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At least 289 records · Page 16Linked to original sources
PubMed2005

Pleiotropic costs of niche expansion in the RNA bacteriophage phi 6.

Natural and experimental systems have failed to universally demonstrate a trade-off between generalism and specialism. When a trade-off does occur it is difficult to attribute its cause to antagonistic pleiotropy without dissecting the genetic basis of adaptation, and few previous experiments provide these genetic data. Here we investigate the evolution of expanded host range (generalism) in the RNA virus phi6, an experimental model system allowing adaptive mutations to be readily identified. We isolated 10 spontaneous host range mutants on each of three novel Pseudomonas hosts and determined whether these mutations imposed fitness costs on the standard laboratory host. Sequencing revealed that each mutant had one of nine nonsynonymous mutations in the phi6 gene P3, important in host attachment. Seven of these nine mutations were costly on the original host, confirming the existence of antagonistic pleiotropy. In addition to this genetically imposed cost, we identified an epigenetic cost of generalism that occurs when phage transition between host types. Our results confirm the existence in phi6 of two costs of generalism, genetic and environmental, but they also indicate that the cost is not always large. The possibility for cost-free niche expansion implies that varied ecological conditions may favor host shifts in RNA viruses.

Adaptation, Physiological↗
PubMedDate not supplied

[An analysis of the possible routes of viral macroevolution].

A complex analysis of virus groups was carried out in order to find out possible ways of their macroevolution. The analysis was based on the detection of similar groups of viruses which could be considered to be evolutionally close. The similarity was evaluated both by a complex of virus properties (physicochemical, morphological, etc.) and using systemic analysis of means of genetic information transmission (MGIT) describing the features of replication and transmission properties. The developed systemic approach using the analysis of the MGIT system and integral differences between viruses by the totality of their properties helped to form models of virus evolution taking into account, in particular, their mono- or polyphyletic origin, more definite knowledge on pravirus(es) MGIT, etc. A monophyletic model of macroevolution of viruses was constructed.

Biological Evolution↗
PubMed2006

Phylogeny and evolution of old world arenaviruses.

The intention of this study was to investigate the genomics, phylogeny and evolution of the Old World arenaviruses based on sequence data representing the four viral genes. To achieve this aim, we sequenced the complete S and L RNA segments of Ippy virus (IPPYV), Mobala virus (MOBV) and Mopeia virus (MOPV). Full-length sequences of the NP, GPC, Z and L genes were used to reconstruct phylogenetic relationships and to compare resulting tree topologies. Each of the five Old World arenavirus species (namely Lassa virus [LASV], IPPYV, MOBV, MOPV and Lymphocytic choriomeningitis virus [LCMV]) are monophyletic; seven selected strains of LASV showed a similar topology regardless of the gene under analysis; IPPYV rooted the three other African arenaviruses; the four African arenaviruses are rooted by the ubiquitous LCMV; and the tree topologies of the three African arenaviruses other than LASV are identical regardless of the gene used for analysis. No evidence for significant evolutionary events such as intra- or intersegmental recombination was obtained.

Arenaviruses, Old World↗
PubMed1984

Properties of defective interfering particles of Sindbis virus generated in vertebrate and mosquito cells.

Defective interfering (DI) particles of Sindbis virus were generated during serial, undiluted passage of a cloned virus stock in both chick embryo fibroblast (CEF) cells and Aedes albopictus mosquito cells. DI particle-containing stocks were identified by their ability to interfere with standard virus replication and to synthesize small DI RNA species in the cell type in which they were generated. DI RNA species generated during serial passage in CEF cells were able to replicate in both vertebrate and A. albopictus cells. Some of the DI RNA species generated during serial passage in A. albopictus cells replicated efficiently in both cell types while others, sometimes present in the same DI particle stock, failed to replicate in cells of vertebrate origin. These results suggest that evolution of DI RNA species during serial passage of Sindbis virus in mosquito cells may result in the loss or alteration of nucleotide sequences required for RNA synthesis in vertebrate cells.

Aedes↗
PubMed1999

Molecular mechanisms of coxsackievirus persistence in chronic inflammatory myopathy: viral RNA persists through formation of a double-stranded complex without associated genomic mutations or evolution.

Enterovirus infection and persistence have been implicated in the pathogenesis of certain chronic muscle diseases. In vitro studies suggest that persistent enteroviruses mutate, evolving into forms that are less lytic and display altered tropism, but it is less clear whether these mechanisms operate in vivo. In this study, persistent coxsackievirus RNA from the muscle of mice afflicted with chronic inflammatory myopathy (CIM) was characterized and compared with RNA from a virus that had established a persistent infection of G8 mouse myoblasts for 30 passages in vitro. Competitive strand-specific reverse transcription-PCR and susceptibility to RNase I treatment revealed that plus- and minus-strand viral RNAs were present at nearly equivalent levels in muscle and that they persisted in a double-stranded conformation. All regions of the viral genome persisted and were amplified as a series of seven overlapping fragments. Restriction endonuclease fingerprinting coupled with sequencing indicated that there was no evolution of the viral genome associated with its persistence in muscle. This contrasted with the productive persistent infection that was established in myoblast cultures, where plus-strand RNA predominated and persistent virus developed distinct mutations. In vitro persistence proceeded by a carrier culture mechanism and was completely dependent on production of infectious virus, since persistent viral RNA was not detected in cultures subjected to antibody-mediated curing. These experiments demonstrate that persistence of coxsackievirus RNA in muscle is not facilitated by distinct genetic changes in the virus that give rise to replication-defective forms but occurs primarily through production of stable double-stranded RNA that is produced as the acute viral infection resolves. The data suggest a mechanism for coxsackievirus persistence in myofibers and perhaps other nondividing cells whereby cells that survive infection could harbor persistent viral RNA for extended times without producing detectable levels of infectious virus.

