PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “virus evolution”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 865 records · Page 48Linked to original sources
PubMed2004

Conserved translational frameshift in dsDNA bacteriophage tail assembly genes.

A programmed translational frameshift similar to frameshifts in retroviral gag-pol genes and bacterial insertion elements was found to be strongly conserved in tail assembly genes of dsDNA phages and to be independent of sequence similarities. In bacteriophage lambda, this frameshift controls production of two proteins with overlapping sequences, gpG and gpGT, that are required for tail assembly. We developed bioinformatic approaches to identify analogous -1 frameshifting sites and experimentally confirmed our predictions for five additional phages. Clear evidence was also found for an unusual but analogous -2 frameshift in phage Mu. Frameshifting sites could be identified for most phages with contractile or noncontractile tails whose length is controlled by a tape measure protein. Phages from a broad spectrum of hosts spanning Eubacteria and Archaea appear to conserve this frameshift as a fundamental component of their tail assembly mechanisms, supporting the idea that their tail genes share a common, distant ancestry.

Amino Acid Sequence↗
PubMed2005

Lineage extinction and replacement in dengue type 1 virus populations are due to stochastic events rather than to natural selection.

Between 1996 and 1998, two clades (B and C; genotype I) of dengue virus type 1 (DENV-1) appeared in Myanmar (Burma) that were new to that location. Between 1998 and 2000, a third clade (A; genotype III) of DENV-1, which had been circulating at that locality for at least 25 years, became extinct. These changes preceded the largest outbreak of dengue recorded in Myanmar, in 2001, in which more than 95% of viruses recovered from patients were DENV-1, but where the incidence of severe disease was much less than in previous years. Phylogenetic analyses of viral genomes indicated that the two new clades of DENV-1 did not arise from the, now extinct, clade A viruses nor was the extinction of this clade due to differences in the fitness of the viral populations. Since the extinction occurred during an inter-epidemic period, we suggest that it was due to a stochastic event attributable to the low rate of virus transmission in this interval.

Aedes↗
PubMed2005

Genomic and evolutionary aspects of Mimivirus.

We recently described a giant double stranded DNA virus called Mimivirus, isolated from amoebae, which might represent a new pneumonia-associated human pathogen. Its unique morphological and genomic characteristics allowed us to propose Mimivirus as a member of a new distinct Nucleocytoplasmic Large DNA viruses family, the Mimiviridae. Mimivirus-specific features, namely its size and its genomic complexity, ranged it between viruses and cellular organisms. This paper reviews our current knowledge on Mimivirus structure, life cycle and genome analysis and discusses its putative evolutionary origin in the tree of species of the three domains of life.

Acanthamoeba↗
PubMed2006

Mimivirus and the emerging concept of "giant" virus.

The recently discovered Acanthamoeba polyphaga Mimivirus is the largest known DNA virus. Its particle size (750 nm), genome length (1.2 million bp) and large gene repertoire (911 protein coding genes) blur the established boundaries between viruses and parasitic cellular organisms. In addition, the analysis of its genome sequence identified many types of genes never before encountered in a virus, including aminoacyl-tRNA synthetases and other central components of the translation machinery previously thought to be the signature of cellular organisms. In this article, we examine how the finding of such a giant virus might durably influence the way we look at microbial biodiversity, and lead us to revise the classification of microbial domains and life forms. We propose to introduce the word "girus" to recognize the intermediate status of these giant DNA viruses, the genome complexity of which makes them closer to small parasitic prokaryotes than to regular viruses.

Acanthamoeba↗
PubMed2001

Evolution of intermediates of influenza virus hemagglutinin-mediated fusion revealed by kinetic measurements of pore formation.

