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At least 127 records · Page 7Linked to original sources
PubMed2001

The evolution of human influenza viruses.

The evolution of influenza viruses results in (i) recurrent annual epidemics of disease that are caused by progressive antigenic drift of influenza A and B viruses due to the mutability of the RNA genome and (ii) infrequent but severe pandemics caused by the emergence of novel influenza A subtypes to which the population has little immunity. The latter characteristic is a consequence of the wide antigenic diversity and peculiar host range of influenza A viruses and the ability of their segmented RNA genomes to undergo frequent genetic reassortment (recombination) during mixed infections. Contrasting features of the evolution of recently circulating influenza AH1N1, AH3N2 and B viruses include the rapid drift of AH3N2 viruses as a single lineage, the slow replacement of successive antigenic variants of AH1N1 viruses and the co-circulation over some 25 years of antigenically and genetically distinct lineages of influenza B viruses. Constant monitoring of changes in the circulating viruses is important for maintaining the efficacy of influenza vaccines in combating disease.

Biological Evolution↗
PubMed2001

An error-prone T7 RNA polymerase mutant generated by directed evolution.

Viruses replicate their genomes at exceptionally high mutation rates. Their offspring evolve rapidly and therefore, are able to evade common immunological and chemical antiviral agents. In parallel, virus genomes cannot tolerate a further increase in mutation rate: Experimental evidence exists that even few additional mutations are sufficient for the extinction of a viral population. A future antiviral strategy might therefore aim at increasing the error-producing capacity of viral replication enzymes. We employed the principles of directed evolution and developed a scheme for the stringent positive selection of error-prone polymerase activity. A mutant T7 RNA polymerase with a nucleotide substitution error rate at least 20-fold greater than that of the wild-type was selected. This enzyme synthesized highly heterogeneous RNA products in vitro or in vivo and also decreased the replication efficiency of wild-type bacteriophage T7 during infection.

Bacteriophage T7↗
PubMed2005

HIV-1 envelope evolution and vaccine efficacy.

Transmission of human immunodeficiency virus type 1 (HIV-1) selects for envelope variants with a number of defined properties, including use of CCR5 as the preferred coreceptor, binding to CCR5 in a distinct manner compared to HIV-1 isolated later in infection, shorter variable (V) regions, and fewer N-linked glycosylation sites. These features define the ideal target for an envelope-containing vaccine designed to elicit neutralizing antibody. If a candidate vaccine were sufficiently potent to elicit sterilizing immunity, virus evolution would not be an issue. However, all results to date suggest that an envelope-containing vaccine will have a lesser impact, and that virus evolution will contribute to escape from the vaccine-induced antibody response. The key question is whether or not the early selection pressure imposed by neutralizing antibody will have a long term impact on HIV disease progression. Several recent reports suggest that HIV-1 will evolve to rapidly escape antibody selection, and that the cost to the virus in terms of entry fitness will be small. Durable effects of vaccination are predicted to be associated with a reduction in peak viremia and viral set point at the time of primary infection.

AIDS Vaccines↗
PubMed2026

Oropouche virus: viral evolution, epidemiological trends, and challenges for control.

PURPOSE OF REVIEW: In recent years, OROV has emerged as a significant public health threat beyond the Amazon region. Here we review current epidemiological, virological, clinical and ecological knowledge of OROV to inform health practitioners, public health authorities and the scientific community and to facilitate the development of effective control strategies for OROV. RECENT FINDINGS: We describe the epidemiological, virological, ecological and clinical characteristics of OROV, focusing on lessons from the recent expansion, and highlighting needs for control and management of this emerging arbovirus. SUMMARY: This review aims to inform health practitioners, public health authorities and the scientific community of the recent reemergence and expansion of OROV beyond the Amazon Basin. The ecology, epidemiology, virology of OROV and clinical presentations of OROV infection are discussed, and knowledge gaps are identified.

Humans↗
PubMed2001

Equine infectious anemia virus genomic evolution in progressor and nonprogressor ponies.

A primary mechanism of lentivirus persistence is the ability of these viruses to evolve in response to biological and immunological selective pressures with a remarkable array of genetic and antigenic variations that constitute a perpetual natural experiment in genetic engineering. A widely accepted paradigm of lentivirus evolution is that the rate of genetic variation is correlated directly with the levels of virus replication: the greater the viral replication, the more opportunities that exist for genetic modifications and selection of viral variants. To test this hypothesis directly, we examined the patterns of equine infectious anemia virus (EIAV) envelope variation during a 2.5-year period in experimentally infected ponies that differed markedly in clinical progression and in steady-state levels of viral replication as indicated by plasma virus genomic RNA assays. The results of these comprehensive studies revealed for the first time similar extents of envelope gp90 variation in persistently infected ponies regardless of the number of disease cycles (one to six) and viremia during chronic disease. The extent of envelope variation was also independent of the apparent steady-state levels of virus replication during long-term asymptomatic infection, varying from undetectable to 10(5) genomic RNA copies per ml of plasma. In addition, the data confirmed the evolution of distinct virus populations (genomic quasispecies) associated with sequential febrile episodes during acute and chronic EIA and demonstrated for the first time ongoing envelope variation during long-term asymptomatic infections. Finally, comparison of the rates of evolution of the previously defined EIAV gp90 variable domains demonstrated distinct differences in the rates of nucleotide and amino acid sequence variation, presumably reflecting differences in the ability of different envelope domains to respond to immune or other biological selection pressures. Thus, these data suggest that EIAV variation can be associated predominantly with ongoing low levels of virus replication and selection in target tissues, even in the absence of substantial levels of plasma viremia, and that envelope variation continues during all stages of persistent infection as the virus successfully avoids clearance by host defense mechanisms.

