On the origin of RNA tumor viruses.
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Bacteriophages↗
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Nidovirales: evolving the largest RNA virus genome.
This review focuses on the monophyletic group of animal RNA viruses united in the order Nidovirales. The order includes the distantly related coronaviruses, toroviruses, and roniviruses, which possess the largest known RNA genomes (from 26 to 32kb) and will therefore be called "large" nidoviruses in this review. They are compared with their arterivirus cousins, which also belong to the Nidovirales despite having a much smaller genome (13-16kb). Common and unique features that have been identified for either large or all nidoviruses are outlined. These include the nidovirus genetic plan and genome diversity, the composition of the replicase machinery and virus particles, virus-specific accessory genes, the mechanisms of RNA and protein synthesis, and the origin and evolution of nidoviruses with small and large genomes. Nidoviruses employ single-stranded, polycistronic RNA genomes of positive polarity that direct the synthesis of the subunits of the replicative complex, including the RNA-dependent RNA polymerase and helicase. Replicase gene expression is under the principal control of a ribosomal frameshifting signal and a chymotrypsin-like protease, which is assisted by one or more papain-like proteases. A nested set of subgenomic RNAs is synthesized to express the 3'-proximal ORFs that encode most conserved structural proteins and, in some large nidoviruses, also diverse accessory proteins that may promote virus adaptation to specific hosts. The replicase machinery includes a set of RNA-processing enzymes some of which are unique for either all or large nidoviruses. The acquisition of these enzymes may have improved the low fidelity of RNA replication to allow genome expansion and give rise to the ancestors of small and, subsequently, large nidoviruses.
Evolution, Molecular↗
[Evolution of RNA-dependent RNA polymerases of positive riboviruses].
A comparative analysis is presented of 24 known amino acid sequences of RNA-dependent RNA polymerases of positive strand RNA viruses infecting animals, plants and bacteria. Using a newly proposed methodology of group alignment for weakly similar sequences, evolutionary conserved fragments of all these proteins were unambiguously aligned. A unique pattern (consensus) of 7 invariant amino acid residues was revealed which is absent from the sequences of other RNA and DNA polymerases and is thought to unequivocally identify the RNA-dependent RNA polymerases of positive strand RNA viruses. Based on the obtained alignment a tentative phylogenetic tree of viral RNA polymerases was constructed for the first time. The RNA-dependent RNA polymerases of positive strand RNA viruses are concluded to comprise a distinct family of evolutionary related proteins.
Amino Acid Sequence↗
The extent of codon usage bias in human RNA viruses and its evolutionary origin.
Revealing the determinants of codon usage bias is central to the understanding of factors governing viral evolution. Herein, we report the results of a survey of codon usage bias in a wide range of genetically and ecologically diverse human RNA viruses. This analysis showed that the overall extent of codon usage bias in RNA viruses is low and that there is little variation in bias between genes. Furthermore, the strong correlation between base and dinucleotide composition and codon usage bias suggested that mutation pressure rather than natural (translational) selection is the most important determinant of the codon bias observed. However, we also detected correlations between codon usage bias and some characteristics of viral genome structure and ecology, with increased bias in segmented and aerosol-transmitted viruses and decreased bias in vector-borne viruses. This suggests that translational selection may also have some influence in shaping codon usage bias.
Base Composition↗
RNA tumor virus genes and the transforming genes: genetic transmission, infectious spread, and modes of expression.
The genetic conservation and evolution of virogenes in mammalian species are described in relation to the horizontal, vertical, and congenital transmission of type C RNA oncogenic viruses within members of a given species, or among members of near and/or distantly related species. Examples of oncogenic virus infection between ancestors of the mouse, cat, pig, and primates as well as the integration of the virus into the host's genome are documented. The possible normal functions of the virogenes as a part of the cellular genome of many species are explored. Recent evidence of genetic recombination (genetic mixing) among distinct type C viruses is also reviewed, thus completing an overview of the evolutionary past, present, and complex future relationships of oncogenic RNA viruses and mammalian species.
Animals↗
Secondary structure as a constraint on the evolution of a plant viral satellite RNA.