Cells expressing wild-type influenza virus hemagglutinin (HA) or HA with a point mutation within the transmembrane domain (G520L) were bound to red blood cells and exposed to low pH for short times at suboptimal temperatures followed by reneutralization. This produced intermediate states of fusion. The ability of intermediate states to proceed on to fusion when temperature was raised was compared kinetically. In general, for wild-type HA, fusion occurred more quickly by directly lowering pH at 37 degrees C in the bound state than by raising temperature at the intermediate stage. When pH was lowered for 1-2 min, kinetics of fusion upon raising temperature of an intermediate slowed the longer the intermediate was maintained at neutral pH. But for a more sustained (10 min) acidification, kinetics was independent of the time the intermediate was held at neutral pH before triggering fusion by raising temperature. In contrast, generating intermediates in the same way with G520L yielded kinetics of fusion that did not depend on the time intermediates were maintained after reneutralization. For both HA and G520L, the extents of fusion did not depend on the temperature at which pH was lowered, but fusion from the intermediate was extremely sensitive to the temperature to which the cells were raised. The measured kinetics and temperature dependencies suggest that the rate-limiting step of fusion occurs subsequent to formation of any of the intermediates; the conformational change of HA into its final configuration may be the rate-limiting step.

Animals↗
PubMed1988

Evolution of sex in RNA viruses.

The distribution of deleterious mutations in a population of organisms is determined by the opposing effects of two forces, mutation pressure and selection. If mutation rates are high, the resulting mutation-selection balance can generate a substantial mutational load in the population. Sex can be advantageous to organisms experiencing high mutation rates because it can either buffer the mutation-selection balance from genetic drift, thus preventing any increases in the mutational load (Muller, 1964: Mut. Res. 1, 2), or decrease the mutational load by increasing the efficiency of selection (Crow, 1970: Biomathematics 1, 128). Muller's hypothesis assumes that deleterious mutations act independently, whereas Crow's hypothesis assumes that deleterious mutations interact synergistically, i.e., the acquisition of a deleterious mutation is proportionately more harmful to a genome with many mutations than it is to a genome with a few mutations. RNA viruses provide a test for these two hypotheses because they have extremely high mutation rates and appear to have evolved specific adaptations to reproduce sexually. Population genetic models for RNA viruses show that Muller's and Crow's hypotheses are also possible explanations for why sex is advantageous to these viruses. A re-analysis of published data on RNA viruses that are cultured by undiluted passage suggests that deleterious mutations in such viruses interact synergistically and that sex evolved there as a mechanism to reduce the mutational load.

Models, Genetic↗
PubMedDate not supplied

[Immunologic thrombopenic purpura and HIV infection in heroin addicts].

The authors have studied the clinical aspects and mechanism of the thrombocytopenia observed in heroin addicts in the light of recently published data. This relatively frequent complication of intravenous drug addiction must be related to the immunological disturbances caused by carriage of the HIV virus. The evolutive characteristics of thrombocytopenia in such cases and the therapeutic implications of this association between thrombocytopenic purpura and acquired immunodeficiency are discussed.

Acquired Immunodeficiency Syndrome↗
PubMed2000

The causes and consequences of genetic variation in dengue virus.

Despite the fact that dengue is one of the most prevalent viral infections of humans, the mechanisms responsible for its pathogenesis remain uncertain. Evolutionary studies of dengue virus have revealed that its genetic diversity is increasing. This, coupled with evidence that viral strains could naturally differ in virulence, suggests that in the future we might be exposed to viruses with an expanded range of pathogenic properties.

Dengue↗
PubMed2005

Mimivirus gene promoters exhibit an unprecedented conservation among all eukaryotes.

The initial analysis of the recently sequenced genome of Acanthamoeba polyphaga Mimivirus, the largest known double-stranded DNA virus, predicted a proteome of size and complexity more akin to small parasitic bacteria than to other nucleocytoplasmic large DNA viruses and identified numerous functions never before described in a virus. It has been proposed that the Mimivirus lineage could have emerged before the individualization of cellular organisms from the three domains of life. An exhaustive in silico analysis of the noncoding moiety of all known viral genomes now uncovers the unprecedented perfect conservation of an AAAATTGA motif in close to 50% of the Mimivirus genes. This motif preferentially occurs in genes transcribed from the predicted leading strand and is associated with functions required early in the viral infectious cycle, such as transcription and protein translation. A comparison with the known promoter of unicellular eukaryotes, amoebal protists in particular, strongly suggests that the AAAATTGA motif is the structural equivalent of the TATA box core promoter element. This element is specific to the Mimivirus lineage and may correspond to an ancestral promoter structure predating the radiation of the eukaryotic kingdoms. This unprecedented conservation of core promoter regions is another exceptional feature of Mimivirus that again raises the question of its evolutionary origin.

