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At least 1,063 records · Page 59Linked to original sources
PubMed2006

Epistasis correlates to genomic complexity.

Whether systematic genetic interactions (epistasis) occur at the genomic scale remains a challenging topic in evolutionary biology. Epistasis should make a significant contribution to variation in complex traits and influence the evolution of genetic systems as sex, diploidy, dominance, or the contamination of genomes with deleterious mutations. We have collected data from widely different organisms and quantified epistasis in a common, per-generation scale. Simpler genomes, such as those of RNA viruses, display antagonistic epistasis (mutations have smaller effects together than expected); bacterial microorganisms do not apparently deviate from independent effects, whereas in multicellular eukaryotes, a transition toward synergistic epistasis occurs (mutations have larger effects together than expected). We propose that antagonistic epistasis might be a property of compact genomes with few nonpleiotropic biological functions, whereas in complex genomes, synergism might emerge from mutational robustness.

Animals↗
PubMed1999

The Yersinia high-pathogenicity island.

A pathogenicity island present only in highly pathogenic strains of Yersinia (Y. enterocolitica 1B, Y. pseudotuberculosis I and Y. pestis) has been identified on the chromosome of Yersinia spp. and has been designated High-Pathogenicity Island (HPI). The Yersinia HPI carries a cluster of genes involved in the biosynthesis, transport and regulation of the siderophore yersiniabactin. The major function of this island is thus to acquire iron molecules essential for in vivo bacterial growth and dissemination. The presence of an integrase gene and att sites homologous to those of phage P4, together with a G + C content much higher than the chromosomal background, suggests that the HPI is of foreign origin and has been acquired by chromosomal integration of a phage. The HPI can excise from the chromosome of Y. pseudotuberculosis and is found inserted into any of the three copies of the asn tRNA loci present in this species. A unique characteristic of the HPI is its wide distribution in various enterobacteria. Although first identified in Yersinia spp., it has subsequently been detected in other genera such as E. coli, Klebsiella and Citrobacter.

Bacteriophages↗
PubMed2006

Hepatitis B virus genetic diversity.

Hepatitis B virus (HBV) is a human DNA virus, which replicates through an RNA intermediate because of the reverse-transcriptase (RT) activity of its DNA polymerase. As a result, the mutation rate for HBV is higher than the rate observed for most DNA viruses. HBVs are classified into genotypes based on genomic sequencing, and antigenic subtypes based on the antigenic properties of its major surface glycoprotein, the HBV surface antigen (HBsAg). Subgenotypes have been identified within most of the HBV genotypes. The HBV groups defined by the different genotype-HBsAg subtype associations found over the world display characteristic geographical distributions, reflecting the movements of human populations and other epidemiologically significant events. Such HBV groups constitute genetically stable viral populations sharing a common evolutionary history, but additional stable changes, originating from mutation and mutant selection, are observed within all of them. These viral sub-populations are known as the HBV variants, and some of which have medical and public health relevance. Pre-core (pre-C) defective variants have been shown to make HBV infection much less susceptible to interferon treatment, and treatment failures with other antiviral drugs have been associated with selection of resistant variants that display specific mutations in the genome region encoding the viral RT activity. Since the RT region of the genome overlaps the sequence encoding the HBsAg molecule, selection of drug resistant variants involves, in some cases, the indirect selection of HBsAg variants. Viral variants displaying changes in HBsAg seem to be very common among chronic HBV carriers; and some of these variants may emerge under the pressure of the neutralizing antibody response, leading to vaccine resistance and resistance to immunotherapy. Mutations conferring resistance to immunotherapy are noted often among liver transplant recipients and among babies born to HBV-carrier mothers. In addition, some of these HBsAg variants have been associated with lack of detection by HBsAg tests used for the diagnosis of HBV infection, for the identification of chronic carriers, for screening of blood donations for transfusion, and in the manufacture of therapeutic blood products.

Antiviral Agents↗
PubMed1980

Conserved sequence related to the 3'-terminal region of retrovirus RNA'S In normal cellular DNAs.

