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PubMed2003

Escape from Prisoner's Dilemma in RNA phage phi6.

We previously examined competitive interactions among viruses by allowing the RNA phage phi6 to evolve at high and low multiplicities of infection (ratio of infecting viruses to bacterial cells). Derived high-multiplicity phages were competitively advantaged relative to their ancestors during coinfection, but their fixation caused population fitness to decline. These data conform to the evolution of lowered fitness in a population of defectors, as expected from the Prisoner's Dilemma of game theory. However, the generality of this result is unknown; the evolution of viruses at other multiplicities may alter the fitness payoffs associated with conflicting strategies of cooperation and defection. Here we examine the change in matrix variables by propagating the ancestor under strictly clonal conditions, allowing cooperation the chance to evolve. In competitions involving derived cooperators and their selfish counterparts, our data reveal a new outcome where the two strategies are predicted to coexist in a mixed polymorphism. Thus, we demonstrate that the payoff matrix is not a constant in phi6. Rather, clonal selection allows viruses the opportunity to escape the Prisoner's Dilemma. We discuss mechanisms that may afford selfish genotypes an advantage during intrahost competition and the relevance in our system for alternative ecological interactions among viruses.

Bacteriophage phi 6↗
PubMed1994

Molecular evolution and epidemiology of dengue-3 viruses.

The nucleic acid sequences of the pre-membrane/membrane and envelope protein genes of 23 geographically and temporally distinct dengue (DEN)-3 viruses were determined. This was accomplished by reverse transcriptase-PCR amplification of the structural genes followed by automated DNA sequence analysis. Comparison of nucleic acid sequences revealed that similarity among the viruses was greater than 90%. The similarity among deduced amino acids was between 95% and 100%, and in many cases identical amino acid substitutions occurred among viruses from similar geographical regions. Alignment of nucleic acid sequences followed by parsimony analysis allowed the generation of phylogenetic trees, demonstrating that geographically independent evolution of DEN-3 viruses had occurred. The DEN-3 viruses were separated into four genetically distinct subtypes. Subtype I consists of viruses from Indonesia, Malaysia, the Philippines and the South Pacific islands; subtype II consists of viruses from Thailand; subtype III consists of viruses from Sri Lanka, India, Africa and Samoa; subtype IV consists of viruses from Puerto Rico and the 1965 Tahiti virus. Phylogenetic analysis has also contributed to our understanding of the molecular epidemiology and worldwide distribution of DEN-3 viruses.

Amino Acid Sequence↗
PubMed1997

Evolution of the human immunodeficiency virus type 1 subtype-specific V3 domain is confined to a sequence space with a fixed distance to the subtype consensus.

Human immunodeficiency virus type 1 (HIV-1) strains can be separated into genetic subtypes based on phylogenetic analysis of the envelope gene. Once it had been shown that population-wide intrasubtype genetic variation of HIV-1 strains increases in the course of the AIDS epidemic, it remained uncertain whether HIV-1 subtypes are phenotypic entities spreading as distinct virus populations. To examine this, we applied Eigen's concepts of sequence geometry and fitness topography to the analysis of intrasubtype evolution of the gp120 V3 domain of HIV-1 subtypes A, B, C, and D in the course of the global AIDS epidemic. We observed that despite the high evolution rate of HIV-1, the nonsynonymous distances to the subtype consensus of sequences obtained early in the epidemic are similar to those obtained more than 10 years later, in contrast to the synonymous distances, which increased steadily over time. For HIV-1 subtype B, we observed that the evolution rate of the individual sequences is independent of their distance from the subtype B consensus, but for the individual sequences most distant from the consensus evolution away from the consensus is constrained. As a result, individual HIV-1 genomes fluctuate within a sequence space with fixed distance to the subtype consensus. Our findings suggest that the evolution of the V3 domain of HIV-1 subtypes A, B, C, and D is confined to an area in sequence space within a fixed distance to the consensus of a respective subtype. This in turn indicates that each HIV-1 subtype is a distinct viral quasispecies that is well adapted to the present environment, able to maintain its identity in the V3 region over time, and unlikely to merge during progression of the AIDS epidemic.

