Showing papers on "Viral evolution published in 2000"
TL;DR: Viruses are now accepted as bona fide etiologic factors of human cancer; these include hepatitis B virus, Epstein-Barr virus, human papillomaviruses, human T-cell leukemia virus type I and hepatitis C virus, plus several candidate human cancer viruses.
Abstract: The RNA and DNA tumor viruses have made fundamental contributions to two major areas of cancer research. Viruses were vital, first, to the discovery and analysis of cellular growth control pathways and the synthesis of current concepts of cancer biology and, second, to the recognition of the etiology of some human cancers. Transforming retroviruses carry oncogenes derived from cellular genes that are involved in mitogenic signalling and growth control. DNA tumor viruses encode oncogenes of viral origin that are essential for viral replication and cell transformation; viral oncoproteins complex with cellular proteins to stimulate cell cycle progression and led to the discovery of tumor suppressors. Viral systems support the concept that cancer development occurs by the accumulation of multiple cooperating events. Viruses are now accepted as bona fide etiologic factors of human cancer; these include hepatitis B virus, Epstein-Barr virus, human papillomaviruses, human T-cell leukemia virus type I and hepatitis C virus, plus several candidate human cancer viruses. It is estimated that 15% of all human tumors worldwide are caused by viruses. The infectious nature of viruses distinguishes them from all other cancer-causing factors; tumor viruses establish long-term persistent infections in humans, with cancer an accidental side effect of viral replication strategies. Viruses are usually not complete carcinogens, and the known human cancer viruses display different roles in transformation. Many years may pass between initial infection and tumor appearance and most infected individuals do not develop cancer, although immunocompromised individuals are at elevated risk of viral-associated cancers. Variable factors that influence viral carcinogenesis are reviewed, including possible synergy between viruses and environmental cofactors. The difficulties in establishing an etiologic role for a virus in human cancer are discussed, as well as the different approaches that proved viral links to cancer. Future directions for tumor virus studies are considered.
397 citations
TL;DR: Evidence is presented that influenza A and B viruses encoding altered viral NS1 proteins are highly attenuated in the mouse host, yet provide protection from challenge with wild-type viruses.
Abstract: We propose a rational approach to the generation of live viral vaccines: alteration of virally encoded type I IFN antagonists to attenuate virulence while retaining immunogenicity. We have explored this concept by using the influenza virus. Previously we have shown that the NS1 protein of influenza A virus possesses anti-IFN activity. We now present evidence that influenza A and B viruses encoding altered viral NS1 proteins are highly attenuated in the mouse host, yet provide protection from challenge with wild-type viruses.
347 citations
TL;DR: This thesis has introduced some properties of RNA viruses that are relevant for studying evolution and tested the role of deleterious and beneficial mutations in the degree of adaptation of vesicular stomatitis virus, a nonsegmented virus of negative strand.
Abstract: RNA viruses are excellent experimental models for studying evolution under the theoretical framework of population genetics. For a proper justification of this thesis we have introduced some properties of RNA viruses that are relevant for studying evolution. On the other hand, population genetics is a reductionistic theory of evolution. It does not consider or make simplistic assumptions on the transformation laws within and between genotypic and phenotypic spaces. However, such laws are minimized in the case of RNA viruses because the phenotypic space maps onto the genotypic space in a much more linear way than on higher DNA-based organisms. Under experimental conditions, we have tested the role of deleterious and beneficial mutations in the degree of adaptation of vesicular stomatitis virus (VSV), a nonsegmented virus of negative strand. We also have studied how effective population size, initial genetic variability in populations, and environmental heterogeneity shapes the impact of mutations in the evolution of vesicular stomatitis virus. Finally, in an integrative attempt, we discuss pros and cons of the quasispecies theory compared with classic population genetics models for haploid organisms to explain the evolution of RNA viruses.
183 citations
TL;DR: Advances in the understanding of host plant response to virus infection reveal some generalized patterns of host defense to a diversity of viruses.