The nucleotide sequences related to the 3'-terminal protion of retrovirus genomic RNA have been detected in the DNA of animals, including humans. The DNA complementary to the 400 to 700 nucleotides from the 3'-terminal end of retrovirus RNA (cDNA3'), which contains the enriched conserved region, was hybridized with DNA from a variety of animal cells. Under the conditions of annealing in 0.72 M NaCl at 67 degrees C and hydroxyapatite chromatography at 55 degrees C, 20 to 50% of the radioactivity of the cDNA3' prepared from two retroviruses, a murine Rauscher virus (RLV) and a baboon virus (M7), annealed with normal cellular DNA of animals, including human tissue. The thermal denaturation profile revealed considerable mismatching between the duplex of the cDNA3' and human DNA, cDNA3' of retroviruses is most homologous to cellular DNA of the host species of origin and is less homologous to cellular DNA of species that are distant in the phylogeny of the host species. The conservation and evolution of nucleotide sequences related to the 3' end of retrovirus genomes in animal DNAs, including humans, suggest that the sequences may have important functions.

Animals↗
PubMed1997

Evolution of human immunodeficiency virus type 1 env sequence variation in patients with diverse rates of disease progression and T-cell function.

We examined the relationship between env sequence variation and disease progression in 10 human immunodeficiency virus type 1 (HIV-1)-seropositive subjects selected from a longitudinal cohort receiving zidovudine therapy. Five subjects were chosen for stable clinical status and CD4 counts (slow progressors), and five were selected for rapid clinical deterioration and CD4 count decline (rapid progressors). The slow progressors had significantly lower plasma viral RNA loads and greater lymphoproliferative responses to mitogens than the rapid progressors. DNA sequences representing the C1 through C3 regions of env were amplified from two peripheral blood mononuclear cell DNA samples from each subject separated by an average of 2.5 years. Molecular clones of these amplicons were then sequenced, and DNA sequence and deduced amino acid sequence distances were compared. Inter-time point sequence comparison showed a higher rate of sequence evolution for the rapid progressors in three of five matched pairs of rapid progressors and slow progressors and for the slow progressors in the remaining two subject pairs. However, intra-time point sequence comparisons showed that four of five slow progressors developed a more diverse quasispecies over time and one showed no change. In contrast, four of five rapid progressors showed no change in quasispecies diversity over time and one showed a significant decrease in diversity. The overall C1 through C3 region quasispecies diversity in the slow progressors at baseline was lower than that for the rapid progressors, but this difference was not significant at the follow-up time points. These diversity relationships were obscured if sequence analyses were limited to the 300-bp C2 to V3 region. Thus, HIV-1 quasispecies diversity increased over time in subjects with more functional immune systems.

Base Sequence↗
PubMed1993

Genetic and antigenic analyses of influenza A (H1N1) viruses, 1986-1991.

Eighteen strains of human influenza A (H1N1) viruses isolated between August 1986 and January 1991 were analyzed in this study. Examination of the total viral genome of 12 strains by T1 mapping revealed that considerable genetic heterogeneity exists among these viruses. Partial sequencing of each of the non-HA RNA segments of 4 viruses having divergent T1 oligonucleotide maps indicated that only one was a reassortant virus that had genes from both the influenza A (H1N1) and (H3N2) subtypes. This reassortant obtained its PB2 gene from a virus of the H3N2 subtype and the other 7 RNA segments from an H1N1 parent. Sequencing studies of the HA1 domains of the hemagglutinin (HA) genes of these 18 strains revealed that although these viruses are antigenically similar to the reference strains A/Taiwan/1/86 and A/Singapore/6/86, 7 conserved amino acid substitutions that are shared by recently isolated H1N1 viruses have occurred in the main stream of evolution of the H1N1 subtype. Our data indicate that: (1) Genetic reassortment continues to contribute to genetic variability of H1N1 viruses. (2) Genetic variants of non-reassortant H1N1 viruses are co-circulating in the world. (3) The HA's of recent H1N1 viruses are related to those of the 1986 reference strains. (4) Although there has been little detectable antigenic variability, the HA genes of human epidemic influenza A (H1N1) viruses have continued to evolve at an evolutionary rate similar to that for the H1N1 and H3N2 viruses analyzed previously.

Amino Acid Sequence↗
PubMed2006

Direct repeats in the 3' untranslated regions of mosquito-borne flaviviruses: possible implications for virus transmission.

