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PubMed2006

Evolution of multi-drug resistant hepatitis B virus during sequential therapy.

Multi-drug resistant hepatitis B virus (HBV) has been reported in hepatitis B patients who received sequential antiviral therapy. In vitro studies showed that HBV constructs with mutations resistant to lamivudine and adefovir have marked reduction in sensitivity to combination of lamivudine and adefovir, whereas constructs with mutations resistant to either drug remain sensitive to the other drug. We conducted this study to determine whether mutations conferring resistance to multiple antiviral agents co-locate on the same HBV genome in vivo and to describe the evolution of these mutations. Sera from six patients who had been found to have multi-drug resistant HBV mutations to lamivudine+adefovir, lamivudine+hepatitis B immunoglobulin (HBIG), or lamivudine+entecavir on direct sequencing were cloned after nested polymerase chain reaction (PCR). Analysis of 215 clones from 11 samples with multi-drug resistant mutations on direct sequencing showed that 183 (85%) clones had mutations to both therapies on the same genome; 31 clones had lamivudine-resistant mutants only. Clonal analysis of serial samples from three patients showed progressive evolution from all clones with lamivudine-resistant HBV mutations only to mixtures of clones that have multi-drug resistant mutations and clones that have lamivudine-resistant HBV mutations only, and ultimately all clones having multi-drug resistant HBV mutations. In conclusion, mutations conferring resistance to multiple antiviral agents co-locate on the same viral genome, suggesting that combination therapy directed against mutants resistant to each treatment may not be adequate in suppressing multi-drug resistant HBV. De novo combination therapy may prevent the emergence of multi-drug resistant mutants.

Adult↗
PubMed2004

[Molecular evolution and geographic origins of type 1 human lymphotrophic virus in Colombia detected by RFLP polymorphism].

The human T-lymphotropic virus type I (HTLV-I) infection is a public health problem in many endemic areas of Colombia. The subtyping of HTLV-I was based on the analysis of restriction fragment length polymorphisms (RFLP) in 3'LTR proviral DNA. From 31 HTLV-I isolates collected throughout Colombia, a RFLP analysis in a 737 bp 3'LTR fragment was performed. Fifty-eight percent (18/31) were identified as the Cosmopolitan subtype a, 19.4% (6/31) in the West African subtype b, 12.9% (4/31) in the Cosmopolitan subtype b and 9.6% (3/31) in the West African subtype c. The phylogenetic analysis of 3'LTR nucleotide sequences indicated that all the isolates in the current study were in the subgroup B or Japanese, in contrast with the highly divergent isolates from native Amerindians grouped in subgroup a or Transcontinental. The supported hypothesis was that of a post-Columbus introduction of virus represented in the African-American communities of the Colombian South Pacific. Some viral isolates from Colombian native Amerindians exhibited a nucleotide variation compatible with a Paleolithic introduction of the virus. The genetic diversity of HTLV-I in Colombia is complex and probably represents several independent introductions of lymphotropic virus.

Base Sequence↗
PubMed2005

Characterisation of three equine influenza A H3N8 viruses from Germany (2000 and 2002): evidence for frozen evolution.

Reported here are the results of antigenic and genetic characterisation of equine influenza strains causing local outbreaks reported to the Equine Diagnostic Centre in Berlin, Germany. In 2000, equine influenza virus was detected in a nasal swab from a non-vaccinated horse using a rapid diagnostic kit, but was not successfully isolated. Partial direct sequencing of the haemagglutinin (HA1) gene, indicated that the virus was a European lineage H3N8 subtype strain representative of strains isolated in several European countries during 2000. In 2002, two equine influenza viruses were isolated from nasal swabs both taken from unvaccinated horses with acute respiratory symptoms housed at the same stables. Antigenic characterisation using a panel of ferret antisera suggested that these isolates also belonged to the European lineage of H3N8 viruses. Analysis of deduced HA1 amino acid sequences confirmed that the HA1 of both isolates were identical and belonged to the European lineage. However, from phylogenetic analysis, both strains appeared to be more closely related to viruses isolated between 1989 and 1995 than to viruses isolated more recently in Europe. These results suggested that viruses with fewer changes than those on the main evolutionary lineage may continue to circulate. The importance of expanding current equine influenza surveillance efforts is emphasised.

Amino Acid Sequence↗
PubMed1988

Evolution of the structural proteins of human immunodeficiency virus: selective constraints on nucleotide substitution.

