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At least 181 records · Page 10Linked to original sources
PubMed1997

Evolution of human immunodeficiency virus subtype A in women seroconverting post partum and in their offspring post-natally infected by ingestion of breast milk.

The evolution of genomic RNA of human immunodeficiency virus type 1 (HIV-1), subtype A, was studied in three Rwandan mother-child pairs over a period of 12-30 months. In two pairs a homogeneous subtype A V3 sequence population was observed at seroconversion and the virus populations in the children resembled those in the mothers. One of these mother-child pairs was infected with an A/C recombinant virus (Ap17/Cp24). In the third pair, a heterogeneous V3 sequence population was observed in the maternal seroconversion sample but the V3 sequence population in the child's sample was homogeneous. In each individual the intra- and intersample variation (between the seroconversion and follow-up samples) increased over time in both the V3 region and p17gag. Independent evolution for 1-2 years did not abolish the epidemiological relationship between virus populations in mother and child.

Amino Acid Sequence↗
PubMed2006

Evolutionary influences in arboviral disease.

Arthropod-borne viruses (arboviruses) generally require horizontal transmission by arthropod vectors among vertebrate hosts for their natural maintenance. This requirement for alternate replication in disparate hosts places unusual evolutionary constraints on these viruses, which have probably limited the evolution of arboviruses to only a few families of RNA viruses (Togaviridae, Flaviviridae, Bunyaviridae, Rhabdoviridae, Reoviridae, and Orthomyxoviridae) and a single DNA virus. Phylogenetic studies have suggested the dominance of purifying selection in the evolution of arboviruses, consistent with constraints imposed by differing replication environments and requirements in arthropod and vertebrate hosts. Molecular genetic studies of alphaviruses and flaviviruses have also identified several mutations that effect differentially the replication in vertebrate and mosquito cells, consistent with the view that arboviruses must adopt compromise fitness characteristics for each host. More recently, evidence of positive selection has also been obtained from these studies. However, experimental model systems employing arthropod and vertebrate cell cultures have yielded conflicting conclusions on the effect of alternating host infections, with host specialization inconsistently resulting in fitness gains or losses in the bypassed host cells. Further studies using in vivo systems to study experimental arbovirus evolution are critical to understanding and predicting disease emergence, which often results from virus adaptation to new vectors or amplification hosts. Reverse genetic technologies that are now available for most arbovirus groups should be exploited to test assumptions and hypotheses derived from retrospective phylogenetic approaches.

Adaptation, Physiological↗
PubMed2005

The two ages of the RNA world, and the transition to the DNA world: a story of viruses and cells.

Most evolutionists agree to consider that our present RNA/DNA/protein world has originated from a simpler world in which RNA played both the role of catalyst and genetic material. Recent findings from structural studies and comparative genomics now allow to get a clearer picture of this transition. These data suggest that evolution occurred in several steps, first from an RNA to an RNA/protein world (defining two ages of the RNA world) and finally to the present world based on DNA. The DNA world itself probably originated in two steps, first the U-DNA world, following the invention of ribonucleotide reductase, and later on the T-DNA world, with the independent invention of at least two thymidylate synthases. Recently, several authors have suggested that evolution from the RNA world up to the Last Universal Cellular Ancestor (LUCA) could have occurred before the invention of cells. On the contrary, I argue here that evolution of the RNA world taken place in a framework of competing cells and viruses (preys, predators and symbionts). I focus on the RNA-to-DNA transition and expand my previous hypothesis that viruses played a critical role in the emergence of DNA. The hypothesis that DNA and associated mechanisms (replication, repair, recombination) first evolved and diversified in a world of DNA viruses infecting RNA cells readily explains the existence of viral-encoded DNA transaction proteins without cellular homologues. It also potentially explains puzzling observations from comparative genomic, such as the existence of two non-homologous DNA replication machineries in the cellular world. I suggest here a specific scenario for the transfer of DNA from viruses to cells and briefly explore the intriguing possibility that several independent transfers of this kind produced the two cell types (prokaryote/eukaryote) and the three cellular domains presently known (Archaea, Bacteria and Eukarya).

Archaea↗
PubMed1985

Rates of evolution of the retroviral oncogene of Moloney murine sarcoma virus and of its cellular homologues.