Direct repeats (DRs) of 20-45 nucleotide conserved sequences (CS) and repeated CS (RCS), separated by non-conserved sequences up to 100 nucleotides long, were previously described in the 3' untranslated region (3'UTR) of the three major mosquito-borne flavivirus (MBFV) subgroups, represented by Japanese encephalitis virus, Yellow fever virus and Dengue virus. Each subgroup exhibits a specific pattern of DRs, the biological significance of which has not yet been adequately addressed. The DRs were originally identified using conventional alignment programs based on the assumption that genetic variation is driven primarily by nucleotide substitutions. Since there are no recognized alignment programs that can adequately accommodate very divergent sequences, a method has been devised to construct and analyse a substantially improved 3'UTR alignment between these highly divergent viruses, based on the concept that deletions and/or insertions, in addition to substitutions, are important drivers of 3'UTR evolution. This 'robust alignment' approach demonstrated more extensive homologies in the 3'UTR than had been recognized previously and revealed the presence of similar DRs, either intact or as sequence 'remnants', in all the MBFV subgroups. The relevance of these observations is discussed in relation to (i) the function of DRs as elements of replication enhancement, (ii) the evolution of RNA secondary structures and (iii) the significance of DRs and secondary structures in MBFV transmissibility between vertebrate and invertebrate hosts.

3' Untranslated Regions↗
PubMed1995

Nucleotide sequence variation of the envelope protein gene identifies two distinct genotypes of yellow fever virus.

The evolution of yellow fever virus over 67 years was investigated by comparing the nucleotide sequences of the envelope (E) protein genes of 20 viruses isolated in Africa, the Caribbean, and South America. Uniformly weighted parsimony algorithm analysis defined two major evolutionary yellow fever virus lineages designated E genotypes I and II. E genotype I contained viruses isolated from East and Central Africa. E genotype II viruses were divided into two sublineages: IIA viruses from West Africa and IIB viruses from America, except for a 1979 virus isolated from Trinidad (TRINID79A). Unique signature patterns were identified at 111 nucleotide and 12 amino acid positions within the yellow fever virus E gene by signature pattern analysis. Yellow fever viruses from East and Central Africa contained unique signatures at 60 nucleotide and five amino acid positions, those from West Africa contained unique signatures at 25 nucleotide and two amino acid positions, and viruses from America contained such signatures at 30 nucleotide and five amino acid positions in the E gene. The dissemination of yellow fever viruses from Africa to the Americas is supported by the close genetic relatedness of genotype IIA and IIB viruses and genetic evidence of a possible second introduction of yellow fever virus from West Africa, as illustrated by the TRINID79A virus isolate. The E protein genes of American IIB yellow fever viruses had higher frequencies of amino acid substitutions than did genes of yellow fever viruses of genotypes I and IIA on the basis of comparisons with a consensus amino acid sequence for the yellow fever E gene. The great variation in the E proteins of American yellow fever virus probably results from positive selection imposed by virus interaction with different species of mosquitoes or nonhuman primates in the Americas.

Aedes↗
PubMed2006

SIV Vpr evolution is inversely related to disease progression in a morphine-dependent rhesus macaque model of AIDS.

Three of six morphine-dependent monkeys progressed rapidly to AIDS and died by 20 weeks in our SIV/SHIV non-human primate model of drug addiction and AIDS. We studied the evolution of the SIV vpr gene in both cerebrospinal fluid (CSF) and plasma in these rapid progressors, in their normal progressor counterparts and in infected, drug-free controls at 12 and 20 weeks post infection. Viral RNA was amplified, cloned, and sequenced to permit phylogenetic analyses of diversity and divergence of the vpr locus. As we found for SIV tat and env, the vpr gene evolves inversely to the rate of disease progression. Further, we found evidence that compartmentalization of the virus in plasma and CSF is significantly greater in the normal progressors than in the morphine-dependent, rapid progressors. Interestingly, although our previous work with the accessory gene nef indicated no association between disease progression and evolution, the accessory factor, vpr, behaves similarly to the essential lentiviral genes tat and env.

Acquired Immunodeficiency Syndrome↗
PubMed2005

Viral evolution of hepatitis C in injection drug users.