Animals↗
PubMed2005

Impact of human immunodeficiency virus type 1 (HIV-1) genetic diversity on performance of four commercial viral load assays: LCx HIV RNA Quantitative, AMPLICOR HIV-1 MONITOR v1.5, VERSANT HIV-1 RNA 3.0, and NucliSens HIV-1 QT.

Human immunodeficiency virus type 1 (HIV-1) evolution and changing strain distribution present a challenge to nucleic acid-based assays. Reliable patient monitoring of viral loads requires the detection and accurate quantification of genetically diverse HIV-1. A panel of 97 HIV-1-seropositive plasma samples collected from Cameroon, Brazil, and South Africa was used to compare the performance of four commercially available HIV RNA quantitative tests: Abbott LCx HIV RNA Quantitative assay (LCx), Bayer Versant HIV-1 RNA 3.0 (bDNA), Roche AMPLICOR HIV-1 MONITOR v1.5 (Monitor v1.5), and bioMérieux NucliSens HIV-1 QT (NucliSens). The panel included group M, group O, and recombinant viruses based on sequence analysis of gag p24, pol integrase, and env gp41. The LCx HIV assay quantified viral RNA in 97 (100%) of the samples. In comparison, bDNA, Monitor v1.5, and NucliSens quantified viral RNA in 96.9%, 94.8%, and 88.6% of the samples, respectively. The two group O specimens were quantified only by the LCx HIV assay. Analysis of nucleotide mismatches at the primer/probe binding sites for Monitor v1.5, NucliSens, and LCx assays revealed that performance characteristics reflected differences in the level of genetic conservation within the target regions.

Genetic Variation↗
PubMed1987

The evolution of multicompartmental genomes in viruses.

The genetic information of many viruses is divided between separately encapsidated nucleic acid molecules. A simple evolutionary model is constructed to explain this phenomenon. All multicompartmental viruses infect plants, and most are RNA viruses. The former fact may be due to the high transmission multiplicities enjoyed by plant viruses. The latter may be due to the low replication fidelity of RNA, although another explanation is also offered. The logic of the analysis is contrasted with that of previous explanations. In particular, this paper proceeds from a "selfish DNA" viewpoint. It is not necessary to suppose that the division of the genome fills any adaptive function for the virus. The theory makes testable predictions about the parameters of multicompartmental viruses.

Biological Evolution↗
PubMed2002

Evolutionary history of Cucumber mosaic virus deduced by phylogenetic analyses.

Cucumber mosaic virus (CMV) is an RNA plant virus with a tripartite genome and an extremely broad host range. Previous evolutionary analyses with the coat protein (CP) and 5' nontranslated region (NTR) of RNA 3 suggested subdivision of the virus into three groups, subgroups IA, IB, and II. In this study 15 strains of CMV whose nucleotide sequences have been determined were used for a complete phylogenetic analysis of the virus. The trees estimated for open reading frames (ORFs) located on the different RNAs were not congruent and did not completely support the subgrouping indicated by the CP ORF, indicating that different RNAs had independent evolutionary histories. This is consistent with a reassortment mechanism playing an important role in the evolution of the virus. The evolutionary trees of the 1a and 3a ORFs were more compact and displayed more branching than did those of the 2a and CP ORFs. This may reflect more rigid host-interactive constraints exerted on the 1a and 3a ORFs. In addition, analysis of the 3' NTR that is conserved among all RNAs indicated that evolutionary constraints on this region are specific to the RNA component rather than the virus isolate. This indicates that functions other than replication are encoded in the 3' NTR. Reassortment may have led to the genetic diversity found among CMV strains and contributed to its enormous evolutionary success.

3' Untranslated Regions↗
PubMed2001

Molecular evolution of Puumala hantavirus.

Puumala virus (PUUV) is a negative-stranded RNA virus in the genus Hantavirus, family Bunyaviridae. In this study, detailed phylogenetic analysis was performed on 42 complete S segment sequences of PUUV originated from several European countries, Russia, and Japan, the largest set available thus far for hantaviruses. The results show that PUUV sequences form seven distinct and well-supported genetic lineages; within these lineages, geographical clustering of genetic variants is observed. The overall phylogeny of PUUV is star-like, suggesting an early split of genetic lineages. The individual PUUV lineages appear to be independent, with the only exception to this being the Finnish and the Russian lineages that are closely connected to each other. Two strains of PUUV-like virus from Japan form the most ancestral lineage diverging from PUUV. Recombination points within the S segment were searched for and evidence for intralineage recombination events was seen in the Finnish, Russian, Danish, and Belgian lineages of PUUV. Molecular clock analysis showed that PUUV is a stable virus, evolving slowly at a rate of 0.7 x 10(-7) to 2.2 x 10(-6) nt substitutions per site per year.

