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PubMed1995

Molecular evolution of viruses: an interim summary.

The origin and molecular evolution of viruses in this issue is dealt with at two levels: (1) tracing the past evolutionary pathways of viruses belonging to RNA virus families, retroviruses, and small and large DNA viruses; (2) tracing current changes in the RNA and DNA viral genomes that lead to the evolution of new virus mutants. In this interim summary, a time scale for the evolutionary processes is given, based on the accumulated published knowledge concerning the postulated origins of life on planet Earth, and the hypothesis that living cells with RNA genomes may have emerged (the "RNA world hypothesis") that then developed into cells with DNA genomes in eukaryotic and prokaryotic cells (1-3). The ideas about the evolution of RNA and DNA viruses from ancient cellular RNA and DNA molecules over a period of 3.5 billion years are discussed. It may be possible that by studying virus genes and molecular processes in virus-infected cells, and their involvement in the shaping of the genomes of bacteria, yeast, plants, insects, mammals, and humans, it will be possible to understand the importance of viruses in past evolution and to predict their possible impact on current and future evolutionary trends in biology.

DNA, Viral↗
PubMedDate not supplied

Evolution of coxsackie B virus during in vitro persistent infection: detection of protein mutations using two-dimensional polyacrylamide gel electrophoresis.

Serotype 5 coxsackie B virus (CBV5) can establish in vitro persistent infections in human rhabdomyosarcoma (RD) cells. This paper describes the characterisation of the virus released from the persistently infected RD cell line designated piRD-3673. Although infectious virus was released for 42 sequential passages of piRD-3673 cells, no gross virus-specific cytopathic effect was detected when the cells were examined by light microscopy. Two-dimensional polyacrylamide gel electrophoresis was used to compare the virus released from piRD-3673 cells with the CBV5 isolate (CBV-3673) used to initiate the persistent virus infection. Two of the virus intracellular proteins (apparent molecular weights 33,000 and 39,000, designated p33 and p39, respectively) increased in their net basic charge for the virus released from piRD-3673 cells compared to CBV-3673; a reduction in the apparent molecular weights of p33 and p39 was also observed. The charge alteration for both p33 and p39 was a two-stage process, the accumulative effect of which resulted in p33 increasing in pI from 6.14 to 6.53 and p39 increasing in pI from 6.29 to 6.63. The first mutation of p33 and p39 occurred between passages 7 and 10 of piRD-3673 cells and affected both the charge and apparent molecular weight of these two proteins. The second mutation at passage 15 of piRD-3673 cells caused only a change in the charge of p33 and p39. Two other virus proteins (p54 and p75) showed no evidence of mutation over the same passage history of piRD-3673 cells. The virus released from piRD-3673 cells also differed from CBV-3673 by two further criteria, a reduction in plaque-forming efficiency in HEp-2 cells and increased virus replication in RD cells. These data on virus evolution are discussed in relation to the maintenance of persistent CBV infections and the presence of naturally occurring CBV variants.

Coxsackievirus Infections↗
PubMed1994

RNA virus quasispecies: significance for viral disease and epidemiology.

The experimental evidence available for animal and plant RNA viruses, as well as other RNA genetic elements (viroids, satellites, retroelements, etc.), reinforces the view that many different types of genetic alterations may occur during RNA genome replication. This is fundamentally because of infidelity of genome replication and large population sizes. Homologous and heterologous recombination, as well as gene reassortments occur frequently during replication of retroviruses and most riboviruses, especially those that use enzymes with limited processivity. Following the generation of variant genomes, selection, which is dependent on environmental parameters in ways that are poorly understood, sorts out those genome fits enough to generate viable quasispecies. Chance events can also be destabilizing, as illustrated by recent results on fitness loss and other phenotypic changes accompanying bottleneck transmission. Variation, selection, and random sampling of genomes occur continuously and unavoidably during virus evolution. Evolution of RNA viruses is largely unpredictable because of the stochastic nature of mutation and recombination events, as well as the subtle effects of chance transmission events and host/environmental factors. Among environmental factors, alterations resulting from human intervention (deforestation, agricultural activities, global climatic changes, etc.) may alter dispersal patterns and provide new adaptive possibilities to viral quasispecies. Current understanding of RNA virus evolution suggests several strategies to control and diagnose viral diseases. The new generation of chemically defined vaccines and diagnostic reagents (monoclonal antibodies, peptide antigens, oligonucleotides for polymerase chain reaction amplification, etc.) may be adequate to prevent disease and detect some or even most of the circulating quasispecies of any given RNA pathogen. However, the dynamics of viral quasispecies mandate careful consideration of those reagents to be incorporated into diagnostic kits. Broadening diagnosis without jeopardizing specificity of detection will be challenging. There is a finite probability (impossible to quantify at present) that a defined vaccine may promote selection of escape mutants or a particular diagnostic kit may fail to detect a viral pathogen. Of particular concern are the potential long-term effects of weak selective pressures that may initially go unnoticed. Variant viruses resulting from evolutionary pressure imposed by vaccines or drugs may insidiously and gradually replace previous quasispecies. The great potential for variation and phenotypic diversity of some important RNA virus pathogens (human immunodeficiency virus, the hepatitis viruses, the newly recognized human hantaviruses, etc.) has become clear. Prevention and therapy should rely on multicomponent vaccines and antiviral agents to address the complexity of RNA quasispecies mutant spectra.(ABSTRACT TRUNCATED AT 400 WORDS)