153 citations
TL;DR: It is suggested that the majority of the mutations in both lineages were fixed as a result of successive sampling, from the heterogeneous populations, of random portions containing predominantly neutral and possibly adverse mutations.
Abstract: We determined nucleotide sequences of the VP1 and 2AB genes and portions of the 2C and 3D genes of two evolving poliovirus lineages: circulating wild viruses of T geotype and Sabin vaccine-derived isolates from an immunodeficient patient. Different regions of the viral RNA were found to evolve nonsynchronously, and the rate of evolution of the 2AB region in the vaccine-derived population was not constant throughout its history. Synonymous replacements occurred not completely randomly, suggesting the need for conservation of certain rare codons (possibly to control translation elongation) and the existence of unidentified constraints in the viral RNA structure. Nevertheless the major contribution to the evolution of the two lineages came from linear accumulation of synonymous substitutions. Therefore, in agreement with current theories of viral evolution, we suggest that the majority of the mutations in both lineages were fixed as a result of successive sampling, from the heterogeneous populations, of random portions containing predominantly neutral and possibly adverse mutations. As a result of such a mode of evolution, the virus fitness may be maintained at a more or less constant level or may decrease unless more-fit variants are stochastically generated. The proposed unifying model of natural poliovirus evolution has important implications for the epidemiology of poliomyelitis.
140 citations
TL;DR: It is likely that the numerous infections of poultry and other birds with H9 subtype influenza viruses during the 1990s originate from separate introductions from feral birds.
Abstract: A 380 nucleotide region (bases 613 to 992) of the HA1 part of the haemagglutinin (H) gene was obtained for 35 influenza viruses of H9 subtype isolated from around the world over the past 33 years. These were analyzed phylogenetically and compared with sequences from 19 H9 subtype viruses available in the Genbank database. These viruses do not show such clear geographical lineages as other subtypes (i.e. H5 or H7) and there is a high degree of variation at the cleavage site of the haemagglutinin. Genetically distinct lineages of H9 viruses have circulated contemporaneously in different locations. Thus, it is likely that the numerous infections of poultry and other birds with H9 subtype influenza viruses during the 1990s originate from separate introductions from feral birds. The observed heterogeneity of these viruses may reflect the gene pool for H9 viruses, which is maintained in shorebirds and gulls (Charadriiformes).
139 citations
TL;DR: These events established that avian viruses could infect humans without acquiring human influenza genes by reassortment in an intermediate host and highlighted challenges associated with the detection of human immune responses to avian influenza viruses and the development of appropriate vaccines.
Abstract: Avian species, particularly waterfowl, are the natural hosts of influenza A viruses. Influenza viruses bearing each of the 15 hemagglutinin and nine neuraminidase subtypes infect birds and serve as a reservoir from which influenza viruses or genes are introduced into the human population. Viruses with novel hemagglutinin genes derived from avian influenza viruses, with or without other accompanying avian influenza virus genes, have the potential for pandemic spread when the human population lacks protective immunity against the new hemagglutinin. Avian influenza viruses were thought to be limited in their ability to directly infect humans until 1997, when 18 human infections with avian influenza H5N1 viruses occurred in Hong Kong. In 1999, two human infections with avian influenza H9N2 viruses were also identified in Hong Kong. These events established that avian viruses could infect humans without acquiring human influenza genes by reassortment in an intermediate host and highlighted challenges associated with the detection of human immune responses to avian influenza viruses and the development of appropriate vaccines.
127 citations
TL;DR: Based on M protein amino acid sequences, NDV separates as a clade most closely related to morbilliviruses and not with their current designated category, the rubulaviruses among the Paramyxoviridae, Consequently, avian paramyxoviruses should have their own taxonomic subfamily among theParamyxvirinae.
86 citations
TL;DR: Currently, deletion mutants appear to be outcompeting nondeleted viruses in the field, highlighting the importance of the porcine antibody response against the minor structural glycoproteins of European-type PRRSV for viral evolution.
