Viruses scout evolution's path.
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Biological Evolution↗
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Results for “virus evolution”
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Evolution of virus and defective-interfering RNAs in BHK cells persistently infected with Sindbis virus.
We analyzed a BHK cell line persistently infected with Sindbis virus for 16 months and a virus (Sin-16) cloned from these cells. Sin-16 virus was resistant to the defective interfering particles present in the original infection. We found that (i) cells infected with Sin-16 were impaired in the processing of a viral precursor glycoprotein, (ii) high-multiplicity passaging of Sin-16 gave rise to a variant that was able to generate and be inhibited by defective-interfering particles to which the original Sin-16 virus was resistant, and (iii) the persistently infected culture contained a heterogeneous mixture of defective Sindbis virus RNAs which were not packaged into extracellular particles. To determine whether these intracellular RNAs could interfere with the replication of Sin-16, we analyzed cells that were cloned from the persistently infected culture. One clone (A3) synthesized a single defective viral RNA which was lost with continued passaging in culture. Infection of A3 cells with Sin-16 showed that the presence of the defective RNA greatly enhanced cell survival and led to enrichment of this RNA. In contrast, cured cells were highly susceptible to killing by Sin-16, and survivors did not synthesize this RNA. Thus, A3 cells were not genetically altered in their response to Sin-16, but were protected from the cytopathic effects of infection by an RNA with the characteristics of a defective-interfering RNA.
Animals↗
Virus and target cell evolution in human immunodeficiency virus type 1 infection.
Human immunodeficiency virus (HIV) infection leads to a prolonged struggle between a rapidly evolving viral population and a potent immune response. In the vast majority of infected individuals, the virus wins this struggle. In my laboratory, we focus on understanding both the viral and immune factors that contribute to this outcome. The results of our studies and those of many others indicate that HIV can escape a potent immune response by a combination of mechanisms including rapid mutation, shedding of decoy antigens, modulation of host major histocompatibility complex, and destruction of cytotoxic T lymphocytes. The target cells for viral infection change as the virus evolves to use different chemokine coreceptors for entry. The initial targets are activated and resting memory T cells that express both CD4 and CCR5, but both naive and memory CD4 T cells are targeted by viruses capable of using CXCR4 for entry, and macrophages become the primary target cells when most CD4 T cells are depleted. Compelling evidence is emerging that the availability of target cells for infection is as limiting for the spread of virus as the immune response.
HIV Infections↗
Hepatocellular carcinoma among hemodialysis patients infected with hepatitis C virus--early evolution and rapid progression.
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Acute Disease↗
[The arenavirus in the New World: a virus in evolution and emerging diseases].
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Arenaviridae Infections↗
A theory of modular evolution for bacteriophages.
The modular theory of virus evolution has clear experimental support among the temperate bacteriophages of the enteric bacteria. However, there is also similar genetic and DNA heteroduplex evidence for such evolution among other families of bacteriophages: the virulent bacteriophages of the enterics comprise several families: the T-even group, the T3-T7 group (which has many members among different species of bacteria, including bacteria as widely divergent as E. coli and Caulobacter crescentus. It nicely explains the diffusion of very similar homologous bacteriophages into hosts whose own DNAs have diverged very greatly from each other in nucleotide sequence. It also accounts for the rigorous maintenance of regulatory schemes while units of function (including regions coding for proteins) diverge more rapidly. It should also be noted that the considerations that make modular evolution seem advantageous for bacteriophages apply equally well to viruses of higher organisms. Furthermore, the kinds of heteroduplex similarity observed among animal viruses are reminiscent of what is found for bacteriophages. Viruses found in widely divergent hosts show much greater similarity than would be expected; quite possibly animal viruses also evolve as a population of interchangeable modules.
Bacteriophage lambda↗
The pivotal role of phosphatidylinositol 3-kinase-Akt signal transduction in virus survival.
Over the course of evolution, viruses have developed the ability to modulate a variety of host cell signalling pathways. Inhibition of apoptosis, in particular, has become recognized as an important contributory factor in virus survival. Apoptotic inhibition contributes to the establishment of latent and chronic infections and has been implicated in viral oncogenesis. The phosphatidylinositol 3-kinase (PI3K)-Akt pathway is utilized by many cell types for inhibition of apoptosis and cellular survival. Virus modulation of this pathway provides an alternative to the expression of viral oncogenes or the direct inhibition of pro-apoptotic proteins. It has become evident that many viruses require up-regulation of this pathway to sustain long-term infections and it is modulated, in some cases, by specific viral products to create an environment favourable for cellular transformation. In other cases, PI3K-Akt signalling simply helps to create an environment favourable for virus replication and virion assembly. This review details the modulation and function of PI3K-Akt signalling for virus survival.