Biological Evolution↗
PubMed1998

Molecular evolution of viruses--Past and Present, Part 2--An introduction.

The evolution of viruses is reviewed within the perspective of the concepts on the evolution of the lipid membrane bound vesicular structures in the prebiotic soup through the ideas on evolution of cells during the RNA World and the transition into the DNA World. The ancient Archeae bacteria and their retrons that carry the bacterial reverse transcriptase gene and their unique protein splicing capability provide an indication of the evolutionary path for retroviruses and, independently, for RNA and DNA viruses of the prokaryotic Archeae bacteria and the eukaryotic yeast and fungi.

Archaea↗
PubMed2005

Quasispecies theory in the context of population genetics.

BACKGROUND: A number of recent papers have cast doubt on the applicability of the quasispecies concept to virus evolution, and have argued that population genetics is a more appropriate framework to describe virus evolution than quasispecies theory. RESULTS: I review the pertinent literature, and demonstrate for a number of cases that the quasispecies concept is equivalent to the concept of mutation-selection balance developed in population genetics, and that there is no disagreement between the population genetics of haploid, asexually-replicating organisms and quasispecies theory. CONCLUSION: Since quasispecies theory and mutation-selection balance are two sides of the same medal, the discussion about which is more appropriate to describe virus evolution is moot. In future work on virus evolution, we would do good to focus on the important questions, such as whether we can develop accurate, quantitative models of virus evolution, and to leave aside discussions about the relative merits of perfectly equivalent concepts.

Biological Evolution↗
PubMed2005

Origin and evolution of viruses: escaped DNA/RNA sequences as evolutionary accelerators and natural biological weapons.

Knowledge of the origin and evolution of viruses could provide a better understanding of a number of phenomena in the field of evolution such as the origin and development of multi-cellular organisms, the rapid diversification of species over the last 600-700 million years and the lack of transitional forms in the evolution of species ("missing links") etc. One of the possible effects of escaped DNA/RNA sequences or viruses on the evolution of multi-cellular organisms, especially vertebrates, could be the phenomenon of horizontal transmission and dissemination of genes. Interestingly, if so, this effect could be considered as a model of primeval and natural genetic engineering. Other possible links between the evolution of multi-cellular organisms and viruses are connected with the fact that viruses represent the source of different forms of selective pressure such as epidemics of infectious diseases, autoimmunity, malignant alteration, reproductive efficiency, etc. At the same time, these two models of "long-term evolutionary relations" could represent "key factors" in the evolution between viruses and multi-cellular organisms. The capability of a genome to produce and emit DNA/RNA sequences or de novo created viruses which can be a vector of genes horizontal transmission and/or cause selective pressure on concurrent or predator species gives a new characteristic to viruses--the possibility of their acting as natural biological weapons. Finally, possibly evolutionary advantages of this genome capability could be one of explanations for the phenomena such as genome instability and its ability to emit DNA/RNA sequences and/or de novo created viruses, as well as evolutionary conservation of this unique phenomena.

Animals↗
PubMed2003

Progressive reversion of human immunodeficiency virus type 1 resistance mutations in vivo after transmission of a multiply drug-resistant virus.