Base Sequence↗
PubMed2025

The potential impacts of human genetics on virus emergence.

Human monogenic traits can confer resistance to viral infection in exposed individuals or predisposition to severe disease in infected individuals. Enhanced susceptibility can be driven directly by mutations in genes essential for control of the virus or indirectly via the production of autoantibodies against components of host defense. While the impact of viruses on individuals carrying these genotypes permitted their identification and has been amply studied, little is known about the impact of these human genotypes on the natural history of viruses, including not only persisting but also emerging viruses. We envisage several scenarios, including the possibility that genetically susceptible individuals serve as patient zeros, superspreaders, or mutation incubators, or that genetically resistant individuals even permit the selection of new viral mutants. Viruses are continually shared between individuals and even host species, where they can benefit from adaption to new environments. Current human viruses, as well as novel viruses from animal reservoirs, will continue to threaten the human population. Improvements in the scale of human genomic sequencing and analysis will permit testing hypotheses about the impact of human genetics on the origin and trajectory of viral infections, including future pandemics, which may ultimately help to prevent or curtail impending outbreaks.

Humans↗
PubMed1999

Widespread intra-serotype recombination in natural populations of dengue virus.

Diversity analysis of 71 published dengue virus gene sequences revealed several strains that appeared to be mosaics comprising gene regions with conflicting evolutionary histories. Subsequent maximum likelihood breakpoint estimation identified seven recombinants, including members of three of the four dengue virus serotypes, with breakpoints in the premembrane/membrane gene, the envelope gene, and at the junction of the envelope and first nonstructural genes. Many of the individual recombinants contain sequence representing separate genetic subtypes. The results were highly statistically significant and were confirmed by phylogenetic analysis of the regions of interest. These findings indicate that recombination may play a very significant role in shaping genetic diversity in dengue virus and, as such, have important implications for its biology and its control.

Dengue Virus↗
PubMed2002

Evolution of pigeon Newcastle disease virus strains.

Twenty-seven Newcastle disease virus isolates obtained during the years 1998 and 1999 from racing pigeons were shown to be antigenically indistinguishable from the pigeon paramyxovirus type 1 (PPMV-1) viruses isolated in the years 1983 and 1984. Partial sequencing of 240 base pairs of the F gene demonstrated at least 94.7% identity at the nucleotide level between isolates from 1983 and 1984, and more recent viruses isolated in 1998 and 1999. Most of the nucleotide changes observed were silent mutations as only six amino acid changes were observed. Three amino acid substitutions were observed in the F2/F1 cleavage site. The sequence of the F2/F1 cleavage site of all isolates was typical for pathogenic paramyxovirus 1 viruses. Amino acids at the F2/F1 cleavage site changed from (112)GRQKRF(117) to (112)RRQKRF(117), (112)RRKKRF(117) or (112)RRRKRF(117). The motif (112)RRQKRF(117) was present in the majority of the isolates but the intracerebral pathogenicity indexes of PPMV-1 isolates having this motif was highly variable but largely lower (mean, 0.69) than that reported for PPMV-1 viruses isolated in the years 1983 and 1984 (mean, 1.44).

Amino Acid Sequence↗
PubMed1995

Hepatic toxicity associated with 2'-3' dideoxyinosine in children with AIDS.

Among 34 children with AIDS enrolled in a trial with 2'-3' dideoxyinosine (ddI), six (aged 1-6 years) developed liver abnormalities within 2-18 months after institution of ddI. Two children died of fulminant hepatic failure (one had also an adenovirus infection), and four had a striking elevation of alkaline phosphatases (AP: 1120-7000 IU/L). All of them received sulfa drugs and antifungic treatment with ketoconazole or fluconazole. Three had a serology positive for hepatitis C virus. The evolution of liver enzymes following withdrawal and rechallenge with ddI in the children with elevated AP was an indication of drug-induced toxicity in two patients. In both of the others, readministration of ddI did not cause any subsequent problems. Liver histology in the patients with fulminant hepatitis showed an extensive hepatic necrosis. Liver biopsy done in two other patients revealed a mild granulomatous hepatitis in one and nonspecific changes (i.e., steatosis and a mild inflammation) in the other. Hepatic toxicity has been described with ddI and other nucleoside analogs in adult patients. These six children had many potential causes of liver disease. It may be that ddI is not hepatotoxic per se but that it precipitates liver disease in predisposed patients. We recommend that liver functions be carefully monitored when using this drug.