Animals↗
Evolution of the G and P genes of human respiratory syncytial virus (subgroup A) studied by the RNase A mismatch cleavage method.
The G and P genes of human respiratory syncytial viruses (subgroup A), isolated between 1961 and 1989, were analyzed by RNase A one-dimensional fingerprinting, using the Long strain as the reference. Total RNA extracted from cells infected with the different isolates was hybridized to radiolabeled antisense G or P RNA probes of the Long virus. The RNA:RNA heteroduplexes were digested with RNase A and the resistant products analyzed by gel electrophoresis. Comparative analysis of the cleavage patterns revealed extensive genetic heterogeneity in both genes among viruses isolated in different epidemics. In contrast, 13 viruses isolated in Montevideo during a 3-month period showed much more restricted heterogeneity; thus, 11 viruses represented the predominant type of this outbreak and only 2 other viruses generated different RNA cleavage patterns distantly related to the major type. Statistical analysis of the results obtained indicated progressive accumulation of genetic changes with time along cocirculating evolutionary lineages within the same antigenic subgroup of RS virus. The results are discussed in terms of a model for RS virus evolution.
Antigens, Viral↗
Evolution of influenza A virus PB2 genes: implications for evolution of the ribonucleoprotein complex and origin of human influenza A virus.
Phylogenetic analysis of 20 influenza A virus PB2 genes showed that PB2 genes have evolved into the following four major lineages: (i) equine/Prague/56 (EQPR56); (ii and iii) two distinct avian PB2 lineages, one containing FPV/34 and H13 gull virus strains and the other containing North American avian and recent equine strains; and (iv) human virus strains joined with classic swine virus strains (i.e., H1N1 swine virus strains related to swine/Iowa/15/30). The human virus lineage showed the greatest divergence from its root relative to other lineages. The estimated nucleotide evolutionary rate for the human PB2 lineage was 1.82 x 10(-3) changes per nucleotide per year, which is within the range of published estimates for NP and NS genes of human influenza A viruses. At the amino acid level, PB2s of human viruses have accumulated 34 amino acid changes over the past 55 years. In contrast, the avian PB2 lineages showed much less evolution, e.g., recent avian PB2s showed as few as three amino acid changes relative to the avian root. The completion of evolutionary analyses of the PB1, PB2, PA and NP genes of the ribonucleoprotein (RNP) complex permits comparison of evolutionary pathways. Different patterns of evolution among the RNP genes indicate that the genes of the complex are not coevolving as a unit. Evolution of the PB1 and PB2 genes is less correlated with host-specific factors, and their proteins appear to be evolving more slowly than NP and PA. This suggests that protein functional constraints are limiting the evolutionary divergence of PB1 and PB2 genes. The parallel host-specific evolutionary pathways of the NP and PA genes suggest that these proteins are coevolving in response to host-specific factors. PB2s of human influenza A viruses share a common ancestor with classic swine virus PB2s, and the pattern of evolution suggests that the ancestor was an avian virus PB2. This same pattern of evolution appears in the other genes of the RNP complex. Antigenic studies of HA and NA proteins and sequence comparisons of NS and M genes also suggest a close ancestry for these genes in human and classic swine viruses. From our review of the evolutionary patterns of influenza A virus genes, we propose the following hypothesis: the common ancestor to current strains of human and classic swine influenza viruses predated the 1918 human pandemic virus and was recently derived from the avian host reservoir.
Amino Acid Sequence↗
Molecular epidemiology of rabies virus in France: comparison with vaccine strains.
A molecular epidemiological study of the rabies virus currently prevalent in France was carried out by directly sequencing polymerase chain reaction-amplified genes. The rabies virus pseudogene psi was chosen as the most divergent genomic area, and as such the best 'clock' for measuring virus evolution. Sequence comparisons between 12 wild rabies virus isolates indicated strong conservation whatever the host and wherever the virus had been isolated. This holds true for a unique wild reservoir, the fox. On the other hand, a good correlation between genetic and geographical criteria indicates a slow evolution of the wild virus in parallel with the spatio-temporal progression of the epizootic. In contrast to their intrinsic homogeneity (about 2% divergence), the wild isolate sequences showed a marked divergence from those of vaccine seed strains (about 14.7%). This finding invites world-wide molecular epidemiological studies, particularly in countries in which vaccination failures have been reported.
Animals↗
Foot-and-mouth disease virus lacking the VP1 G-H loop: the mutant spectrum uncovers interactions among antigenic sites for fitness gain.