Consensus Sequence↗
PubMed2002

Viral evolution during structured treatment interruptions in chronically human immunodeficiency virus-infected individuals.

We analyzed the evolution of the human immunodeficiency virus type 1 (HIV-1) env gene in 12 chronically infected individuals who underwent structured treatment interruptions (STIs). Analyses of length variation and of clonal sequences demonstrated highly unpredictable evolution, which may limit the strengthening of HIV-specific immune responses by STIs because of the variability in exposure to viral antigens.

Adult↗
PubMed2001

On the origin and evolution of the human immunodeficiency virus (HIV).

The human AIDS viruses--HIV-1 and HIV-2--impose major burdens on the health and economic status of many developing countries. Surveys of other animal species have revealed that related viruses--the SIVs are widespread in a large number of African simian primates where they do not appear to cause disease. Phylogenetic analyses indicate that these SIVs are the reservoirs for the human viruses, with SIVsm from the sooty mangabey monkey the most likely source of HIV-2, and SIVcpz from the common chimpanzee the progenitor population for HIV-1. Although it is clear that AIDS has a zoonotic origin, it is less certain when HIV-1 and HIV-2 first entered human populations and whether cross-species viral transmission is common among primates. Within infected individuals the process of HIV evolution takes the form of an arms race, with the virus continually fixing mutations by natural selection which allow it to escape from host immune responses. The arms race is less intense in SIV-infected monkeys, where a weaker immune response generates less selective pressure on the virus. Such a difference in virus-host interaction, along with a broadening of co-receptor usage such that HIV strains are able to infect cells with both CCR5 and CXCR4 chemokine receptors, may explain the increased virulence of HIV in humans compared to SIV in other primates.

Animals↗
PubMed1998

Structured-tree topology and adaptive evolution of the simian immunodeficiency virus SIVsm envelope during serial passage in rhesus macaques according to likelihood mapping and quartet puzzling.

Species-specific strains of simian immunodeficiency virus (SIV) are nonpathogenic in African primates. The SIV strain most closely related to human immunodeficiency virus type 2 (HIV-2) is SIVsm, the strain specific to the sooty mangabey (Cercocebus atys). Infection of Asian primates with SIV causes AIDS and allows the study of the adaptive evolution of a lentivirus to replicate efficiently in a new host, providing a useful animal model of HIV infection and AIDS in humans. Serial passage of SIVsm from sooty mangabeys in rhesus macaques drastically shortened the time of disease progression from 1.5 years to 1 month as the retrovirus adapted to these Asian hosts. In the present study we analyzed the quasispecies nature of the SIVsm envelope gene (env) during serial population passage in rhesus macaques. We asked ourselves if phylogenetic evidence could be provided for the structured topology of the SIVsm env tree and subsequently for the adaptive evolution of SIVsm env. Likelihood mapping showed that phylogenetic reconstruction of the passage was possible because a high percentage of the sequence data had a "tree-like" form. Subsequently, quartet puzzling was used and produced a phylogeny with a structure parallel to the known infection history. The adaptation of SIVsm to Asian rhesus macaques appears to be an ordered process in which the env evolves in a tree-like manner, particularly in its constant regions.

Adaptation, Biological↗
PubMed1998

Phylogenetic analyses of the matrix and non-structural genes of equine influenza viruses.