Acquired Immunodeficiency Syndrome↗
PubMed1997

Viral phenotype, antiretroviral resistance and clinical evolution in human immunodeficiency virus-infected children.

BACKGROUND: The syncytium-inducing (SI) viral phenotype and the emergence of viral strains resistant to zidovudine have been described in persons infected with HIV, and in some cases they have been associated with poor prognosis. METHODS: HIV isolates obtained from 37 HIV-infected children were analyzed to determine whether the SI viral phenotype and the mutation on the 215 position of the reverse transcriptase (M215) could be used as markers of disease progression. We performed peripheral blood coculture mononuclear cells, and we analyzed the induction of syncytia using the MT-2 cell line. The emergence of mutations on the 215 position was determined by PCR. RESULTS: We found a statistically significant association (P < 0.05) between SI viral phenotype and (1) recurrent serious bacterial infections, (2) absolute CD4+ cell counts <2 SD, (3) progression to AIDS and (4) death. Sixty percent of the children treated with zidovudine developed 215 mutant viral strains without statistically significant association with clinical or immunologic findings. The SI viral phenotype was statistically associated with the presence of the 215 mutation (P < 0.05). CONCLUSIONS: SI viral phenotype is a marker associated with a poor clinical and immunologic progression of the disease and it may facilitate the emergence of mutant strains in children treated with zidovudine.

Adolescent↗
PubMed2003

Why are dengue virus serotypes so distantly related? Enhancement and limiting serotype similarity between dengue virus strains.

Dengue virus, the causative agent of dengue fever, has four major serotypes characterized by large genetic and immunological distances. We propose that the unusually large distances between the serotypes can be explained in the light of a process of antibody-dependent enhancement (ADE) leading to increased mortality. Antibody-dependent enhancement results from a new infection with a particular serotype in an individual with acquired immunity to a different serotype. Classical dengue fever causes negligible mortality, but ADE leads to the risk of developing the significantly more dangerous dengue haemorrhagic fever (DHF) and dengue shock syndrome (DSS). A mathematical model is presented that describes the epidemiological dynamics of two serotypes of a pathogen where there is the possibility of co-infection and reinfection by a different serotype, along with increased mortality as a result of enhancement. We show that if there is no or slightly increased mortality after reinfection (enhancement), serotypes with a small immunological distance can stably coexist. This suggests that a cloud of serotypes with minor serological differences will constitute the viral population. By contrast, if enhancement is sufficiently great, a substantial immunological distance is necessary for two serotypes to stably coexist in the population. Therefore, high mortality owing to enhancement leads to an evolutionarily stable viral community comprising a set of distantly separated serotypes.

Antibody-Dependent Enhancement↗
PubMed1995

Molecular epidemiology of dengue-1 and dengue-4 viruses.

Genetic variation between geographically and temporally distinct isolates of dengue-1 (DEN-1) and dengue-4 (DEN-4) viruses was investigated. The nucleotide sequences of a fragment of the envelope protein gene encoding amino acids 28 to 87 of 35 DEN-1 isolates and 28 DEN-4 isolates were determined. Maximum nucleotide sequence variation was 6.9% and 4.9% for DEN-1 and DEN-4 viruses, respectively. Taking a divergence of 6% between the nucleotide sequences as the cut-off value, three genotype groups were defined for DEN-1 viruses, whereas only one was observed for DEN-4 viruses. Molecular analysis of isolates from the South Pacific permits the classification of the recent strains of DEN-1 (1988-1989 epidemics) into a genotype distinct from the genotype which comprises earlier strains. This observation suggests that the recent epidemics were due to the introduction of a new genotype rather than to the re-emergence of the earlier strain.

Animals↗