Injection drug users represent the largest cohort of patients with established hepatitis C virus (HCV) infection as well as the group that is at highest risk for new infections. Most published studies have focused on the clinical consequences of established HCV infection and have not examined the consequences of new infection. The aim of the current study was to measure the virological consequences of HCV in patients with ongoing injection drug use that might pose a risk for new and/or for superinfection with additional strains of HCV. We examined the following groups: (a) those with resolved HCV infection with ongoing injection drug use, (b) those with chronic infection who continued to inject and (c) those with chronic infection who no longer injected. Our study demonstrated a spectrum of responses. The majority of patients appeared to be 'protected' from new infection. None of six patients with resolved infection had detectable HCV RNA by quantitative or qualitative PCR when followed for 1 year. Similarly, despite ongoing injection drug use, no patient with persistent infection had a 'switch' in HCV genotype indicative of possible superinfection. Virological analysis of HCV quasispecies to detect possible infection with new variants of HCV in patients with apparently 'stable' infection, indicated divergence of virus over time, divergence that was unrelated to injection drug behaviour. Thus, patients with ongoing or prior HCV infection appear to develop immunity that protects against further infection with HCV despite repeated exposure.

Adult↗
PubMed1987

Molecular evolution and phylogeny of the human AIDS viruses LAV, HTLV-III, and ARV.

A phylogenetic tree for the human lymphadenopathy-associated virus (LAV), the human T-cell lymphotrophic virus type III (HTLV-III), and the acquired immune deficiency syndrome (AIDS)-associated retrovirus (ARV) has been constructed from comparisons of the amino acid sequences of their gag proteins. A method is proposed for estimating the divergence times among these AIDS viruses and the rates of nucleotide substitution for their RNA genomes. The analysis indicates that the LAV and HTLV-III strains diverged from one another after 1977 and that their common ancestor diverged from the ARV virus no more than 10 years earlier. Hence, the evolutionary diversity among strains of the AIDS viruses apparently has been generated within the last 20 years. It is estimated that the genome of the AIDS virus has a nucleotide substitution rate on the order of 10(-3) per site per year, with the rate in the second half of the genome being double that in the first half.

Biological Evolution↗
PubMed2003

Characterization and evolution of NS5A quasispecies of hepatitis C virus genotype 1b in patients with different stages of liver disease.

The quasispecies nature of hepatitis C virus (HCV) is thought to play a central role in modulating viral functions. Recent work has linked NS5A protein with viral replication, resistance to interferon (IFN), and control of cellular growth, probably through the interaction of its protein kinase R (double stranded RNA-activated protein kinase, PKR) binding domain (PKR-bd) with cellular PKR, but knowledge of how PKR-bd viral population evolves during disease progression is limited. Since we have previously described an association between amino acid composition of the PKR-bd and the presence of HCC, in this report we further investigated the dynamic behavior of viral population parameters by sequencing an average of 20 clones per sample in 27 samples from 19 untreated patients with different degrees of liver disease, 8 of whom were followed over time. Viral population parameters varied widely from patient to patient, but no differences were observed in the complexity, diversity, types of nucleotide changes, or evolutionary pattern of the quasispecies according to the stage of liver disease. In five samples, we detected "quasispecies-tails"; that is, clones whose minimum genetic distance to the remaining clones of their own quasispecies were higher than the maximum genetic distance found between any other two clones of the same sample. In summary, independent of the degree of liver disease, or the mutations detected within the consensus sequence of the PKR-bd, the NS5A of HCV presents a flexible and variable quasispecies structure that remains largely stable during the natural course of an HCV infection, highlighting the central role of NS5A protein in viral life cycle.

Amino Acid Sequence↗
PubMed1984

Nucleotide sequence of a cloned duck hepatitis B virus genome: comparison with woodchuck and human hepatitis B virus sequences.

