immunogenic, disulfide-linked viral structural glycoprotein, which must be included among the other five previously described VZV-specific fucosylated species--gp118, gp98, gp62, and gp45.

Antibody Formation↗
PubMed1990

Interaction of RNase P from Escherichia coli with pseudoknotted structures in viral RNAs.

In a previous study it was shown that RNase P from E. coli cleaves the tRNA-like structure of turnip yellow mosaic virus (TYMV) RNA in vitro (Guerrier-Takada et al. (1988) Cell, 53, 267-272). Cleavage takes place at the 3' side of the loop that crosses the deep groove of the pseudoknot structure present in the aminoacyl acceptor domain. In the present study fragments of TYMV RNA with mutations in the pseudoknot, generated by transcription in vitro, were tested for susceptibility to cleavage by RNase P. Changes in the specificity with respect to the site of cleavage and decreases in the rate of cleavage were observed with most of these substrates. The behaviour of various mutants in the reaction catalyzed by RNase P is in agreement with the present model of the TYMV RNA pseudoknot (Dumas et al. (1987), J. Biomol. Struct. Dyn. 263, 652-657). Base substitutions in the loop that crosses the shallow groove of the pseudoknot structure resulted, however, in an unexpected decrease in the rate of cleavage, probably due to conformational changes in the substrates. Studies on other tRNA-like structures revealed an important role in the reaction with RNase P for both the nucleotide at the 3' side of the loop that spans the deep groove and the nucleotide at position 4, which correspond to positions--1 and 73, respectively, in tRNA precursors.

Base Sequence↗
PubMed2000

Crystal structure of viral serpin crmA provides insights into its mechanism of cysteine proteinase inhibition.

CrmA is an unusual viral serpin that inhibits both cysteine and serine proteinases involved in the regulation of host inflammatory and apoptosis processes. It differs from other members of the serpin superfamily by having a reactive center loop that is one residue shorter, and by its apparent inability to form SDS-stable covalent complexes with cysteine proteinases. To obtain insight into the inhibitory mechanism of crmA, we determined the crystal structure of reactive center loop-cleaved crmA to 2.9 A resolution. The structure, which is the first of a viral serpin, suggests that crmA can inhibit cysteine proteinases by a mechanism analogous to that used by other serpins against serine proteinases. However, one striking difference from other serpins, which may be significant for in vivo function, is an additional highly charged antiparallel strand for b sheet A, whose sequence and length are unique to crmA.

Amino Acid Sequence↗
PubMed1977

Differential synthesis of mammalian type C viral gene products in infected cells.

Radioimmunological techniques were applied to the quantitation of the translational products of the gag, pol, and env genes of mammalian type C viruses. Analysis of the viral proteins associated with simian sarcoma-associated virus (SSA V) and SSA V-infected cells revealed in each that the level of reverse transcriptase was less than 1% of that of the major viral structural protein, p30. The rate of intracellular degradation of reverse transcriptase in SSA V-infected cells was found to be no greater than that of several viral structural proteins, indicating that the lower levels of viral enzyme resulted from its decreased synthesis. By screening individual cells infected at limiting SSA V dilution, it was possible to isolate a clone (clone 16), which demonstrated levels of viral p12, p30, and gp70 similar to those found in wild-type SSA V-infected cells, and which released noninfectious virions in large quantity. The noninfectious virions and clone 16 cells were shown to lack immunologically or enzymologically detectable reverse transcriptase. With serial passage of clone 16 cells, reverse transcriptase activity became spontaneously detectable in tissue culture fluids, concomitant with the appearance of infectious virus. The reverse transcriptase associated with this virus was indistinguishable from SSA V polymerase, indicating that the genetic alteration restricting SSA V pol gene expression in clone 16 cells was reversible. These results further demonstrate the strict requirement of reverse transcriptase for establishment of type C virus infection. Possible mechanisms to account for the patterns of type C viral gene expression detected in SSA V-infected cells are discussed.

Cell Line↗
PubMed1978

Encephalitis following vaccination against distemper and infectious hepatitis in the dog. An optical and ultrastructural study.

A 4-month-old, male, healthy dog developed CNS-symptoms 10 days after the second vaccination with live, attenuated distemper and canine hepatitis virus. The animal was euthanized after 2 weeks of illness. Light and electron microscopic examination of the CNS showed a partly necrotizing encephalomyelitis with numberous intranuclear and intracytoplasmic inclusion bodies, and the presence of probable pseudomyxovirus nucleocapsids and of crystalloid and tubuloreticular aggregates. Although there was conformity of inclusion bodies and probable viral structures as revealed by electron microscopy, the latter showed a much wider distribution. In addition, viral structures of a different type were found in polymorphonuclear leukocytes and vascular endothelial cells. Several morphological criteria led to the supposition that they are Picornaviruses, or possibly Arenaviruses. It is thought that their role in the disease process was at best an indirect one.

Animals↗
PubMed1965

Autoradiographic study on sheeppox virus infection.

Terrinha, António M. (National Laboratory for Veterinary Research, Lisbon, Portugal), José D. Vigário, José L. Nunes Petisca, J. Moura Nunes, and Armando L. Bastos. Autoradiographic study on sheeppox virus infection. J. Bacteriol. 90:1703-1709. 1965.-An autoradiographic study of sheep embryo cell cultures infected with sheeppox virus showed that viral deoxyribonucleic acid (DNA) synthesis starts at 10 to 11 hr after infection. The number of cells which supported viral DNA synthesis increased until 22 to 23 hr. The extent of cytoplasmic continuity between cells might permit the cell-to-cell transfer of mature virus or perhaps viral DNA. There is evidence of an inhibitory action on cellular DNA synthesis in cells which supported viral DNA synthesis, but, in all cellular populations infected, a small proportion of cells was encountered which supported viral DNA synthesis in compartment S. No evidence for cellular division of sheeppox virus-infected cells has been found. Enzymatic digestion by deoxyribonuclease combined with autoradiography provided an indirect demonstration of the time at which the first viral structural proteins were found to be synthesized, that is, 18 hr after infection. A progressive increase in synthesis of viral structural proteins was demonstrated. Virus maturation occurred within the cells in the cytoplasm, predominantly in the same sites as viral DNA synthesis.