A method is proposed for computing the rates of nucleotide substitution for an oncogene of a retrovirus (v-onc), its cellular homologue (c-onc), and the retrovirus genome simultaneously. The method has been applied to DNA sequences of the v-mos gene of Moloney murine sarcoma virus (Mo-MuSV) and the c-mos and gag genes of Mo-MuSV and Moloney murine leukemia virus (Mo-MuLV). The rates of nucleotide substitution for c-mos, the gag gene, and v-mos are estimated to be 1.71 X 10(-9), 6.3 X 10(-4), and 1.31 X 10(-3) per site per year, respectively. The rate of evolution of c-mos is comparable to that of many functional genes in DNA genomes, suggesting some important biological function played by cellular oncogenes. The rates of nucleotide substitution in the v-mos and gag genes are very high and are similar to those of RNA viral genes such as the hemagglutinin and neuraminidase genes in the influenza A virus. Thus, oncogenes seem to exemplify a general feature of genome evolution: the rate of evolution of RNA genomes can be more than a million times greater than that of DNA genomes because of a high mutation rate in the RNA genome.

Animals↗
PubMed1998

Evolution of a quadripartite hybrid virus by interspecific exchange and recombination between replicase components of two related tripartite RNA viruses.

Cucumber mosaic virus (CMV) and tomato aspermy virus (TAV) belong to the Cucumovirus genus. They have a tripartite genome consisting of single-stranded RNAs, designated 1, 2, and 3. Previous studies have shown that viable pseudorecombinants could be created in vitro by reciprocal exchanges between CMV and TAV RNA 3, but exchanges of RNAs 1 and 2 were replication deficient. When we coinoculated CMV RNAs 2 and 3 along with TAV RNAs 1 and 2 onto Nicotiana benthamiana, a hybrid quadripartite virus appeared that consisted of TAV RNA 1, CMV RNAs 2 and 3, and a distinctive chimeric RNA originating from a recombination between CMV RNA 2 and the 3'-terminal 320 nucleotides of TAV RNA 2. This hybrid arose by means of segment reassortment and RNA recombination to produce an interspecific hybrid with the TAV helicase subunit and the CMV polymerase subunit. To our knowledge, this is the first report demonstrating the evolution of a new plant or animal virus strain containing an interspecific hybrid replicase complex.

Base Sequence↗
PubMedDate not supplied

[The time scale in poxvirus evolution].

Unlike vertebrates and RNA-containing viruses, the objective estimate of molecular clock for DNA-containing viruses was so far absent. An extended central conservative genomic region of orthopoxviruses (about 102 kbp) and the sequence of DNA polymerase gene (about 3 kbp) of the viruses belonging to various genera from the family Poxviridae were analyzed. During this analysis, the known dating of variola virus (VARV) transfer from West Africa to South America (XVI century) and our own data on close phylogenetic relations between the modem West African and South American VARV isolates were used. As a result of this work, it was calculated for the first time that the rate of mutation accumulation in these DNA-containing viruses amounted to 0.9-1.2 x 10(-6) substitutions per site per year. The poxviruses started separating from the ancestor virus to form the modem genera approximately 500 thousand years ago; the ancestor of the genus Orthopoxvirus separated about 300 thousand years ago; and its division into the modem studied species took place approximately 14 thousand years ago.

DNA, Viral↗
PubMed2006

The ancient Virus World and evolution of cells.

BACKGROUND: Recent advances in genomics of viruses and cellular life forms have greatly stimulated interest in the origins and evolution of viruses and, for the first time, offer an opportunity for a data-driven exploration of the deepest roots of viruses. Here we briefly review the current views of virus evolution and propose a new, coherent scenario that appears to be best compatible with comparative-genomic data and is naturally linked to models of cellular evolution that, from independent considerations, seem to be the most parsimonious among the existing ones. RESULTS: Several genes coding for key proteins involved in viral replication and morphogenesis as well as the major capsid protein of icosahedral virions are shared by many groups of RNA and DNA viruses but are missing in cellular life forms. On the basis of this key observation and the data on extensive genetic exchange between diverse viruses, we propose the concept of the ancient virus world. The virus world is construed as a distinct contingent of viral genes that continuously retained its identity throughout the entire history of life. Under this concept, the principal lineages of viruses and related selfish agents emerged from the primordial pool of primitive genetic elements, the ancestors of both cellular and viral genes. Thus, notwithstanding the numerous gene exchanges and acquisitions attributed to later stages of evolution, most, if not all, modern viruses and other selfish agents are inferred to descend from elements that belonged to the primordial genetic pool. In this pool, RNA viruses would evolve first, followed by retroid elements, and DNA viruses. The Virus World concept is predicated on a model of early evolution whereby emergence of substantial genetic diversity antedates the advent of full-fledged cells, allowing for extensive gene mixing at this early stage of evolution. We outline a scenario of the origin of the main classes of viruses in conjunction with a specific model of precellular evolution under which the primordial gene pool dwelled in a network of inorganic compartments. Somewhat paradoxically, under this scenario, we surmise that selfish genetic elements ancestral to viruses evolved prior to typical cells, to become intracellular parasites once bacteria and archaea arrived at the scene. Selection against excessively aggressive parasites that would kill off the host ensembles of genetic elements would lead to early evolution of temperate virus-like agents and primitive defense mechanisms, possibly, based on the RNA interference principle. The emergence of the eukaryotic cell is construed as the second melting pot of virus evolution from which the major groups of eukaryotic viruses originated as a result of extensive recombination of genes from various bacteriophages, archaeal viruses, plasmids, and the evolving eukaryotic genomes. Again, this vision is predicated on a specific model of the emergence of eukaryotic cell under which archaeo-bacterial symbiosis was the starting point of eukaryogenesis, a scenario that appears to be best compatible with the data. CONCLUSION: The existence of several genes that are central to virus replication and structure, are shared by a broad variety of viruses but are missing from cellular genomes (virus hallmark genes) suggests the model of an ancient virus world, a flow of virus-specific genes that went uninterrupted from the precellular stage of life's evolution to this day. This concept is tightly linked to two key conjectures on evolution of cells: existence of a complex, precellular, compartmentalized but extensively mixing and recombining pool of genes, and origin of the eukaryotic cell by archaeo-bacterial fusion. The virus world concept and these models of major transitions in the evolution of cells provide complementary pieces of an emerging coherent picture of life's history. REVIEWERS: W. Ford Doolittle, J. Peter Gogarten, and Arcady Mushegian.