Matrix (M) and nonstructural (NS) genes of thirteen equine H3N8 and H7N7 influenza viruses were sequenced and analyzed from an evolutionary point of view. The M and NS genes of H3N8 viruses isolated between 1989 and 1993 evolved into two minor branch clusters, including isolates from Europe and the American continent, respectively. It was noteworthy to reveal that the nucleotide sequences of the M and NS genes of an earlier American strain showed highest homology to those of recent European viruses. "Frozen evolution" was observed in the M and NS genes of A/eq/LaPlata/1/88. It was also evident that the NS gene of an H7N7 virus from 1977 was very similar to that of a 1979-H3N8 virus, while the M gene was closest phylogenetically to that of the earliest H7N7 virus isolated in 1956. Furthermore, the M2 protein of A/eq/Newmarket/1/77 virus contained a carboxyl terminal deletion of three amino acids. The evolutionary rates of the M and NS genes of H3N8 equine influenza viruses were estimated to be 5.4 x 10(-4) and 5.1 x 10(-4) substitutions per site per year, respectively, which were slower than those of human viruses.

Amino Acid Sequence↗
PubMed2004

[Comparison of hepatitis C viral RNA and core antigen kinetics in the therapeutic follow up of hepatitis C virus and human immunodeficiency virus co-infected patients, treated by bitherapy interferon-ribavirin, within the framework of RIBAVIC protocol].

AIM OF STUDY: The RIBAVIC protocol, established by ANRS in 2001 and closed in 2003, compared the efficacy and the tolerance of two bitherapy anti-Hepatitis C Virus for HIV-HCV co-infected patients: IFN-ribavirin and PEG-IFN-ribavirin for 48 weeks. Two hundred patients from protocol were tested for hepatitis C virus core antigen, to study this viral marker kinetics, before and under treatment, in comparison with hepatitis C virus RNA evolution. MATERIAL AND METHODS: The available samples for the 204 patients of our study were tested for RNA detection (COBAS AMPLICOR v2.0, Roche Diagnostics) and quantification (VERSANT HCV RNA v3.0, Bayer Diagnostics) and for quantification of core antigen (Ortho trak-C Assay, Ortho Clinical Diagnostics). The viral kinetics were established from samples quantified at D0, W2, W4, W12, W24, W48, W52, W72 (W =week), according to virological response assessed by PCR, six month after the end of treatment (non responders, sustained responders, relapsers et breakthroughs). RESULTS: We obtained, for each type of response, similar evolution of both viral markers. Trak-C assay show to be enough sensitive, with similar results whatever genotype of hepatitis C virus. The Pearson's correlation is excellent (R =0.94; P <0.001). The intergenotype correlation is correct too, whatever HCV genotype (1, 2, 3, 4). CONCLUSIONS: The HCV core antigen quantification by trak-C assay is a new tool for the follow-up of the treatment of patients with chronic hepatitis C and HIV co-infected.

Antigens, Viral↗
PubMed2002

Recent developments in the epidemiology of virus diseases.

There is continual variation in viral epidemics regarding clinical symptoms, duration and disappearance, and the emergence of new diseases. This can be observed in both human and animal diseases. This evolution of virus diseases is mainly related to three factors: aetiological agent, host and environment. As far as genetic alterations of the virus are concerned, two major mechanisms are involved: mutations such as recombination and reassortment; and selection for resistance or susceptibility. This review focuses on the epidemiology of newly emerged virus diseases in man and animals, such as acquired immunodeficiency syndrome, haemorraghic fevers, bovine spongiform encephalopathy, canine haemorraghic disease and respiratory syndrome in horses.

Animals↗
PubMed1993

Viral evolution and insects as a possible virologic turning table.

