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At least 181 records · Page 10Linked to original sources
PubMed1979

A new endogenous primate type C virus isolated from the Old World monkey Colobus polykomos.

A new, genetically transmitted retrovirus has been isolated from the Old World monkey Colobus polykomos. This virus, designated CPC-1, is readily transmitted to both feline and human cells in culture. Nucleic acid hybridization studies reveal that there are 50-70 copies of the CPC-1 genome in colobus cellular DNA. Related virogene sequences can be detected in the DNA of all other Old World monkeys, as well as in the DNA of at least one ape species, the chimpanzee, indicating that this virus has been genetically transmitted in primates for 30-40 million years. CPC-1 is partially related to the type C virus previously isolated from stumptail monkeys (MAC-1). These two viruses have nucleic acid sequence homology, antigenic crossreactivity in their major viral structural protein, and a very similar host range in vitro. CPC-1 and MAC-1 therefore belong to the same class of genetically transmitted primate type C viruses and, as such, represent the first example in primates of analogous endogenous retroviruses isolated from two distantly related species.

Animals↗
PubMed1977

Complementation between temperature-sensitive (ts) and host range nontransforming (hr-t) mutants of polyoma virus.

Two major classes of polyoma mutants are defective in cell transformation: early temperature-sensitive mutants of the tsA type which are defective in viral DNA synthesis and transformation at 39 degrees, but not at 32 degrees; and host range nontransforming (hr-t) mutants which fail to transform at either temperature. Mixed infection of mouse 3T3 cells by hr-t mutants and early tsA-type mutants results in enhanced growth of the tsA-type mutants at 39 degrees, indicating that the hr-t mutants can supply the early viral function required for viral DNA synthesis. The hr-t mutants also complement late is mutants which fail to produce infectious progeny at 39 degrees because of alterations in the 45,000-dalton major virion protein. Mixed infection of hamster BHK or rat Y1 cells by hr-t and tsA-type mutants results in efficient transformation at 39 degrees, indicating that the two classes of mutants can complement for transformation. No complementation is observed in pair-wise crosses among the early tsA-type mutants alone. The tsA-type mutants are located in the distal portion of the early region of the polyoma genome [Miller, L. K., and Fried, M. (1976) J. Virol. 18, 824-832]. The hr-t mutants are located in the proximal portion [Feunteun, J., Sompayrac, L., Fluck, M., and Benjamin, T. (1976) Proc. Nat. Acad. Sci. USA]. These results suggest that the early region of the polyoma genome is divided into two functional regions which can complement for transformation. The ts3 mutant of polyoma is located in the proximal portion of the late region.

Cell Line↗
PubMed1989

Mutagenesis of the in-frame opal termination codon preceding nsP4 of Sindbis virus: studies of translational readthrough and its effect on virus replication.

Sindbis virus (SIN) contains an in-frame opal termination codon in the nonstructural protein-coding region separating nsP3 and nsP4 and provides a useful tool to study the readthrough phenomenon of the termination codon in host cells and its role in viral replication. We have changed the opal codon by site-directed mutagenesis of a full-length SIN cDNA clone to either sense amino acids (serine, tryptophan, or arginine) or the other two translation termination codons (amber or ochre). Transcripts from all of the mutant cDNA clones were infectious when used to transfect chicken embryo fibroblasts. The resulting progeny virus stocks were then used to study the effects of these mutations on viral protein and RNA synthesis, growth properties, host range, and fitness compared with the parental strain. None of the mutants showed temperature sensitivity in plaquing efficiency or plaque morphology on chicken embryo fibroblast monolayers. Relative to the wild-type parent, the mutants containing sense replacements overproduced nsP34 but not nsP4 and made slightly decreased levels of nsP3, with a delay in its appearance. This indicates that the cleavage separating nsP3 and nsP4 occurs in these mutants and also that the level of nsP4 is not regulated solely by readthrough of the opal codon. The amber and ochre mutants produced decreased levels of nsP34, and the ochre mutant grew significantly more slowly than the other mutants or wild-type virus. For all five mutants, RNA synthesis early in infection was inhibited compared with that of the parental virus. This effect was apparent at multiplicities of infection of 20 PFU per cell but not at 100 PFU per cell. Using in situ hybridization to distinguish between mutant and wild-type plaques, we have studied the behavior of the serine mutant in a high-multiplicity growth competition experiment with wild-type virus. The wild-type virus eventually outcompeted the mutant after several passages, and these results indicate that this mutation has resulted in effects that are at least partially cis acting. Furthermore, by studying the growth, plaque formation, and protein synthesis of the mutants in various cell types, we have observed host range effects of the mutations, especially in mosquito and human cells. In addition, we have demonstrated, at least indirectly, that opal, amber, and ochre termination codons in the SIN nucleotide context can be suppressed in cultured cells of chicken, human, hamster, and mosquito origin.