Acute Disease↗
PubMed1998

The origin and evolution of viruses (a review).

Viroids and prions might have existed early at the border of inanimate and living worlds. Most extant viruses can be characterized as derivatives of ancestors originating from episomal elements of prokaryotes (DNA phages) and later from eukaryotes. Retroviruses very likely originated from cellular retrotransposons. Retrograde evolution of some large viruses from obligatory intracellular bacteria is possible but the ontogenesis of extant bacteria does not include a viral form of existence (the filterable L forms are not viruses) and well-defined viruses do not regenerate back into vegetative bacterial forms. Biologists experimenting with the evolution of prokaryotic and eukaryotic ancient cells cannot ignore the earliest appearance of viruses within or outside the living matter. Viruses participated in and gave direction to the evolution and natural selection by coexisting with uni- and multicellular organisms for billions of years. The coevolution of viruses and their host cells is characterized by incessant attacks and counterattacks through gene rearrangements and mutations (induced in the virus by an immunological counterattack of the host or by transgression of species barriers by the virus) and recombinations. Recombinations occurred between viral and viral or viral and host genes. Acts of "molecular piracy" as practiced by ancient viruses endowed the virus with the expression of several host genes for the advantage of the virus in its replicative cycle and host-to-host spread. Probably the first immortalized and malignantly transformed cells were induced by viruses as viruses evolved anti-apoptotic measures. While infected cells resort to apoptotic death before the assembly of a new viral progeny, prominent are the anti-apoptotic measures viruses evolved in order to assure the completion of their full replicative cycle. Further, viruses may escape neutralization by host antibodies and may survive a counterattack by the host's T cells directed at virally infected cells of its own. Viruses may induce a form of tolerance and coexist with their host without inducing disease. Persistent and apparently or deceivingly apathogenic or even attenuated viral "quasi-species" populations may contain individual particles that regain virulence due to recombinations and/or gene rearrangements, especially when transgressing species barriers. Xenotropic viruses of animals may replicate in human cells and vice versa confounding experiments with xenotransplants or with use of veterinary viral vaccines for the treatment of human diseases.

Animals↗
PubMed2000

Tempo and mode of human and simian T-lymphotropic virus (HTLV/STLV) evolution revealed by analyses of full-genome sequences.

We investigated the tempo and mode of evolution of the primate T-lymphotropic viruses (PTLVs). Several different models of nucleotide substitution were tested on a general phylogenetic tree obtained using the 20 full-genome HTLV/STLV sequences available. The likelihood ratio test showed that the Tamura and Nei model with discrete gamma-distributed rates among sites is the best-fitting substitution model. The heterogeneity of nucleotide substitution rates along the PTLV genome was further investigated for different genes and at different codon positions (cdp's). Tests of rate constancy showed that different PTLV lineages evolve at different rates when first and second cdp's are considered, but the molecular-clock hypothesis holds for some PTLV lineages when the third cdp is used. Negative selection was evident throughout the genome. However, in the gp46 region, a small fragment subjected to positive selection was identified using a Monte Carlo simulation based on a likelihood method. Employing correlations of the virus divergence times with anthropologically documented migrations of their host, a possible timescale was estimated for each important node of the PTLV tree. The obtained results on these slow-evolving viruses could be used to fill gaps in the historical records of some of the host species. In particular, the HTLV-I/STLV-I history might suggest a simian migration from Asia to Africa not much earlier than 19,500-60,000 years ago.

Animals↗
PubMed2003

Evolution of hepatitis C virus in blood donors and their respective recipients.

This paper describes the study of hepatitis C virus (HCV) evolution in the largest cohort of HCV-infected blood donors (BDs)/blood recipients (BRs) reported to date (25 pairs). A molecular analysis of partial sequences in the E1 (envelope) and NS5-B (polymerase) genes was performed. Phylogenetic reconstruction showed that the evolution of dominant strains was qualitatively and quantitatively different in BDs and BRs. The evolutionary rate was significantly higher in BRs, in which, in addition, most substitutions observed were antonymous. These findings corroborate the hypothesis that a large part of virus evolution - which was evaluated to be equivalent to approximately 20 years of chronic evolution - is acquired during the early phase of infection. These findings should be taken into account for the modelling of the long-term evolution of HCV and their possible contribution to improve our understanding of HCV natural history is discussed.

Blood Donors↗
PubMed1987

Molecular evolution of viruses; 'trees', 'clocks' and 'modules'.

Comparisons of the nucleotide sequences of viral genomes, and derived amino acid sequences, mostly confirm the traditional taxonomic groupings of viruses. These comparisons have also shown unexpected homologies between genes of viruses from different groups previously thought to be unrelated, and between some viral and non-viral genes. Comparisons of the three-dimensional structures of the particle proteins of some viruses have also revealed unexpected relationship, and, together with the sequence homologies, suggest that some ancestral viruses had 'modular' origins. Some of the sequence differences have been used to construct phylogenies. However, there is evidence that viral gene 'molecular clocks' do not always keep time consistently over very long or very short evolutionary time periods. Clues on evolution mostly come from comparative studies of living or fossil organisms. Fossils of viruses are not known, and thus clues of the origins and evolution of viruses are obtained by comparing extant forms. For example, by comparing isolates of different viruses, or strains of viruses, one can infer the properties of their ancestors, and by comparing isolates obtained during an epidemic, and sequentially related to one another, one can observe directly the type and timing of evolutionary changes.

Amino Acid Sequence↗