Journal Article↗
PubMed2006

Evolution of virus-derived sequences for high-level replication of a subviral RNA.

Turnip crinkle virus (TCV) and its 356-nt satellite RNA satC share 151 nt of 3'-terminal sequence, which contain 8 positional differences and are predicted to fold into virtually identical structures, including a series of four phylogenetically inferred hairpins. SatC and TCV containing reciprocal exchanges of this region accumulate to only 15% or 1% of wild-type levels, respectively. Step-wise conversion of satC and TCV 3'-terminal sequences into the counterpart's sequence revealed the importance of having the cognate core promoter (Pr), which is composed of a single hairpin that differs in both sequence and stability, and an adjacent short 3'-terminal segment. The negative impact of the more stable TCV Pr on satC could not be attributed to lack of formation of a known tertiary interaction involving the 3'-terminal bases, nor an effect of coat protein, which binds specifically to TCV-like Pr and not the satC Pr. The satC Pr was a substantially better promoter than the TCV Pr when assayed in vitro using purified recombinant TCV RdRp, either in the context of satC or when assayed downstream of non-TCV-related sequence. Poor activity of the TCV Pr in vitro occurred despite solution structure probing indicating that its conformation in the context of satC is similar to the active form of the satC Pr, which is thought to form following a required conformational switch. These results suggest that evolution of satC following its initial formation generated a Pr that can function more efficiently in the absence of additional TCV sequence that may be required for full functionality of the TCV Pr.

Base Sequence↗
PubMed2006

Characterization of White bream virus reveals a novel genetic cluster of nidoviruses.

The order Nidovirales comprises viruses from the families Coronaviridae (genera Coronavirus and Torovirus), Roniviridae (genus Okavirus), and Arteriviridae (genus Arterivirus). In this study, we characterized White bream virus (WBV), a bacilliform plus-strand RNA virus isolated from fish. Analysis of the nucleotide sequence, organization, and expression of the 26.6-kb genome provided conclusive evidence for a phylogenetic relationship between WBV and nidoviruses. The polycistronic genome of WBV contains five open reading frames (ORFs), called ORF1a, -1b, -2, -3, and -4. In WBV-infected cells, three subgenomic RNAs expressing the structural proteins S, M, and N were identified. The subgenomic RNAs were revealed to share a 42-nucleotide, 5' leader sequence that is identical to the 5'-terminal genome sequence. The data suggest that a conserved nonanucleotide sequence, CA(G/A)CACUAC, located downstream of the leader and upstream of the structural protein genes acts as the core transcription-regulating sequence element in WBV. Like other nidoviruses with large genomes (>26 kb), WBV encodes in its ORF1b an extensive set of enzymes, including putative polymerase, helicase, ribose methyltransferase, exoribonuclease, and endoribonuclease activities. ORF1a encodes several membrane domains, a putative ADP-ribose 1"-phosphatase, and a chymotrypsin-like serine protease whose activity was established in this study. Comparative sequence analysis revealed that WBV represents a separate cluster of nidoviruses that significantly diverged from toroviruses and, even more, from coronaviruses, roniviruses, and arteriviruses. The study adds to the amazing diversity of nidoviruses and appeals for a more extensive characterization of nonmammalian nidoviruses to better understand the evolution of these largest known RNA viruses.

Coronaviridae↗
PubMed1992

Identification of the domains required for direct interaction of the helicase-like and polymerase-like RNA replication proteins of brome mosaic virus.