Autoradiography↗
PubMed2026

Viral community structure in New Zealand's aquatic birds is associated with scavenging behavior.

Wild migratory birds play a major role in the global spread of viruses, yet the ecological drivers underpinning viral diversity and transmission, particularly host behavior, remain poorly understood. Aotearoa/New Zealand provides a powerful system to address this, including unique species that reflect its geographical isolation, yet with international connections provided by migratory birds across the East Asian-Australasian Flyway and Antarctic regions. Herein, we conducted a large-scale metatranscriptomic survey of wild birds across New Zealand and its subantarctic islands, in which we collected 1,348 samples from 690 individuals across 31 host species spanning four avian orders. We identified 118 avian viruses from 17 families, including 107 novel species, expanding our knowledge of avian viral diversity. Notably, viral community composition was most strongly associated with bird scavenging behavior, which explained more variation than host taxonomy, geography, or migratory status. Scavenging birds and opportunistic scavengers harbored more diverse viromes than non-scavengers, consistent with increased viral exposure across trophic levels. This was supported by the detection of 12 mammalian-associated viruses, primarily in scavengers, including hedgehog hepatovirus, rabbit hemorrhagic disease virus 2, and sea lion astroviruses, with host sequence data confirming dietary origin. We also detected viruses of epidemiological and evolutionary interest, including a low-pathogenic avian influenza A(H1N9) virus from red knots (Calidris canutus) and a divergent tobanivirus from Auckland Island teal (Anas aucklandica), which represented the first putative avian member of the Tobaniviridae. These findings suggest that virome structure in wild birds is associated with scavenging behavior, thus highlighting the importance of incorporating host ecology into viral surveillance and risk assessment.

New Zealand↗
PubMed1990

Role of early genes in pathogenesis of adenovirus pneumonia.

Intranasal inoculation of type 5 adenovirus into the cotton rat Sigmodon hispidus produces a pneumonia pathologically similar to that in humans, and it, therefore, provides an excellent animal model to investigate the pathogenesis of this disease. The goal of this study was to test the hypothesis that accumulation of viral structural proteins is responsible for a major portion of the cell-damage-producing disease. Since viral DNA replication is essential for synthesis of the viral structural proteins, which are products of late genes, the hypothesis was tested using mutants defective in genes required for DNA synthesis. Most experiments were done with the conditionally lethal temperature-sensitive (ts) mutant H5ts125, which contains a mutation in the early region 2A (E2A) gene encoding the DNA-binding protein. The data show that infection with 1 x 10(9.0) plaque-forming units of H5ts125 induced a pneumonia that was as extensive and qualitatively the same as that after wild-type adenovirus type 5 infection, although H5ts125 did not replicate to produce infectious virus. When cotton rats were infected with 1 x 10(8.0) plaque-forming units of wild-type adenovirus type 5 or H5ts125, the pneumonias that followed were pathologically similar; in the latter phases, however, wild-type virus produced slightly more extensive pneumonia than did H5ts125, probably because its replication permitted infection of more susceptible cells.

Adenoviridae Infections↗
PubMed1998

Immunological basis for protection in a murine model of tick-borne encephalitis by a recombinant adenovirus carrying the gene encoding the NS1 non-structural protein.

The humoral immune response to flaviviruses is mainly directed to the major envelope protein, E, and a glycosylated non-structural protein, NS1. Cell-mediated immune responses, however, appear to be directed mainly against non-structural proteins. Experiments described here show that a defective recombinant adenovirus (Rad51) containing the gene encoding the NS1 protein of tick-borne encephalitis virus can induce a strong protective immune response against several pathogenic tick-borne flaviviruses in an experimental animal model, and can enhance the efficacy of conventional vaccine preparations. A protective immune response against a lethal virus challenge can also be induced by the passive transfer of antibodies, B cells or T cells from animals vaccinated with Rad51. Raised levels of non-neutralizing antibodies and cytokines associated with a T helper cell-type 1 immune response are also observed. These data demonstrate the importance of non-structural viral proteins in the protective immune response against flaviviruses and support the use of non-structural viral proteins as vaccine components.

Adenoviridae↗
PubMed1981

Glycoprotein enrichment in Moloney leukemia virus structural proteins released from interferon-treated cells.

Interferon treatment of Moloney-leukemia-virus-infected cells (3T3/MLV) leads to the formation of virus particles enriched with viral structural glycoproteins, in addition to the inhibition of virus production. A preferential inhibitory effect on incorporation of RNA and proteins rather than glycoproteins was found in the released virus particles from interferon-treated cells. Enrichment in 70,000- and 45,000-dalton glycoprotein (gP-70, gP-45) in these particles was further demonstrated by polyacrylamide analysis of viral proteins pulse-labeled with [3H]-leucine. Viral glycoproteins released as soluble antigens were also determined. A 40% reduction was found in gP-70 and gP-45 released from interferon-treated cells. Radioimmunoprecipitation of pulse-chase-labeled cellular viral proteins showed no effect of interferon on the formation of viral structural 30,000-, 15,000- to 12,000-dalton proteins, and gP-70 and gP-45 from their respective precursors. The uncoordinate effect of interferon inhibition on viral 30,000-dalton protein and gP-70 is discussed.

Animals↗