Three lines of observation demonstrate the role of arthropods in transmission and evolution of viruses. a) Recent outbreaks of viruses from their niches took place and insects have played a major role in propagating the viruses. b) Examination of the list of viral families and their hosts shows that many infect invertebrates (I) and vertebrates (V) or (I) and plants (P) or all kingdoms (VIPs). This notion holds true irrespective of the genome type. At first glance the argument seems to be weak in the case of enveloped and non-enveloped RNA viruses with single-stranded (ss) segmented or non-segmented genomes of positive (+) or negative polarity. Here, there are several families infecting V or P only; no systematic relation to arthropods is found. c) In the non-enveloped plant viruses with ss RNA genomes there is a strong tendency for segmentation and individual packaging of the genome pieces. This is in contrast to ss+ RNA animal viruses and can only be explained by massive transmission by seed or insects or both, because individual packaging necessitates a multihit infection. Comparisons demonstrate relationships in the nonstructural proteins of double-stranded and ss+ RNA viruses irrespective of host range, segmentation, and envelope. Similar conclusions apply for the negative-stranded RNA viruses. Thus, viral supergroups can be created that infect V or P and exploit arthropods for infection or transmission or both. Examples of such relationships and explanations for viral evolution are reviewed and the arthropod orders important for cell culture are given.

Amino Acid Sequence↗
PubMedDate not supplied

Evolution of influenza A(H1N1) viruses during a period of low antigenic drift in 1986-91: sequence of the HA1 domain of influenza A/Finland/158/91.

This study used the nucleotide sequence coding for the HA1 domain of virus haemagglutinin to show that influenza A/Finland/158/91, which represents the H1N1 subtype viruses prevalent in Finland in 1990/91, was a direct descendant of a virus (A/NN/1605/88) isolated during the 1988/89 epidemic season in Japan. The elevated rate of 7.4 x 10(-3) nucleotide substitutions per site per year is discussed. The new branch of H1N1 subtype viruses is characterized by loss of a glycosylation site, which may affect subsequent antigenic drift.

Amino Acid Sequence↗
PubMed1979

Evolution of human influenza A viruses in nature: recombination contributes to genetic variation of H1N1 strains.

In June of 1977, a new influenza A pandemic was started by strains of the H1N1 serotype. Oligonucleotide fingerprint analysis of the RNA from viruses isolated during the early stage of this pandemic demonstrated that genetic variation among these 1977 strains could be attributed to sequential mutation [Young, J.F., Desselberger, U. & Palese, P. (1979) Cell, 18, 73-83]. Examination of more recent strains revealed that the H1N1 variants that were isolated in the winter of 1978-1979 differed considerably from the H1N1 viruses isolated the previous year. Oligonucleotide and peptide map analysis of the new prototype strain (A/Cal/10/78) suggested that it arose by recombination. It appears that only the HA, NA, M, and NS genes of this virus are derived from the earlier H1N1 viruses and that the P1, P2, P3, and NP genes most likely originate from an H3N2 parent. These data suggest that genetic variation in influenza virus strains of the same serotype is not restricted to mutation alone, but can also involve recombination (reassortment).

Antigens, Viral↗
PubMed2004

Frequent human leukocyte antigen class I alleles are associated with higher viral load among HIV type 1 seroconverters in Thailand.

The loss of viral control by the host may be due to the evolution of viruses with mutations that limit presentation by human leukocyte antigen (HLA) to cytotoxic T cells. The authors hypothesized that the consequence of such evolution might be that persons with common HLA class I alleles would be less able to control viremia, on average, than would those with rare alleles. HLA class I typing was completed for 128 injection drug users who seroconverted in a prospective cohort study in Bangkok, Thailand. Logistic regression was used to model viral load (greater than or equal to the median) at 9 and 12 months after seroconversion with an HLA score that profiled the relative prevalence of each individual's alleles. At 12 months after seroconversion, injection drug users with the most common HLA alleles (highest quartile HLA score) had an almost 4-fold increased risk for higher viral load (> or = 32,055 copies/mL) than injection drug users with less common HLA alleles (adjusted odds ratio, 3.92; 95% confidence interval, 1.3-11.8). These findings support the importance of frequency-dependent effects of host genes on HIV type 1 evolution in different populations and suggest that HLA-driven viral evolution critically influences control of viremia in early HIV type 1 infection.

Alleles↗
PubMed1992

Independent evolution of monkeypox and variola viruses.