The nucleotide sequence of an EcoRI duck hepatitis B virus (DHBV) clone was elucidated by using the Maxam and Gilbert method. This sequence, which is 3,021 nucleotides long, was compared with the two previously analyzed hepatitis B-like viruses (human and woodchuck). From this comparison, it was shown that DHBV is derived from an ancestor common to the two others but has a slightly different genomic organization. There was no intergenic region between genes 5 and 8, which were fused into a single open reading frame in DHBV. Genes for the surface and core proteins were assigned to open reading frames 7 and 5/8. Amino acid comparisons showed some structural relationship between gene 6 product and avian reverse transcriptase, suggesting either evolution from a common ancestor or convergence to some particular structure to fulfill a specific function. This should be correlated with the synthesis of an RNA intermediate during DNA replication. This is also taken as an argument in favor of the hypothesis that gene 6 codes for the DNA polymerase that is found within the virion. DNA sequence comparison also showed that the two mammalian hepatitis B viruses are more homologous to each other than they are to DHBV, indicating that DHBV starts to evolve on its own earlier than the two other viruses, as do birds compared with mammals. From this it is proposed that the viruses evolved in a fashion parallel to the species they infect.

Amino Acid Sequence↗
PubMed2006

Murine retrovirus escapes from murine APOBEC3 via two distinct novel mechanisms.

APOBEC3G (A3G) is an antiretroviral host factor that functions by deaminating dC to dU in retroviral cDNA. HIV-1 Vif protein counteracts A3G via a ubiquitin-proteasome pathway. In the case of a simple retrovirus such as the murine leukemia virus (MLV), it remains unclear why it can replicate in cells expressing APOBEC3 (A3) even though it doesn't possess any accessory proteins such as Vif. In this study, we demonstrate that MLV escapes from murine A3 (mA3) via two distinct novel mechanisms. First, viral RNA (vRNA) blocks the binding of mA3 to Gag, resulting in the exclusion of mA3 from MLV virions. Second, viral protease (vPR) cleaves mA3 after maturation of virions. Here, we suggest that each virus has its own strategy to escape from A3 proteins and that these mechanisms might be used by other viruses that do not possess Vif-like protein. On the other hand, mice possess another form of mA3, delta exon5, that escapes from the cleavage by vPR to show more antiviral activity than the wild type mA3. This also suggests that battles between host intrinsic immunity and viruses have led to the evolution of proteins on both sides.

Animals↗
PubMed2006

Analysing the evolutionary history of HCV: puzzle of ancient phylogenetic discordance.

Though recombination is an important evolutionary strategy in RNA viruses, only two cases of HCV recombinant strains have been reported. Our objective was to analyze the evolutionary history of the HCV genotypes aiming to obtain evidence of significant phylogenetic discordance due to either recombination or selective forces leading to convergent/divergent evolution. The data support an evolutionary preservation of the interferon-resistance related genomic region (ISDR) for the genotypes 1 and 4. On the other hand, there was no evidence that recombination has occurred in the past with the possible exception of genotype 4. Moreover, it is evidenced that genotypes 3 and 10 split more recently than genotypes 6-9 and 11. This analysis reverberates a commonly found pattern in rapidly evolving viruses, that is the strongly disturbed evolutionary history which deforms the uniform distribution of the phylogenetic relationships across the genome, and introduces a conservative inference framework for approaching this kind of data.

Evolution, Molecular↗
PubMed2006

Full-length sequence analysis of SIVmus in wild populations of mustached monkeys (Cercopithecus cephus) from Cameroon provides evidence for two co-circulating SIVmus lineages.

Mustached monkeys (Cercopithecus cephus), which form a significant component of primate bushmeat in west central Africa, are infected with simian immunodeficiency virus (SIVmus). We identified and genetically characterized five new SIVmus strains infecting wild living mustached monkeys from Cameroon. Phylogenetic analysis of partial pol sequences revealed that SIVmus strains form two distinct groups within the clade comprised of lentiviruses isolated from Cercopithecus nictitans (SIVgsn), Cercopithecus mona (SIVmon) and C. cephus (SIVmus). Characterisation of three full-length SIVmus genomes confirmed the presence of two distinct lineages infecting mustached monkeys. These two variants of SIVmus, here designated SIVmus-1 and SIVmus-2, were isolated from animals sharing habitats within the same geographic region. Phylogenetic analyses showed that the diversification of SIVmus, SIVgsn and SIVmon involved inter-lineage recombination, and suggested that one of the SIVmus lineages likely resulted from cross-species transmission and recombination involving SIVmus and an as yet uncharacterized SIV. These results indicate that cross-species transmission and recombination play a major role in the evolution of primate lentiviruses among sympatric primate species.

Animals↗