The Arg-Gly-Asp (RGD) triplet found in the G-H loop of capsid protein VP1 of foot-and-mouth disease virus (FMDV) is critically involved in the interaction of FMDV with integrin receptors and with neutralizing antibodies. Multiplication of FMDV C-S8c1 in baby hamster kidney 21 (BHK-21) cells selected variant viruses exploiting alternative mechanisms of cell recognition that rendered the RGD integrin-binding triplet dispensable for infectivity. By constructing chimeric viruses, we show that dispensability of the RGD in these variant FMDVs can be extended to surrounding amino acid residues. Replacement of eight amino acid residues within the G-H loop of VP1 by an unrelated FLAG marker yielded infectious virus. Evolution of FLAG-containing viruses in BHK-21 cells generated complex quasispecies in which individual mutants included amino acid replacements at other antigenic sites of FMDV. Inclusion of such replacements in the parental FLAG clone resulted in an increase of relative fitness of the viruses. These results suggest structural or functional connections between antigenic sites of FMDV and underscore the value of mutant spectrum analysis for the identification of fitness-promoting genetic modifications in viral populations. The possibility of producing viable viruses lacking antigenic site A may find application in the design of new anti-FMD vaccines.
Adaptation, Physiological↗
Virus complement evasion strategies.
The immune system has a variety of tools at its disposal to combat virus infections. These can be subdivided roughly into two categories: 'first line defence', consisting of the non-specific, innate immune system, and 'adaptive immune response', acquired over time following virus infection or vaccination. During evolution, viruses have developed numerous, and often very ingenious, strategies to counteract efficient recognition of virions or virus-infected cells by both innate and adaptive immunity. This review will focus on the different strategies that viruses use to avoid recognition by one of the components of the immune system: the complement system. Complement evasion is of particular importance for viruses, since complement activation is a crucial component of innate immunity (alternative and mannan-binding lectin activation pathway) as well as of adaptive immunity (classical, antibody-dependent complement activation).
Animals↗
The evolution of virulence in a plant virus.
The evolution of virulence is a rapidly growing field of research, but few reports deal with the evolution of virulence in natural populations of parasites. We present here an observational and experimental analysis of the evolution of virulence of the plant virus Cucumber mosaic virus (CMV) during an epidemic on tomato in eastern Spain. Three types of CMV isolates were found that caused in tomato plants either a systemic necrosis (N isolates), stunting and a severe reduction of leaf lamina (Y isolates), or stunting and leaf curl (A isolates). These phenotypes were due to the presence of satellite RNAs (satRNAs) necrogenic (in N isolates) or attenuative (in A isolates) of the symptoms caused by CMV without satRNA (Y isolates). For these three types of isolates, parameters of virulence and transmission were estimated experimentally. For virulence the ranking of isolates was N > Y > A, for transmissibility, Y > A > N. The predictions of theoretical models for the evolution of virulence were analyzed with these parameters and compared with observations from the field. A single-infection model predicted adequately the observed long-term evolution of the CMV population to intermediate levels of virulence. A coinfection model that considered competition between isolates with an effect on transmission explained the invasion of the CMV population by N isolates at the beginning of the epidemic, and its predictions also agreed with field data on the long-term evolution of the CMV population. An important conclusion from both models was that the density of the aphid vector's population is a major factor in the evolution of CMV virulence. This may be relevant for the design of control strategies for CMV-induced diseases.
Biological Evolution↗
Microevolution and virulence of dengue viruses.
The evolution of dengue viruses has had a major impact on their virulence for humans and on the epidemiology of dengue disease around the world. Although antigenic and genetic differences in virus strains had become evident, it is mainly due to the lack of animal models of disease that has made it difficult to detect differences in virulence of dengue viruses. However, phylogenetic studies of many different dengue virus samples have led to the association between specific genotypes (within serotypes) and the presentation of more or less severe disease. Currently, dengue viruses can be classified as being of epidemiologically low, medium, or high impact; i.e., some viruses may remain in sylvatic cycles of little or low transmissibility to humans, others produce dengue fever (DF) only, and some genotypes have been associated with the potential to cause the more severe dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS) in addition to DF. Although the factors that contribute to dengue virus epidemiology are complex, studies have suggested that specific viral structures may contribute to increased replication in human target cells and to increased transmission by the mosquito vector; however, the immune status and possibly the genetic background of the host are also determinants of virulence or disease presentation. As to the question of whether dengue viruses are evolving toward virulence as they continue to spread throughout the world, phylogenetic and epidemiological analyses suggest that the more virulent genotypes are now displacing those that have lower epidemiological impact; there is no evidence for the transmission of antigenically aberrant, new strains.
Animals↗
Inference and prediction of courses of the diseases caused by pathologic viruses by estimating molecular evolution of within-host virus.