Evolution and transmission of multiply drug-resistant human immunodeficiency virus type 1 (HIV-1) may limit therapeutic options as global treatment efforts expand. However, the stability of these mutants in the absence of drug selection pressure is not known. We performed a longitudinal analysis of plasma virus from a person who acquired HIV-1 that contained multiple reverse transcriptase (RT) and protease (PR) mutations. In the absence of therapy, 5 of 12 drug resistance mutations reverted in a stepwise fashion to wild type over the course of 52 weeks. Reversion of the M184V mutation alone did not change viral replicative capacity (RC), but it led to enhanced resistance to zidovudine and tenofovir. However, reversions of a second RT mutation and 3 PR mutations were associated with an increase in viral RC, and this was temporally correlated with a marked decrease in CD4 cell number. This study demonstrates the gradual stepwise back-mutation of certain drug resistance mutations in vivo in the absence of ongoing drug selection pressure. Moreover, it suggests that, despite initially impaired viral fitness, a transmitted HIV-1 isolate with multiple drug resistance mutations can evolve to develop increased RC and significant pathogenicity.

Adult↗
PubMed1995

A short introduction to the origin and molecular evolution of viruses.

The present review deals with conceptual and experimental approaches to two aspects of the origin and molecular evolution of viruses. In the section "Role of Retrons, Retroelements, and Reverse Transcriptase in the Evolution of Retroviruses and in Eukaryotic Genome Plasticity", Temin's concept that retrons are an ancient genetic element that during evolution of the species gave rise to retroviruses is presented. An opposing view of Xiong and Eickbush that the most probable ancestor of current retroelements is a retrotransposable element with gag- and pol-like genes is presented. Minus-strand RNA viruses are also discussed. The second aspect of this review is the molecular evolution of viruses at the level of the virus genome. Spiegelman's experiment on the evolution of self-replicating nucleic acid molecules outside living cells and Eigen's experimental and conceptual approaches to this subject are presented, along with studies on the evolutionary rates of base substitutions in viral RNA and defective molecules generated during replication.

Animals↗
PubMed2005

Origin and evolution of viruses causing classical swine fever in Cuba.

We have analyzed the origin and evolution of viruses from the classical swine fever (CSF) epidemic that affects Cuba since 2001 by nucleotide sequencing of regions within the E2 glycoprotein and the NS5B (polymerase) genes. The sequence of 190 nucleotides from E2 gene was determined for 10 CSF viruses isolated at different locations of the island, and used for phylogenetic analyses, including sequences from viruses of the 1993--1997 epizootic, previously determined, as well as those from representatives of the different CSFV genotypes. The phylogenetic tree obtained indicates that viruses circulating at present belong to the subgroup 1.2 and are closely related to those isolated during the 1993--1997 epizootic, including the strain Margarita used for vaccine potency tests in Cuba. However, the pattern of evolution revealed by these analyses was different than that observed previously, in which western isolates were almost identical to Margarita strain, while eastern isolates showed a higher level of genetic diversification. In this case, all the viruses analyzed grouped in an independent, define cluster that is closely related, albeit distinguishable, from that of Margarita-related viruses that previously circulated in the western part of Cuba. In addition, the 2001--2003 viruses showed a branched pattern with a level of sequence diversification similar to that observed in the eastern 1993--1997 viruses. Interestingly, a significant fraction (about 54%) of the mutations found in the E2 sequence led to amino acid replacements. This high rate of non-synonymous mutations was not found in the previous Cuban epizootic and has not been reported for other CSF outbreaks. In spite of these amino acid replacements, no antigenic changes were observed in the reactivity of different isolates with CSFV-specific MAbs and polyclonal sera. The phylogenetic tree derived from 409 nucleotides of NS5B gene of seven isolates and Margarita strain, was consistent with that obtained from E2 sequences. In this region, encoding a non-structural protein, a low level of fixation of non-synonymous mutations was observed. The results obtained suggests that epidemiological factors affecting CSFV spread during the current epizootic in Cuba can favour the fixation of non-synonymous mutation in the E2 gene, which could be associated with a lower severity in the clinical signs developed by most of the affected animals.

Amino Acid Sequence↗
PubMed1990

[The origin and evolution of viruses].

This paper describes various hypotheses for the origin of viruses, prerequisites for the introduction of a virus into a host population, and the concerted evolution of virus and host. In general, viruses evolve through mutations and genetic recombinations. Selection pressure is exerted by various host defence mechanisms and possible ways of virus transmission. The virus variants showing a high reproduction rate without killing their host are most likely to be selected for. In addition, the viral infection vice versa exert a selection pressure on the host population resulting in the elimination of highly susceptible individuals and an increased number of resistant individuals. The apparent consequence is a tendency for the virus to be less virulent and the host to be more resistant.

Biological Evolution↗
PubMed1994

Evolution of alphaviruses in the eastern equine encephalomyelitis complex.