71 citations
TL;DR: The likely origin of the H5N1 viruses has been deduced from molecular analysis of these and other viruses isolated from the region from which the molecular basis for these avian viruses to infect humans is identified.
Abstract: The original article to which this Erratum refers was published in Reviews in Medical Virology 10(4) 2000, 255-277.
63 citations
TL;DR: This review focuses on the genetic patchwork of retroviruses and how mixing of sequence patches by recombination may lead to repair in terms of re-established replication and facilitate increased viral fitness, enhanced pathogenic potential, and altered virus tropisms.
Abstract: Retroviral particles contain a diploid RNA genome which serves as template for the synthesis of double-stranded DNA in a complex process guided by virus-encoded reverse transcriptase. The dimeric nature of the genome allows the proceeding polymerase to switch templates during copying of the copackaged RNA molecules, leading to the generation of recombinant proviruses that harbor genetic information derived from both parental RNAs. Template switching abilities of reverse transcriptase facilitate the development of mosaic retroviruses with altered functional properties and thereby contribute to the restoration and evolution of retroviruses facing altering selective forces of their environment. This review focuses on the genetic patchwork of retroviruses and how mixing of sequence patches by recombination may lead to repair in terms of re-established replication and facilitate increased viral fitness, enhanced pathogenic potential, and altered virus tropisms. Endogenous retroelements represent an affluent source of functional viral sequences which may hitchhike with virions and serve as sequence donors in patch repair. We describe here the involvement of endogenous viruses in genetic reassortment and patch repair and review important examples derived from cell culture and animal studies. Moreover, we discuss how the patch repair phenomenon may challenge both safe usage of retrovirus-based gene vehicles in human gene therapy and the use of animal organs as xenografts in humans. Finally, the ongoing mixing of distinct human immunodeficiency virus strains and its implications for antiviral treatment is discussed.
TL;DR: It is found that CTL-induced pathology is observed if the rate of viral replication is fast relative to the CTL responsiveness of the host, and according to the model, fast viral replication can result in the evolution of virus strains that are susceptible to chemokine-mediated inhibition ofiral replication.
TL;DR: Here, relative sequence diversification of different proteins encoded by viral genomes is found to be linear, indicating that adaptive immunity doesn't necessarily shape the relative accumulation of amino acid substitutions.
Abstract: RNA viruses and retroviruses fix substitutions approximately 1 million-fold faster than their hosts. This diversification could represent an inevitable drift under purifying selection, the majority of substitutions being phenotypically neutral. The alternative is to suppose that most fixed mutations are beneficial to the virus, allowing it to keep ahead of the host and/or host population. Here, relative sequence diversification of different proteins encoded by viral genomes is found to be linear. The examples encompass a wide variety of retroviruses and RNA viruses. The smoothness of relative divergence spans quasispeciation following clonal infection, to variation among different isolates of the same virus, to viruses from different species or those associated with different diseases, indicating that the majority of fixed mutations likely reflects drift. This held for both mammalian and plant viruses, indicating that adaptive immunity doesn't necessarily shape the relative accumulation of amino acid substitutions. When compared to their hosts RNA viruses evolution appears conservative.
TL;DR: The model shows that coexistence between coviruses and the self-sufficient viruses that spawned them is unlikely, and describes an abrupt transition from mutualistic two-species to single-species dynamics, showing a new sense in which questions such as 'Is a lichen one species or two?' can be given a definite answer.
Abstract: Coviruses are viruses with the property that their genetic information is divided up among two or more different viral particles. I model the evolution of coviruses using information on both viral virulence and the interactions between viruses and molecules that parasitize them: satellite viruses, satellite RNAs and defective interfering viruses. The model ultimately, and inevitably contains within it single-species dynamics as well as mutualistic, parasitic, cooperative and competitive relationships. The model shows that coexistence between coviruses and the self-sufficient viruses that spawned them is unlikely, in the sense that the quantitative conditions for coexistence are not easy to satisfy I also describe an abrupt transition from mutualistic two-species to single-species dynamics, showing a new sense in which questions such as 'Is a lichen one species or two?' can be given a definite answer.