Brome mosaic virus is a positive-strand RNA virus whose RNA replication requires viral protein 1a, which has putative helicase and capping functions, and 2a, which has putative polymerase function. Since domains of related sequence are conserved in a wide range of plus-strand RNA viruses, analysis of 1a and 2a function should have applicability to many other viruses. We have recently demonstrated that 1a and 2a form a complex in vivo and in vitro. Using immune coprecipitation and mutant polypeptides made in reticulocyte lysates, we have now mapped both the 1a and 2a domains necessary for complex formation. The sequences needed to bind 2a map to the carboxy-terminal helicase-like domain of 1a. Truncated polypeptides containing this domain were able to bind to 2a, while several small insertions in the helicase-like domain disrupted binding. The sequence required for binding 1a lies within a 115-residue subset of the 2a N-terminal segment preceding the polymerase-like domain. Truncations or fusion polypeptides containing this segment can bind 1a. We also determined that highly purified 2a protein made in insect cells can form a complex with highly purified 1a helicase-like domain made in Escherichia coli, suggesting that no other factor is required to mediate 1a-2a interaction. Previous genetic analyses of 1a and 2a are consistent with this mapping and show that the newly defined 1a and 2a binding regions are required for RNA synthesis. The locations of these interacting regions are discussed with regard to models of viral replication and the evolution of positive-strand RNA virus genomes.

Base Sequence↗
PubMed1993

The fastest genome evolution ever described: HIV variation in situ.

Human immunodeficiency virus is an RNA virus in which the degree of genetic variation observed is phenomenal--up to 20% within an infected individual. This is essentially due to remorseless cycles of viral replication, most probably due to chronic activation of the immune system. It can be estimated that the number of variants in existence worldwide must be in excess of 10(14)-10(18), and given the nature of RNA viruses even more novel variants should emerge.

Biological Evolution↗
PubMed1994

Landscapes: complex optimization problems and biopolymer structures.

The evolution of RNA molecules in replication assays, viroids and RNA viruses can be viewed as an adaptation process on a 'fitness' landscape. The dynamics of evolution is hence tightly linked to the structure of the underlying landscape. Global features of landscapes can be described by statistical measures like number of optima, lengths of walks and correlation functions. The evolution of a quasispecies on such landscapes exhibits three dynamical regimes depending on the replication fidelity: Above the "localization threshold" the population is centered around a (local) optimum. Between localization and "dispersion threshold" the population is still centered around a consensus sequence, which, however, changes in time. For very large mutation rates the population spreads in sequence space like a gas. The critical mutation rates separating the three domains depend strongly on characteristics properties of the fitness landscapes. Statistical characteristics of RNA landscapes are accessible by mathematical analysis and computer calculations on the level of secondary structures: these RNA landscapes belong to the same class as well known optimization problems and simple spin glass models. The notion of a landscape is extended to combinatory maps, thereby allowing for a direct statistical investigation of the sequence structure relationships of RNA at the level of secondary structures. Frequencies of structures are highly non-uniform: we find relatively few common and many rare ones, as expressed by a generalized form of Zipf's law. Using an algorithm for inverse folding we show that sequences sharing the same structure are distributed randomly over sequence space. Together with calculations of structure correlations and a survey of neutral mutations this provides convincing evidence that RNA landscapes are as simple as they could possibly be for evolutionary adaptation: Any desired secondary structure can be found close to an arbitrary initial sequence and at the same time almost all bases can be substituted sequentially without ever changing the shape of the molecule. Consequences of these results for evolutionary optimization, the early stages of life, and molecular biotechnology are discussed.

Adaptation, Biological↗
PubMed2003

Levels of selection in positive-strand virus dynamics.

Conflicting selection pressures occurring over the life cycle of an organism constitute serious challenges to the robustness of replication. Viruses present a credible model system for analysing problems that arise through evolutionary conflicts of interest. We present a multi-level selection model for the life cycle of positive-strand RNA viruses. The model combines within-cell replication kinetics and protein synthesis, and between-cell population dynamics of virion production and transmission. We show how these two levels of within-host selection interact to produce tradeoffs in the life history strategy of a virus without consideration of host mortality. We find that viruses evolve towards intermediate rather than maximum encapsidation rates. This can be interpreted as selection for intermediate virulence through cellular persistence. We characterize a theoretical persistence threshold arising from the trade-off between genome replication and genetic translation within the cell. We present counter-intuitive relationships whereby increasing genome decay rates and rates of encapsidation lead to increases in the abundance of virus-encoded proteins. Data from poliovirus suggest that viruses might be unable to resolve the vertical conflicts of interests among different levels of selection.

Biological Evolution↗