The genetic variability and evolution of the satellite RNA (satRNA) of cucumber mosaic virus (CMV) was analyzed. Twenty-five CMV-satRNAs compared clustered into three main groups, and no correlation was found between genetic proximity and other characteristics (pathogenicity, geographical origin) of the satRNAs. Values for the number of nucleotide substitutions per site between any two satRNAs suggest that divergence is checked by functional constraints. The analysis of mutations relative to an ancestral sequence, and the number of substitutions per site at first, second and third positions of codons in putative open reading frames, show that the variation of CMV-satRNAs does not follow a pattern typical of coding sequences, and indicates that preservation of the sequence of encoded products is not a constraint to evolution. On the other hand, when the observed variation was analyzed relative to a secondary structure model proposed for CMV-satRNAs, several lines of evidence indicated that the maintenance of the secondary structure is a constraint to evolution: the number of substitutions per site, the number of point insertions and deletions and the number of base substitutions that would disrupt base-pairing were significantly higher for unpaired than for base-paired positions. Also, compensatory mutations at base-paired positions occurred more frequently than expected from random. The results suggest that CMV-satRNAs are non-coding, functional RNAs whose biology would be determined by their direct interaction with components of the host and/or the helper virus.
Base Composition↗
Epistasis and its relationship to canalization in the RNA virus phi 6.
Although deleterious mutations are believed to play a critical role in evolution, assessing their realized effect has been difficult. A key parameter governing the effect of deleterious mutations is the nature of epistasis, the interaction between the mutations. RNA viruses should provide one of the best systems for investigating the nature of epistasis because the high mutation rate allows a thorough investigation of mutational effects and interactions. Nonetheless, previous investigations of RNA viruses by S. Crotty and co-workers and by S. F. Elena have been unable to detect a significant effect of epistasis. Here we provide evidence that positive epistasis is characteristic of deleterious mutations in the RNA bacteriophage phi 6. We estimated the effects of deleterious mutations by performing mutation-accumulation experiments on five viral genotypes of decreasing fitness. We inferred positive epistasis because viral genotypes with low fitness were found to be less sensitive to deleterious mutations. We further examined environmental sensitivity in these genotypes and found that low-fitness genotypes were also less sensitive to environmental perturbations. Our results suggest that even random mutations impact the degree of canalization, the buffering of a phenotype against genetic and environmental perturbations. In addition, our results suggest that genetic and environmental canalization have the same developmental basis and finally that an understanding of the nature of epistasis may first require an understanding of the nature of canalization.
Bacteriophage phi 6↗
What does the molecular structure of viruses tell us about viral functions?
The structures of the protein shell of a number of simple icosahedral RNA plant and animal viruses are now known at atomic resolution. In addition, components of viral capsids such as the haemagglutinin and neuraminidase spikes of influenza virus and the hexon unit of adenovirus are known in similar detail. These structures have provided a wealth of information on viral assembly, viral disassembly, the antigenic surface on viruses available to neutralizing antibodies, the host cell receptor attachment site, fusion of viral particles with the host cell, processing of polyproteins during maturation and the manner in which antiviral agents can interfere with the function of a viral capsid.
Antibodies, Viral↗
Conserved and non-conserved regions in the Sendai virus genome: evolution of a gene possessing overlapping reading frames.
We have sequenced the entire genome of a virulent field isolate of Sendai virus, the Hamamatsu strain, and compared the sequence with that of a distant related strain, the Z strain. Calculation of synonymous and non-synonymous (amino acid changing) nucleotide substitutions revealed regions where changes were permissive and non-permissive, and the experimentally determined functional region were found to be conserved, showing that important regions for function were conserved during evolution. In the cistron-overlapping regions in the P gene, one reading frame was conserved, whereas the other overlapping frame was flexible. The priority of one frame could be a strategy for evolution of an overlapping gene of RNA viruses. We found that the carboxyl two thirds of the C protein was conserved over the amino-terminal one third, possessing priority to the overlapping P polypeptide. This suggests that the carboxyl two thirds of the C protein have a functional importance. We also found a highly variable region between the L coding frame and the 5' trailer sequence. The relevance of these findings to actual viral replication should be clarified in the future.
Base Sequence↗
Screening of the yeast yTHC collection identifies essential host factors affecting tombusvirus RNA recombination.