TL;DR: In this review, cellular homologues encoded by human herpesviruses are focused on and the functional consequences of their expression are discussed.
Abstract: For millions of years viruses have adapted strategies to interfere with the immune defense of the host, which in turn has to deal with this challenge. In general the antiviral defense remains one step behind the pathogen. To achieve this strategic advantage large DNA-containing Viruses encode cellular homologues that mimic or counteract key molecules of the host immune system. Understanding how these cellular homologues enable the viruses to evade the antiviral defense and persist in the host for the lifetime will ultimatively lead also to a better understanding of the principle functions of the immune system. In this review we focused on cellular homologues encoded by human herpesviruses and discuss the functional consequences of their expression.
TL;DR: Experimental evidence for the effects of mutation, selection, and genetic drift on the adaptation and extinction of RNA viruses is reviewed.
Abstract: From a population standpoint, two main features characterize the replication of RNA viruses and viruses that use RNA as a replicative intermediate: high genetic variability, and enormous fluctuations in population size. Their genetic variability mainly reflects a lack of the proof-reading and post-replicative error correction mechanisms that operate during cellular DNA replication, but recombination and segment exchange can also play an important role. Viral population size can change tremendously as a consequence of transmission between hosts or between different tissues within an infected host. A new infection can be initiated with very few particles that subsequently expand many trillion-fold. Repeated bottleneck events can lead to drastic fitness losses or even to viral extinction, whereas continuously large population sizes result in fitness gains and adaptation. Here we review experimental evidence for the effects of mutation, selection, and genetic drift on the adaptation and extinction of RNA viruses.
TL;DR: A review of the use of virus nucleic acid sequences in epidemiological studies can be found in this paper, where examples of how this information can be used to monitor human viruses.
Abstract: Viruses evolve much faster than cellular organisms. Together with recent advances in nucleic acid sequencing and biocomputing, this allows us to distinguish between related strains of viruses, and to deduce the relationships between viruses from different outbreaks or individual patients. Databases of nucleotide sequences contain a large number of viral sequences with which novel sequences from local outbreaks can be compared. In this way the dissemination of viruses can be followed both locally and globally. We here review the biological and technological background to the use of virus nucleic acid sequences in epidemiological studies, and provide examples of how this information can be used to monitor human viruses. Molecular studies are particularly valuable for understanding the dissemination and evolution of viruses. The knowledge obtained is useful in epidemiological reconstructions, in real-time surveillance, and may even enable us to make predictions about the future developments of viral diseases.
TL;DR: The creation of mutators and antimutators during the course of viral infection could play a pivotal role in virus evolution, pathogenesis and emergence, and could also frustrate antiviral therapy.
TL;DR: Hepatitis B viruses replicate by establishing a pool of stable extrachromosomal transcription templates, which allow the virus to react sensitively to changes in its microenvironment by up- or downregulating gene expression.
Abstract: Hepatitis B viruses are DNA viruses characterized by their very small genome size and their unique replication via reverse transcription. The circular genome has been efficiently exploited, thereby limiting genome variation, and leaves no space for genes in addition to those essentially needed during the viral live cycle. Hepatitis B viruses are prototype non-cytopathic viruses causing persistent infection. Human hepatitis B virus (HBV), as well as the closely related animal viruses, most frequently are transmitted vertically from mothers to their offspring. Because infection usually persists for many years, if not lifelong, hepatitis B viruses need efficient mechanisms to hide from the immune response of the host. To escape the immune response, they exploit different strategies. Firstly, they use their structural and non-structural proteins multiplely. One of the purposes is to alter the immune response. Secondly, they replicate by establishing a pool of stable extrachromosomal transcription templates, which allow the virus to react sensitively to changes in its microenvironment by up- or downregulating gene expression. Thirdly, hepatitis B viruses replicate in the liver which is an immunopriviledged site.