A new approach for inferring the evolutionary process of within-host virus is presented in this study. This approach includes a sequential-linking algorithm developed by us that can deal with the sequential viral samples that are obtained at different time points from the same host, and reconstruct a longitudinal phylogenetic tree in which the evolutionary relations between viral variants can be shown. A codon-based model, which uses a Markov process to describe substitutions between codons, is also employed in this approach to calculate synonymous and non-synonymous substitution rates and to distinguish positive selection and neutral evolution. The approach is applied to a data set of the V3 region of the HIV-1 envelope genes sequenced in different years after infection of a single patient. The results suggest that this approach may provide a more realistic description of viral evolution than the traditional evolution models because it accounts for both neutral and adaptive evolution. Most important of all, since this approach make it possible to follow up the evolutionary process of within-host virus by analyzing the sequential viral samples, it could be used in inference and prediction of the course of the diseases caused by pathologic viruses and evaluation of the treatment.
Algorithms↗
Recent influenza B viruses in Europe: a phylogenetic analysis.
BACKGROUND: Influenza B virus evolution is currently in a unique situation having two cocirculating main lineages B/Yamagata/16/88 (YM/88)-like and B/Victoria/2/87 (VI/87)-like viruses. Continuation of this bifurcation would mean development towards distinct forms resembling the HA subtypes of influenza A viruses. OBJECTIVE: We wanted to examine both intraepidemic heterogeneity and recent evolution in these two lineages. The initial purpose was to determine the geographic distribution of the two sublineages of the VI/87-like viruses in Europe in 1989-1990 under circumstances of low epidemic activity. Due to the outbreaks of YM/88-like viruses since 1991, the study was extended to contain the evolution of these viruses and their genetic relationship with the vaccine strains of that time. STUDY DESIGN: The HA1 gene sequences of 33 influenza B strains isolated in ten European countries since 1989 were determined and compared with those available through databases or personal contacts. RESULTS: The two main lineages, YM/88-like and VI/87-like viruses, both continued to circulate. In both lineages, changes in the potential glycosylation sites were observed. Two sublineages of the VI/87 lineage cocirculated during the 1989-1990 season with somewhat different geographic distributions. A high degree of intraepidemic heterogeneity was observed, as well as examples of conserved nucleotide sequences. CONCLUSIONS: It is important to follow the evolution and circulation of VI/87-like viruses. Current vaccines give poor or no protection against VI/87-like viruses in immunologically unprimed children or even in primed adults (Levandowski et al., 1991, Pyhala et al., 1994). Changes in the potential glycosylation pattern in the latest virus isolates of both main lineages have occurred and it is interesting to see the significance of these changes to viral evolution.
Journal Article↗
The origin and evolution of hepatitis viruses in humans.
The spread and origins of hepatitis C virus (HCV) in human populations have been the subject of extensive investigations, not least because of the importance this information would provide in predicting clinical outcomes and controlling spread of HCV in the future. However, in the absence of historical and archaeological records of infection, the evolution of HCV and other human hepatitis viruses can only be inferred indirectly from their epidemiology and by genetic analysis of contemporary virus populations. Some information on the history of the latter may be obtained by dating the time of divergence of various genotypes of HCV, hepatitis B virus (HBV) and the non-pathogenic hepatitis G virus (HGV)/GB virus-C (GBV-C). However, the relatively recent times predicted for the origin of these viruses fit poorly with their epidemiological distributions and the recent evidence for species-associated variants of HBV and HGV/GBV-C in a wide range of non-human primates. The apparent conservatism of viruses over long periods implied by these latter observations may be the result of constraints on sequence change peculiar to viruses with single-stranded genomes, or with overlapping reading frames. Large population sizes and intense selection pressures that optimize fitness may be the factors that set virus evolution apart from that of their hosts.
Amino Acid Sequence↗
Emergence of autologous neutralization-resistant variants from preexisting human immunodeficiency virus (HIV) quasi species during virus rebound in HIV type 1-infected patients undergoing highly active antiretroviral therapy.
The role of neutralizing antibodies (NAbs) during virus rebound in human immunodeficiency virus type 1 (HIV-1)-infected patients undergoing highly active antiretroviral therapy is poorly understood. Three patients in this study had NAbs to preexisting autologous HIV-1 and an episode of virus rebound after a prolonged period of virus suppression. To investigate the influence of NAbs on virus evolution, envelope genotypes of preexisting and rebound viruses were examined. Phylogenetic analysis of env (V1-V5) sequences indicated that rebound viruses had evolved from or preexisted in baseline populations. By use of envelope pseudotype viruses, rebound viruses were found to be significantly resistant to neutralization by autologous antibody in all 3 patients, indicating that rebound viruses were selected by NAbs. The site responsible for conferring neutralization resistance against autologous antibody was identified in the upstream C3 region in 2 of 3 patients.
Adolescent↗