Animals↗
PubMed1983

Host range mutants of human rhinovirus in which nonstructural proteins are altered.

Human rhinovirus type 2 did not replicate in nonpermissive mouse cells; the restriction was not in adsorption but in the early events of virus replication. Mutants which had been adapted to grow in mouse cells had the following characteristics: (i) no change in the structural protein, (ii) a larger nonstructural protein and its precursor protein, and (iii) an altered viral RNA synthesis. The altered nonstructural proteins correlated with a change in host range of the virus and may be involved in viral RNA synthesis.

Animals↗
PubMed1994

The multigenic nature of RNA virus adaptation to plants.

Molecular genetic studies of RNA virus host range suggest that successful systemic infection requires many or all viral genes to have some degree of specific adaptation to the host. In some cases, accommodation to the host appears to be required for viral gene products to fulfil their primary functions in viral multiplication, while in other cases, adaptation seems to be required to avoid eliciting host defenses.

Adaptation, Physiological↗
PubMed1999

Amino acid residues contributing to the substrate specificity of the influenza A virus neuraminidase.

Influenza A viruses possess two glycoprotein spikes on the virion surface: hemagglutinin (HA), which binds to oligosaccharides containing terminal sialic acid, and neuraminidase (NA), which removes terminal sialic acid from oligosaccharides. Hence, the interplay between these receptor-binding and receptor-destroying functions assumes major importance in viral replication. In contrast to the well-characterized role of HA in host range restriction of influenza viruses, there is only limited information on the role of NA substrate specificity in viral replication among different animal species. We therefore investigated the substrate specificities of NA for linkages between N-acetyl sialic acid and galactose (NeuAcalpha2-3Gal and NeuAcalpha2-6Gal) and for different molecular species of sialic acids (N-acetyl and N-glycolyl sialic acids) in influenza A viruses isolated from human, avian, and pig hosts. Substrate specificity assays showed that all viruses had similar specificities for NeuAcalpha2-3Gal, while the activities for NeuAcalpha2-6Gal ranged from marginal, as represented by avian and early N2 human viruses, to high (although only one-third the activity for NeuAcalpha2-3Gal), as represented by swine and more recent N2 human viruses. Using site-specific mutagenesis, we identified in the earliest human virus with a detectable increase in NeuAcalpha2-6Gal specificity a change at position 275 (from isoleucine to valine) that enhanced the specificity for this substrate. Valine at position 275 was maintained in all later human viruses as well as swine viruses. A similar examination of N-glycolylneuraminic acid (NeuGc) specificity showed that avian viruses and most human viruses had low to moderate activity for this substrate, with the exception of most human viruses isolated between 1967 and 1969, whose NeuGc specificity was as high as that of swine viruses. The amino acid at position 431 was found to determine the level of NeuGc specificity of NA: lysine conferred high NeuGc specificity, while proline, glutamine, and glutamic acid were associated with lower NeuGc specificity. Both residues 275 and 431 lie close to the enzymatic active site but are not directly involved in the reaction mechanism. This finding suggests that the adaptation of NA to different substrates occurs by a mechanism of amino acid substitutions that subtly alter the conformation of NA in and around the active site to facilitate the binding of different species of sialic acid.