Smallpox was eradicated more than 10 years ago, but infection with another Orthopoxvirus, monkeypox virus, can result in a clinical picture resembling smallpox. Human infection with monkeypox virus is extremely rare, not easily transmitted, and confined to the rain forest belt of Africa (Z. Jezek and F. Fenner, p. 81-102, in Human Monkeypox, 1988). Evidence that variola virus, the causative agent of smallpox, might be readily derived from monkeypox virus was presented [S. S. Marennikova and E. M. Shelukhina, Nature (London) 276:291-292, 1978; S. S. Marennikova, E. M. Shelukhina, N. N. Maltseva, and G. R. Matsevich Intervirology 11:333-340, 1979], but this was not confirmed [K. R. Dumbell and L. C. Archard, Nature (London) 286:29-32, 1980] and was subsequently discounted (J. J. Esposito, J. H. Nakano, and J. F. Obijeski, Bull. W.H.O. 63:695-703, 1985). Although enough difference between the genomes of monkeypox and variola viruses to rule out a simple interconversion has been demonstrated [K. R. Dumbell and L. C. Archard, Nature (London) 286:29-32, 1980; J. J. Esposito and J. C. Knight, Virology 143:230-251, 1985; J. J. Esposito, J. H. Nakano, and J. F. Obijeski, Bull. W.H.O. 63:695-703, 1985; M. Mackett and L. C. Archard, J. Gen. Virol. 45:683-701, 1979], the possibility that monkeypox virus was a more remote ancestor of variola virus remained. We have now identified a sequence in monkeypox virus DNA which is a homolog of a 1,065-bp open reading frame in the conserved region of the variola virus genome but which has multiple deletions. This is strong evidence that monkeypox virus is not ancestral to variola virus and strengthens confidence in the long-term success of smallpox eradication.

Animals↗
PubMed2002

Genetic diversity and models of viral evolution for the hepatitis C virus.

In this review we discuss the application of theoretical frameworks to the interpretation of viral gene sequence data, with particular reference to the hepatitis C virus (HCV). The increasing availability of such data means that it is now possible (and necessary) to proceed from simple qualitative models of viral evolution, to more quantitative frameworks based on statistical inference, notably population genetics and molecular phylogenetics. We argue that these approaches are invaluable tools to the virologist and are essential for understanding the dynamics of viral infection and the outcome of therapeutic strategies. We use several recent HCV data-sets to illustrate the methods.

Genetic Variation↗
PubMed1992

Evolution of the capsid protein genes of foot-and-mouth disease virus: antigenic variation without accumulation of amino acid substitutions over six decades.

The genetic diversification of foot-and-mouth disease virus (FMDV) of serotype C over a 6-decade period was studied by comparing nucleotide sequences of the capsid protein-coding regions of viruses isolated in Europe, South America, and The Philippines. Phylogenetic trees were derived for VP1 and P1 (VP1, VP2, VP3, and VP4) RNAs by using the least-squares method. Confidence intervals of the derived phylogeny (significance levels of nodes and standard deviations of branch lengths) were placed by application of the bootstrap resampling method. These procedures defined six highly significant major evolutionary lineages and a complex network of sublines for the isolates from South America. In contrast, European isolates are considerably more homogeneous, probably because of the vaccine origin of several of them. The phylogenetic analysis suggests that FMDV CGC Ger/26 (one of the earliest FMDV isolates available) belonged to an evolutionary line which is now apparently extinct. Attempts to date the origin (ancestor) of the FMDVs analyzed met with considerable uncertainty, mainly owing to the stasis noted in European viruses. Remarkably, the evolution of the capsid genes of FMDV was essentially associated with linear accumulation of silent mutations but continuous accumulation of amino acid substitutions was not observed. Thus, the antigenic variation attained by FMDV type C over 6 decades was due to fluctuations among limited combinations of amino acid residues without net accumulation of amino acid replacements over time.

Amino Acid Sequence↗