1 Jan 2000
TL;DR: In this paper, the authors focus on some of the fundamental aspects of transmission, and effects of viruses on individuals and on host populations, focusing on the evolution of viruses in the wild.
Abstract: This chapter deals with the ecology of insect viruses. It focuses on some of the fundamental aspects of transmission, and effects of viruses on individuals and on host populations. Insect viruses can be categorized as being occluded or non-occluded, of being DNA or RNA viruses, and of replicating in the nucleus or cytoplasm of cells. Two general pathways of virus transmission are horizontal, among individuals in the same generation, and between generations through environmental contamination, and vertical, directly from parents to offspring. Virulence is the level of host mortality resulting from parasite infection. Virulent pathogens have high rates of replication within the host. The virulence of insect viruses depends on the type of virus, the host species infected, the age of the host, and variation in resistance between individuals and populations. Virulence may depend on the host species infected.
TL;DR: Results show that in HIV-infected children, multiple variants may initiate infection and early quasispecies diversification is associated with a favorable clinical outcome.
Abstract: The evolution of HIV-1 quasispecies in patients during the first year of life was investigated in 10 vertically infected infants, using heteroduplex analysis of the V3-V5 region of env. Four subjects, who showed little viral evolution during the period of the study, had rapid progression of disease and early loss of CD4(+) cells. The remaining six subjects, who were slow progressors, evolved new viral variants within 6 months, and in one case by 1 month of age. Of the four patients who were PCR positive at birth, one was infected with multiple HIV-1 variants. These results show that in HIV-infected children, multiple variants may initiate infection and early quasispecies diversification is associated with a favorable clinical outcome.
TL;DR: It is proposed that the capture of a ligand gene of the host cells into the viral genome may be one of the important mechanisms of viral evolution to expand its host range and generate new viral species.
TL;DR: Evaluated the extent of variation in the major proviral HIV‐1 population by monitoring proviral DNA sequences in patients receiving potent antiretroviral therapy over a time period of up to 30 months.
Abstract: Different experimental approaches have shown that, despite plasma viral loads under the threshold of detection, HIV-1 frequently continues to replicate in patients receiving potent antiretroviral therapy. However, whether this low-grade viral replication is sufficient for the generation of new major quasispecies has not been studied. Thus, in order to evaluate the extent of variation in the major proviral HIV-1 population, we monitored proviral DNA sequences in such patients over a time period of up to 30 months.
Methods DNA was extracted from peripheral blood mononuclear cells (PBMC) and the V3 region was amplified by nested polymerase chain reaction (PCR) and directly sequenced. Additionally, both HIV-1 RNA and DNA levels and CD4+ T-lymphocyte counts were monitored.
Results Analysing the V3 gene sequences of 17 patients, we observed a sequence evolution in nine patients. Interestingly, the majority of these changes (77%) occurred in the first interval following the initiation of therapy and despite signs of ongoing replication the proviral DNA levels continued to decrease in all patients.
Conclusions Our data suggest that, although available data report that HIV-1 continues to replicate in patients with undetectable viraemia, the extent of viral replication in many of these patients is not sufficient to result in changes in the major viral population.
1 Jan 2000
TL;DR: This chapter deals with the ecology of viruses of cold-blooded vertebrates, which are obligate intracellular parasites whose survival is dependent on how successfully they interact with their host at both the cellular and organismic levels.
Abstract: This chapter deals with the ecology of viruses of cold-blooded vertebrates. Viruses are obligate intracellular parasites whose survival is dependent on how successfully they interact with their host at both the cellular and organismic levels. To complete their “life cycle,” viruses must attach to and replicate within permissive cells, spread from the site of primary infection to specific target tissues, evade the host immune response, and successfully infect another host. The mechanisms by which viruses accomplish these diverse tasks comprise the subject of viral ecology. The host immune response contributes significantly to the success or failure of a given pathogen because virus replication occurs within cells of an infected organism. Too vigorous an immune response eliminates the virus before it has the opportunity to ensure its efficient transmission, whereas too slow an immune response may lead to the death of the host and loss of the species required to sustain its continued existence.