Amino Acids↗
PubMedDate not supplied

Induction of a factor that binds to the polyoma virus A enhancer on differentiation of embryonal carcinoma cells.

The cell type specificity of certain enhancers, competition experiments and the interactions that occur between proteins and enhancer sequences demonstrate that enhancers are the targets of specific factors involved in transcription control. The 246-base pair BclI-PvuII restriction enzyme fragment of polyoma virus has been shown to include two distinct enhancers, Py A and Py B, composed of several subdomains which interact with nuclear proteins from mouse fibroblasts. Embryonal carcinoma (EC) cells do not permit polyoma virus infection: both viral transcription and DNA replication are blocked. Host-range mutants of polyoma virus (EC mutants) capable of overcoming the expression block in EC cells have mutations or sequence rearrangements in their enhancer region. In an attempt to understand the molecular basis of this host restriction we compared the binding patterns displayed on the viral enhancer sequences by nuclear proteins prepared from EC cells or from fibroblasts. We show that one of the fibroblast factors required for Py A enhancer function, almost undetectable in EC cells, is induced after differentiation of these cells into parietal endoderm, suggesting that this protein is crucial in the regulation of viral gene expression during cellular differentiation, and perhaps more generally in the control of gene expression during early embryonic development.

Animals↗
PubMed1985

Relating cistrons and functions in bacteriophage PM2.

An approach to correlate functions with cistrons in bacteriophage PM2 is presented. Two of the temperature-sensitive mutants obtained differed from the wild type in heat sensitivity and four differed in host range. Comparison of the electrophoretic patterns of DNA from cells infected at the restrictive temperature with those obtained in wildtype infection revealed that viral DNA bands were absent with three additional mutants. Complementation analysis assigned the four host range mutants to cistron I and the three mutants defective in DNA synthesis to cistron IV. Recombination frequencies were used to locate cistrons III and IV on the partial genetic map of PM2.

Bacteriophages↗
PubMed1999

[Emergence of "new" viral zoonoses].

In the last two to three decades a significant increase of viral zoonotic infections was observed. These zoonoses are not only newly (or previously unrecognized) emerging diseases, but also due to the reappearance of diseases thought to have been defeated (re-emerging diseases). "New" viral diseases can arise when viruses broaden their host-range (monkey poxvirus; equine morbillivirus), or can be a consequence of intrinsic properties of the virus itself, such as high mutation rates (influenza A virus). Most new or reemerging viral zoonoses are due to infections with hemorrhagic viruses. Many of them are transmitted by insects (arboviruses, e.g. yellow fever virus) or by rodents (e.g. Hanta viruses), others by contact with patients and nosocomial infections (e.g. Ebola virus). The emergence and increase of these diseases are a consequence of anthropogenic environmental changes, such as distortions of the ecological balance and changes in agriculture. In addition, the uncontrolled growth of the cities in tropical and subtropical regions without improvement of the public health measures and the increasing international animal trade and travel also favour the spread and recurrence of these diseases.

Animals↗
PubMed1993

Analysis of the functional and host range-determining regions of the murine ectropic and amphotropic retrovirus envelope proteins.

A series of Moloney murine leukemia virus (Mo-MuLV) envelope gene constructs were analyzed for biological activity. Three classes of recombinant envelopes were examined: insertions, deletions, and chimeras. Insertion (4 to 5 amino acids) and deletion (31 to 62 amino acids) mutants spanned most of the SU (gp70)-coding region and were all biologically inactive. Radioimmunoprecipitation demonstrated that the mutant envelope proteins were incorrectly processed. The Pr80env envelope precursor proteins failed to obtain the proper posttranslational modifications and were not cleaved into SU (gp70) and TM (p15E), suggesting that disruption of Pr80env structure prevents intracellular transport and processing. To analyze the functional domains of the SU portion of the Env protein, we assembled several chimeric constructs. In these constructs, portions of the ecotropic Mo-MuLV envelope gene were replaced with corresponding sequences from the 4070A amphotropic MuLV envelope. Using a retroviral vector pseudotyping assay, 5 of 12 chimeric envelope proteins were shown to be biologically active. Host range was determined by retroviral vector transduction of the appropriate cell, by viral interference studies, and by the productive infection of Chinese hamster ovary cells expressing the murine ecotropic receptor. These results permit assignment of the amino acids responsible for host range determination. Ecotropic host range is determined by the first 88 amino acids of the Mo-MuLV SU, while the amphotropic host range-determining region spans the first 157 amino acids of the 4070A SU.