RNA recombination is a major process in promoting rapid virus evolution in an infected host. A previous genome-wide screen with the yeast single-gene deletion library of 4,848 strains, representing approximately 80% of all genes of yeast, led to the identification of 11 host genes affecting RNA recombination in Tomato bushy stunt virus (TBSV), a small model plant virus (E. Serviene, N. Shapka, C. P. Cheng, T. Panavas, B. Phuangrat, J. Baker, and P. D. Nagy, Proc. Natl. Acad. Sci. USA 102:10545-10550, 2005). To further test the role of host genes in viral RNA recombination, in this paper, we extended the screening to 800 essential yeast genes present in the yeast Tet-promoters Hughes Collection (yTHC). In total, we identified 16 new host genes that either increased or decreased the ratio of TBSV recombinants to the nonrecombined TBSV RNA. The identified essential yeast genes are involved in RNA transcription/metabolism, in protein metabolism/transport, or unknown cellular processes. Detailed analysis of the effect of the identified yeast genes revealed that they might affect RNA recombination by altering (i) the ratio of the two viral replication proteins, (ii) the stability of the viral RNA, and/or (iii) the replicability of the recombinant RNAs. Overall, this and previous works firmly establish that a set of essential and nonessential host genes could affect TBSV recombination and evolution.
Base Sequence↗
Structure and function of the C-terminal domain of the polymerase cofactor of rabies virus.
The phosphoprotein (P) of rabies virus binds the viral polymerase to the nucleoprotein (N)-RNA template for transcription and replication. By limited protease digestion we defined a monomeric C-terminal domain of P that can bind to N-RNA. The atomic structure of this domain was determined and previously described mutations that interfere with binding of P to N-RNA could now be interpreted. There appears to be two features involved in this activity situated at opposite surfaces of the molecule: a positively charged patch and a hydrophobic pocket with an exposed tryptophan side-chain. Other previously published work suggests a conformational change in P when it binds to N-RNA, which may imply the repositioning of two helices that would expose a hydrophobic groove for interaction with N. This domain of rabies virus P is structurally unrelated to the N-RNA binding domains of the phosphoproteins of Sendai and measles virus that are members of the same order of viruses, the non-segmented negative strand RNA viruses. The implications of this finding for the evolution of this virus group are discussed.
Amino Acid Sequence↗
A cellular homolog of hepatitis delta antigen: implications for viral replication and evolution.
Hepatitis delta virus (HDV) is a pathogenic human virus whose RNA genome and replication cycle resemble those of plant viroids. However, viroid genomes contain no open reading frames, whereas HDV RNA encodes a single protein, hepatitis delta antigen (HDAg), which is required for viral replication. A cellular gene whose product interacts with HDAg has now been identified, and this interaction was found to affect viral genomic replication in intact cells. DNA sequence analysis revealed that this protein, termed delta-interacting protein A (DIPA), is a cellular homolog of HDAg. These observations demonstrate that a host gene product can modulate HDV replication and suggest that HDV may have evolved from a primitive viroidlike RNA through capture of a cellular transcript.
Adaptor Proteins, Signal Transducing↗
What is a quasispecies?
The concept of the quasispecies as a society formed from a clone of an asexually reproducing organism is reviewed. A broad spectrum of mutants is generated that compete one with another. Eventually a steady state is formed where each mutant type is represented according to its fitness and its formation by mutation. This quasispecies has a defined wild type sequence, which is the weighted average of all genotypes present. The quasispecies concept has been shown to affect the pathway of evolution and has been studied on RNA viruses which have a particularly high mutation rate. They (and possibly the majority of other species) operate close to the error threshold that allows maximum exploration of sequence space while conserving the information content of the genotype. The consequences of the quasispecies concept for the new 'evolutionary technology' are discussed.
Base Sequence↗
Reduced fecundity is the cost of cheating in RNA virus phi6.
Co-infection by multiple viruses affords opportunities for the evolution of cheating strategies to use intracellular resources. Cheating may be costly, however, when viruses infect cells alone. We previously allowed the RNA bacteriophage phi6 to evolve for 250 generations in replicated environments allowing co-infection of Pseudomonas phaseolicola bacteria. Derived genotypes showed great capacity to compete during co-infection, but suffered reduced performance in solo infections. Thus, the evolved viruses appear to be cheaters that sacrifice between-host fitness for within-host fitness. It is unknown, however, which stage of the lytic growth cycle is linked to the cost of cheating. Here, we examine the cost through burst assays, where lytic infection can be separated into three discrete phases (analogous to phage life history): dispersal stage, latent period (juvenile stage), and burst (adult stage). We compared growth of a representative cheater and its ancestor in environments where the cost occurs. The cost of cheating was shown to be reduced fecundity, because cheaters feature a significantly smaller burst size (progeny produced per infected cell) when infecting on their own. Interestingly, latent period (average burst time) of the evolved virus was much longer than that of the ancestor, indicating the cost does not follow a life history trade-off between timing of reproduction and lifetime fecundity. Our data suggest that interference competition allows high fitness of derived cheaters in mixed infections, and we discuss preferential encapsidation as one possible mechanism.