1 Jan 2000
TL;DR: The totiviruses are discussed, which comprise a subgroup of the fungal and protozoan viruses, which are present in phyla separated by a billion years of evolution and are recognizably related to each other and to no other class of viruses.
Abstract: This chapter discusses viruses of fungi and protozoans. There are two extreme strategies for survival pursued by pathogens: killing the host and spreading rapidly, and coexisting with the host, sometimes providing a selective advantage. This chapter discusses the totiviruses, which comprise a subgroup of the fungal and protozoan viruses. With a single essential double stranded RNA (dsRNA), the totiviruses are present in phyla separated by a billion years of evolution and are recognizably related to each other and to no other class of viruses. This chapter outlines the structure of the viral dsRNAs. Saccharomyces cerevisiae (ScV) strains contain virus particles in the cytoplasm, in which segmented dsRNAs are separately encapsidated, and there is a single essential dsRNA. It presents relationships among dsRNA viruses of lower eukaryotes, and discusses the polymerase domain in the dsRNA viruses of lower eukaryotes, satellite viruses, and other viral symbionts in fungi.
TL;DR: The authors summarise current knowledge on the structure of quasispecies, and the biological implications of this structure.
Abstract: Ribonucleic acid (RNA) viruses evolve as complex distributions of genetically different but closely related variants termed viral quasispecies. The precise genome of a quasispecies cannot be defined, since the consensus genome is an average of many variants. The dynamics of quasispecies has considerable implications for the understanding of the adaptability and pathogenic potential of viruses, and in addition, for the design of preventive and therapeutic measures for the diseases caused by these viruses. The authors summarise current knowledge on the structure of quasispecies, and the biological implications of this structure.
TL;DR: The Fifth European Workshop on Virus Evolution and Molecular Epidemiology was held in Leuven, Belgium, from 30 August to 4 September 1999.
Journal Article•
TL;DR: Viral persistence can cause manifestations of latent or chronic infections, as well as prion-caused slow infections of the central nervous system and defective Di particles play an important role in maintaining viral persistence.
Abstract: The current studies show that viral infections can cause not only acute, but also persistent viral diseases. A certain number of viruses are able to incorporate their nucleic acid into the genome of the host-cell, leading to rearrangement of the cell genes and formation of malignant tumors. Viral persistence can cause manifestations of latent or chronic infections, as well as prion-caused slow infections of the central nervous system. Defective Di particles play an important role in maintaining viral persistence. Viruses are important agents involved in various disorders of the immunological homeostasis of the organism.
TL;DR: This chapter discusses viral vector designs and their applications, and efforts to eliminate viral genes involved in disease have met with considerable success, but even viral structural proteins in high concentrations can result in toxicity.
Abstract: Publisher Summary This chapter discusses viral vector designs and their applications. Effective human gene therapy depends on the efficient delivery and appropriate expression of therapeutic genes. Attempts to solve the gene delivery problem have used a variety of strategies, including naked DNA, DNA bound by lipids and/or facilitating proteins, and recombinant viruses. Viruses remain attractive as potential gene-delivery vehicles, because they are highly evolved for the invasion of organisms and the delivery of genetic material to cells. Some viruses naturally establish long-term persistence or may express genes in specific cell types. The use of viruses for gene delivery has two obvious drawbacks—namely, (1) most viruses cause disease and (2) many tissues where gene therapy is required are not known to harbor latent or persistent viruses. Although efforts to eliminate viral genes involved in disease have met with considerable success, even viral structural proteins in high concentrations can result in toxicity. Highly mutated viruses can no longer replicate, and thus technology for producing viral vectors by the complementation of defective genes using complementing cells or packaging systems is impeded by low vector yields and contamination with wild-type virus rescuants.