3T3 Cells↗
PubMed2004

Baculovirus late expression factors.

Autographa californica nuclear polyhedrosis virus, or AcMNPV, is the type member of the baculoviruses, a family of double-stranded DNA viruses with large circular genomes. The successive and concomitant expression of an assortment of early, late and very late genes is instrumental for successful baculovirus infection, and requires a switch from early dependence on a host cell-derived polymerase II to a novel virus-encoded RNA polymerase that is required for transcription later on in infection. A series of repetitive and highly conserved sequences known as homologous regions, or hrs, function both as origins of DNA replication as well as transcriptional enhancers of late gene expression. An array of AcMNPV genes produced early on in infection, known as late expression factors, or LEFs, are essential for both replication and late gene expression. In this review, an overview of baculovirus LEFs and their roles in viral replication and late gene expression is presented. The role of LEFs in determining baculovirus host range is described. Finally, we compare baculovirus replication and transcription machinery with other viral systems.

Baculoviridae↗
PubMed1992

Viruses and the blood.

Haematological syndromes attributed to viruses demonstrate geographical variations in incidence and great dependence on host factors. Severe haematological disease is the exception rather than the rule in dengue virus infection, and probably depends at least in part on the host immune response to the virus. The increased incidence of hepatitis-associated aplasia in east Asia may reflect distribution of an infectious agent, an environmental toxin, or genetic predisposition, but probably represents some combination of these factors. Agents with apparently universal distribution, such as parvovirus B19 and Epstein-Barr virus, are associated with bone marrow failure only in a very narrow range of hosts. These examples teach us that viral causes cannot automatically be excluded from the differential diagnosis of syndromes whose occurrence is rare or apparently sporadic. Further investigation of these syndromes should include more detailed characterization of host factors, particularly immunological characteristics, and possible infectious and toxic cofactors which are associated with morbidity.

Bone Marrow↗
PubMed1999

Viral vector targeting.

The field of viral vector targeting is advancing rapidly. Recent advances include the successful use of bifunctional crosslinkers to target adenoviral and retroviral vectors, elucidation of the crystal structures of an adenoviral and a retroviral receptor-binding domain, and definition of strategies for inserting short targeting peptides and larger polypeptide-binding domains into the coat proteins of a number of different viral vectors. Novel targeting strategies based on host range restriction and protease activation have been developed, targeted replication-competent vectors have shown promise as anti-cancer agents and the possibility of selecting targeted vectors from vector display libraries has been established.

Animals↗
PubMed2003

Citrus leprosis virus vectored by Brevipalpus phoenicis (Acari: Tenuipalpidae) on citrus in Brazil.

Citrus leprosis is caused by Citrus leprosis virus (CiLV) that is transmitted by mites in the genus Brevipalpus (Acari: Tenuipalpidae). This disease directly reduces production and the life span of the citrus plant. The main symptoms of the disease include lesions on fruits, leaves, and twigs or small branches, causing premature fruit drop, defoliation, and death of the twigs or branches leading to serious tree decline. Leprosis is a highly destructive disease of citrus, wherever it occurs. The Brazilian citrus industry spends over 100 million US dollars annually on acaricides to control the vector, Brevipalpus phoenicis (Geijskes). This review contains information about the history of the etiology of citrus leprosis, its geographical distribution, host range, the role of the mite vectors, viral morphology and relationships with the infected cell, and transmissibility of the virus by the mite. In addition, data on the mite-virus-plant relationship, disease damage, and strategies for controlling disease spread are presented.