Adaptation, Physiological↗
Identification of a major restriction in HIV-1 intersubtype recombination.
Genetic recombination increases diversity in HIV-1 populations, thereby allowing variants to escape from host immunity or antiviral therapies. In addition to the currently described nine subtypes of HIV-1, many of the circulating strains are intersubtype recombinants. In this study, we determined the recombination rate between two HIV-1 subtype C viruses and between a subtype B virus and a subtype C virus during a single round of virus replication. Although HIV-1 subtype C recombines at a high rate, similar to that of HIV-1 subtype B, the recombination rate between a subtype B virus and a subtype C virus is much lower than the intrasubtype recombination rate. A 3-nt sequence difference in the dimerization initiation signal (DIS) region between HIV-1 subtypes B and C accounts for most of the reduction of intersubtype recombination. By matching the DIS sequences, the B/C intersub-type recombination rate was elevated 4-fold; by introducing mismatches in the 3-nt sequences, the B/B intrasubtype recombination rate was reduced 4-fold. Further analyses showed that the intermolecular template-switching frequency was unaffected by the sequence identity of the DIS region. These results support the hypothesis that mismatched sequences in the DIS region alter the formation of heterozygous virions, thereby lowering the observable recombination rate. Here, we present the discovery of a major restriction in HIV-1 intersubtype recombination. These results have important implications for virus evolution, the mechanism of HIV-1 RNA packaging, high negative interference in recombination, and the generation of circulating intersubtype recombinants within the infected population.
Base Sequence↗
HIV and hepatitis delta virus: evolution takes different paths to relieve blocks in transcriptional elongation.
The elongation step of transcription by RNA polymerase II (RNAPII) is controlled both positively and negatively by over a dozen cellular proteins. Recent findings suggest that two distinct viruses, human immunodeficiency virus type 1 and hepatitis delta virus, encode proteins that facilitate viral replication and transcription by targeting the same cellular transcription elongation machinery.
Evolution, Molecular↗
RNA recombination in animal and plant viruses.
An increasing number of animal and plant viruses have been shown to undergo RNA-RNA recombination, which is defined as the exchange of genetic information between nonsegmented RNAs. Only some of these viruses have been shown to undergo recombination in experimental infection of tissue culture, animals, and plants. However, a survey of viral RNA structure and sequences suggests that many RNA viruses were derived form homologous or nonhomologous recombination between viruses or between viruses and cellular genes during natural viral evolution. The high frequency and widespread nature of RNA recombination indicate that this phenomenon plays a more significant role in the biology of RNA viruses than was previously recognized. Three types of RNA recombination are defined: homologous recombination; aberrant homologous recombination, which results in sequence duplication, insertion, or deletion during recombination; and nonhomologous (illegitimate) recombination, which does not involve sequence homology. RNA recombination has been shown to occur by a copy choice mechanism in some viruses. A model for this recombination mechanism is presented.
Base Sequence↗
Domains in viroids: evidence of intermolecular RNA rearrangements and their contribution to viroid evolution.
On the basis of sequence homology a model is proposed for five structural and functional domains in viroids. These domains include (i) a conserved central region capable of forming two alternative structures that may regulate two phases of the viroid replication cycle, (ii) a region associated with pathogenicity, (iii) a domain with high sequence variability, (iv and v) two terminal domains that are interchangeable between viroids. That the evolution of viroids has involved RNA rearrangements of domains is supported by the partial duplication of coconut cadang cadang viroid, which arises de novo during each infection. Similar RNA rearrangements have been established for animal viral defective interfering RNAs, which arise by some form of discontinuous transcription. This mechanism could account for the origin of viroids and also RNA viruses, whereby modules of genetic information may have undergone repeated exchange between RNA pathogens and the RNA of their hosts.
Base Sequence↗