Evolution, Molecular↗
PubMed1997

Evolution of mouse hepatitis virus: detection and characterization of spike deletion variants during persistent infection.

High-frequency RNA recombination has been proposed as an important mechanism for generating viral deletion variants of murine coronavirus. Indeed, a number of variants with deletions in the spike glycoprotein have been isolated from persistently infected animals. However, the significance of generating and potentially accumulating deletion variants in the persisting viral RNA population is unclear. To study this issue, we evaluated the evolution of spike variants by examining the population of spike RNA sequences detected in the brains and spinal cords of mice inoculated with coronavirus and sacrificed at 4, 42, or 100 days postinoculation. We focused on the S1 hypervariable region since previous investigators had shown that this region is subject to recombination and deletion. RNA isolated from the brains or spinal cords of infected mice was rescued by reverse transcription-PCR, and the amplified products were cloned and used in differential colony hybridizations to identify individual isolates with deletions. We found that 11 of 20 persistently infected mice harbored spike deletion variants (SDVs), indicating that deletions are common but not required for persistent infection. To determine if a specific type of SDV accumulated during persistence, we sequenced 106 of the deletion isolates. We identified 23 distinct patterns of SDVs, including 5 double-deletion variants. Furthermore, we found that each mouse harbored distinct variants in its central nervous system (CNS), suggesting that SDVs are generated during viral replication in the CNS. Interestingly, mice with the most severe and persisting neurological disease harbored the most prevalent and diverse quasispecies of SDVs. Overall, these findings illustrate the complexity of the population of persisting viral RNAs which may contribute to chronic disease.

Animals↗
PubMed1995

Using in vitro selection to direct the covalent attachment of human immunodeficiency virus type 1 Rev protein to high-affinity RNA ligands.

We have used an in vitro selection procedure called crosslinking SELEX (SELEX = systematic evolution of ligands by exponential enrichment) to identify RNA sequences that bind with high affinity and crosslink to the Rev protein from human immunodeficiency virus type 1 (HIV-1). A randomized RNA library substituted with the photoreactive chromophore 5-iodouracil was irradiated with monochromatic UV light in the presence of Rev. Those sequences with the ability to photocrosslink to Rev were partitioned from the rest of the RNA pool, amplified, and used for the next round of selection. Rounds of photocrosslinking selection were alternated with rounds of selection for RNA sequences with high affinity to Rev. This iterative, dual-selection method yielded RNA molecules with subnanomolar dissociation constants and high efficiency photocrosslinking to Rev. Some of the RNA molecules isolated by this procedure form a stable complex with Rev that is resistant to denaturing gel electrophoresis in the absence of UV irradiation. In vitro selection of nucleic acids by using modified nucleotides allows the isolation of nucleic acid molecules with potentially limitless chemical capacities to covalently attack a target molecule.

Base Sequence↗
PubMed1992

Genetic evolution and tropism of transmissible gastroenteritis coronaviruses.

Transmissible gastroenteritis virus (TGEV) is an enteropathogenic coronavirus isolated for the first time in 1946. Nonenteropathogenic porcine respiratory coronaviruses (PRCVs) have been derived from TGEV. The genetic relationship among six European PRCVs and five coronaviruses of the TGEV antigenic cluster has been determined based on their RNA sequences. The S protein of six PRCVs have an identical deletion of 224 amino acids starting at position 21. The deleted area includes the antigenic sites C and B of TGEV S glycoprotein. Interestingly, two viruses (NEB72 and TOY56) with respiratory tropism have S proteins with a size similar to the enteric viruses. NEB72 and TOY56 viruses have in the S protein 2 and 15 specific amino acid differences with the enteric viruses. Four of the residues changed (aa 219 of NEB72 isolate and aa 92, 94, and 218 of TOY56) are located within the deletion present in the PRCVs and may be involved in the receptor binding site (RBS) conferring enteric tropism to TGEVs. A second RBS used by the virus to infect ST cells might be located in a conserved area between sites A and D of the S glycoprotein, since monoclonal antibodies specific for these sites inhibit the binding of the virus to ST cells. An evolutionary tree relating 13 enteric and respiratory isolates has been proposed. According to this tree, a main virus lineage evolved from a recent progenitor virus which was circulating around 1941. From this, secondary lineages originated PUR46, NEB72, TOY56, MIL65, BR170, and the PRCVs, in this order. Least squares estimation of the origin of TGEV-related coronaviruses showed a significant constancy in the fixation of mutations with time, that is, the existence of a well-defined molecular clock. A mutation fixation rate of 7 +/- 2 x 10(-4) nucleotide substitutions per site and per year was calculated for TGEV-related viruses. This rate falls in the range reported for other RNA viruses. Point mutations and probably recombination events have occurred during TGEV evolution.

Amino Acid Sequence↗