Evolution of viruses in the eastern equine encephalomyelitis (EEE) complex was studied by analyzing RNA sequences and oligonucleotide fingerprints from isolates representing the North and South American antigenic varieties. By using homologous sequences of Venezuelan equine encephalomyelitis virus as an outgroup, phylogenetic trees revealed three main EEE virus monophyletic groups. A North American variety group included all isolates from North America and the Caribbean. One South American variety group included isolates from the Amazon basin in Brazil and Peru, while the other included strains from Argentina, Guyana, Ecuador, Panama, Trinidad, and Venezuela. No evidence of heterologous recombination was obtained when three separate regions of the EEE virus genome were analyzed independently. Estimates of the overall rate of EEE virus evolution (nucleotide substitution) were 1.6 x 10(-4) substitution per nucleotide per year for the North American group and 4.3 x 10(-4) for the Argentina-Panama South American group. Evolutionary rate estimates for the North American group increased over 10-fold (from about 2 x 10(-5) to 4 x 10(-4)) concurrent with divergence of two monophyletic groups during the early 1970s. The North and South American antigenic varieties diverged roughly 1,000 years ago, while the two main South American groups diverged about 450 years ago. Analysis of multiple strains isolated from an upstate New York transmission focus during the same years suggested that, in certain locations, EEE virus may be relatively isolated for short time periods.

Antigens, Viral↗
PubMed2003

Estimation of population bottlenecks during systemic movement of tobacco mosaic virus in tobacco plants.

More often than not, analyses of virus evolution have considered that virus populations are so large that evolution can be explained by purely deterministic models. However, virus populations could have much smaller effective numbers than the huge reported census numbers, and random genetic drift could be important in virus evolution. A reason for this would be population bottlenecks during the virus life cycle. Here we report a quantitative estimate of population bottlenecks during the systemic colonization of tobacco leaves by Tobacco mosaic virus (TMV). Our analysis is based on the experimental estimation of the frequency of different genotypes of TMV in the inoculated leaf, and in systemically infected leaves, of tobacco plants coinoculated with two TMV genotypes. A simple model, based on the probability that a leaf in coinoculated plants is infected by just one genotype and on the frequency of each genotype in the source, was used to estimate the effective number of founders for the populations in each leaf. Results from the analysis of three leaves per plant in plants inoculated with different combinations of three TMV genotypes yielded highly consistent estimates. Founder numbers for each leaf were small, in the order of units. This would result in effective population numbers much smaller than the census numbers and indicates that random effects due to genetic drift should be considered for understanding virus evolution within an infected plant.

Genotype↗
PubMed2004

A long-term latent reservoir for HIV-1: discovery and clinical implications.

Despite the remarkable success of highly active antiretroviral therapy (HAART) for the treatment of HIV-1 infection, it now appears that the infection is intrinsically incurable with antiretroviral therapy alone. The major reason is that the virus can persist in a latent form in resting memory CD4 cells. These cells arise when infected CD4+ lymphoblasts carrying an integrated copy of the HIV-1 genome revert back to a resting memory state. In this resting state, CD4 cells are minimally permissive for virus gene expression, and infected memory cells can survive for many years. Following re-exposure to the relevant antigen or other activating stimuli, these cells can begin to produce virus again. The existence of a stable reservoir has altered treatment strategies in several ways. HAART is no longer given with the goal of eradication. In addition, the reservoir serves as a permanent archive for wild-type virus and for drug-resistant variants that arise during treatment. Thus, once resistance to a particular drug arises, the patient will always carry that resistance. Interruption in treatment results in the re-emergence of the original wild-type virus, which often replicates better than drug-resistant virus. Although HAART cannot eradicate the infection, current regimens do come close to stopping virus evolution. Free viruses found in the plasma at low levels in patients on HAART resemble viruses in the latent reservoir and do not contain new drug resistance mutations. Thus although HAART cannot produce eradication, lifetime control of the infection with antiretroviral drugs may be possible.

Anti-HIV Agents↗
PubMed1996

[Evolution and epidemiology of influenza A viruses].

Influenza A viruses are suitable for the analysis of virus evolution because the genes of the viruses are well analyzed. The origin of the present human influenza A viruses are deduced to be direct descendent of the viruses which caused Spanish flu in 1918. The analysis of NS gene shows the branching point between avian and human viruses are early 1900. By comparison of the amino acid sequences, HA serotypes could be divided into two groups, i.e., an H1 and an H3 groups. The branching between subtypes H1 and H2 occurred fairly recently. The HA genes of influenza A viruses evolve causing two kinds of antigenic variation, saift and drift, which are caused by different mechanisms.

Animals↗