Animals↗
PubMed1988

Safe and efficient generation of recombinant retroviruses with amphotropic and ecotropic host ranges.

We have constructed a set of packaging cell lines useful for the generation of helper-free recombinant retroviruses with amphotropic and ecotropic host ranges. To eliminate the problems of transfer of packaging functions and helper virus formation encountered with the previously available packaging systems, two mutant Moloney murine leukemia virus-derived proviral genomes carrying complementary mutations in the gag-pol or env regions were sequentially introduced into NIH 3T3 cells by cotransformation. Both genomes contained a deletion of the psi sequence necessary for the efficient encapsidation of retroviral genomes into virus particles and additional alterations at the 3' end of the provirus. We show that the resulting packaging cell lines psi CRIP and psi CRE can be used to isolate clones that stably produce high titers (10(6) colony-forming units/ml) of recombinant retroviruses with amphotropic and ecotropic host ranges, respectively. More importantly, we demonstrate that viral producers derived from the packaging cell lines do not transfer the packaging functions, or yield helper virus, even under conditions where existing packaging cell lines can be shown to yield transfer of packaging functions and/or helper virus. These properties of the psi CRIP and psi CRE packaging lines make them particularly valuable reagents for in vivo gene transfer studies aimed at cell lineage analysis and the development of human gene replacement therapies.

Animals↗
PubMed1993

Molecular determinants of the virulence and infectivity of California serogroup bunyaviruses.

California bunyaviruses cause encephalitis in mammalian hosts after peripheral infection. The virulence of these viruses is determined by their ability to replicate sequentially in striated muscle, cause viremia, and invade and replicate in the central nervous system. These viruses are also able to infect vector mosquitoes following ingestion of a blood meal containing virus. Bunyaviruses are negative stranded RNA viruses with a trisegmented genome, and the large, medium, and small RNA segments encode the polymerase, the glycoproteins, and the nucleoprotein, respectively. Reassortants between virulent and avirulent virus clones have been used to map virulence determinants in mice as well as determinants of infectivity in mosquitoes. Attenuation in mice and infectivity in mosquitoes of some virus clones maps to the medium RNA segment, implying that the virus glycoproteins, which are involved in virus entry, play a role in virulence. Attenuation in mice and mosquito infectivity of other clones maps to the large RNA segment, suggesting that cell-specific differences in the function of the viral polymerase can also determine virulence and host range.

Animals↗
PubMed1996

Expression of chimeric envelope proteins in helper cell lines and integration into Moloney murine leukemia virus particles.

New retroviral constructs with a grafted specificity of infection could become useful gene delivery vehicles with applications in systemic gene therapy. We have constructed retroviral vectors to target gene transfer to human tumor cells. Chimeric envelope proteins have been expressed to obtain viral particles with a defined specificity of infection. Two tumor cell-specific recognition domains were cloned and fused with the viral envelope gene. A recognition domain specific for ErbB-2 expressing tumor cells was derived from a monoclonal antibody directed against the ErbB-2 receptor in the form of a single chain antibody domain (scFv-erbB-2). The receptor binding domain was derived from the heregulin gene (HRG70). This domain provides recognition specificity for ErbB-3 and ErbB-4 receptor expressing tumor cells. The recognition domains were inserted at the amino terminal end into the MoMLV envelope gene. Helper cell lines were established which express the recombinant envelope protein genes, the gag and pol genes and packageable retroviral RNA. The analysis of the helper cell line revealed that the recombinant ErbB-2 scFv-envelope protein was expressed, but not incorporated into viral particles. The scFv-erbB-2 envelope protein was not inserted into the cell membrane and the assembly of retroviral particles was not completed. In contrast, the HRG70-envelope protein was expressed on the surface of the helper cells and incorporated into retroviral particles. The HRG70-envelope protein, however, did not alter the host range of infection. Only cells expressing the ecotropic viral receptor could be infected.

3T3 Cells↗