We have estimated the frequency of synonymous (KS) and amino acid replacement nucleotide substitutions (KA) among gag and env genes of published HIV sequences. The ratio of KS to KA can be used as an indicator of the intensity of the selective constraints on the amino acid sequence of a protein. By this approach we have shown that for both gp120 and gp41, the rate of change in amino acid sequence relative to the overall rate of change in nucleotide sequence is higher than for any other protein yet analyzed. The gag proteins p15 and p17 evolve slightly less rapidly, but p24 is relatively strongly conserved. We have compared the env gene of HIV with those of two other retroviruses for which appropriate data are available. In neither murine leukemia virus nor feline leukemia virus do the envelope glycoproteins evolve particularly rapidly. These results suggest that HIV is unusual among retroviruses in that both gp120 and gp41 are evolving under extremely weak selective constraints relative to the rest of the viral genome; accordingly, much of the observed variation may be selectively neutral.

Amino Acid Sequence↗
PubMed2006

Evolution of gp85 gene of subgroup J avian leukosis virus under the selective pressure of antibodies.

Subgroup J Avian leucosis virus (ALV-J) strain NX0101 was inoculated into chicken embryo fibroblasts (CEF) monolayers in 6-well plates. The six wells of CEF inoculated with NX0101 were divided into groups A (without anti-ALV-J serum in the medium) and B (with anti-ALV-J serum in the medium), then viruses from each well of both groups were separately passed in CEF every 6 d and formed their independent passage lineages. For each lineage of both groups, gp85 genes of the viruses in the 10th, 20th and 30th passages were amplified, cloned and sequenced. The sequence data indicated that the homologies of gp85 at aa level between the primary virus and the passed viruses of different passages of 3 lineages in group A were 97.7%-99.7%; and the homologies of gp85 between the primary virus and the passed viruses of different passages of 3 lineages in group B were 93.8%-96.1%. Analysis of the ratios of nonsynonium (NS) vs synonium (S) mutations of nucleic acids demonstrated that NS/S in 3 highly variable (hr-) regions at aa#110-120, aa#141-151 and aa#189-194 of gp85 in 3 lineages of group A were 2 (8/4), 1(3/3) and 1.3 (4/3), however, NS/S in the same 3 hr-regions of group B were 4.1 (13/3), 4.7 (14/3) and 3.3 (11/3). This study is the first demonstration of influence of immune selective pressure on evolution of ALV-J gp85 by specific antibodies under the controlled in vitro experiments.

Animals↗
PubMed2004

Homologous recombination in bovine pestiviruses. Phylogenetic and statistic evidence.

Bovine pestiviruses (Bovine Viral Diarrea Virus 1 (BVDV 1) and Bovine Viral Diarrea Virus 2 (BVDV 2)) belong to the genus Pestivirus (Flaviviridae), which is composed of positive stranded RNA viruses causing significant economic losses world-wide. We used phylogenetic and bootstrap analyses to systematically scan alignments of previously sequenced genomes in order to explore further the evolutionary mechanisms responsible for variation in the virus. Previously published data suggested that homologous crossover might be one of the mechanisms responsible for the genomic rearrangements observed in cytopathic (cp) strains of bovine pestiviruses. Nevertheless, homologous recombination involves not just homologous crossovers, but also replacement of a homologous region of the acceptor RNA. Furthermore, cytopathic strains represent dead paths in evolution, since they are isolated exclusively from the fatal cases of mucosal disease. Herein, we report evidence of homologous inter-genotype recombination in the genome of a non-cytopathic (ncp) strain of Bovine Viral Diarrea Virus 1, the type species of the genus Pestivirus. We also show that intra-genotype homologous recombination might be a common phenomenon in both species of Pestivirus. This evidence demonstrates that homologous recombination contribute to the diversification of bovine pestiviruses in nature. Implications for virus evolution, taxonomy and phylogenetics are discussed.

Algorithms↗
PubMed2002

What messenger RNA capping tells us about eukaryotic evolution.

The 5' cap is a unique feature of eukaryotic cellular and viral messenger RNA that is absent from the bacterial and archaeal domains of life. The cap is formed by three enzymatic reactions at the 5' terminus of nascent mRNAs. Although the capping pathway is conserved in all eukaryotes, the structure and genetic organization of the component enzymes vary between species. These differences provide insights into the evolution of eukaryotes and eukaryotic viruses.

Acid Anhydride Hydrolases↗
PubMed1990

New viral diseases. A real and potential problem without boundaries.

Viruses are the most mutable and rapidly evolving human parasites. Therefore, it is not surprising that new virus diseases, such as the acquired immunodeficiency syndrome, are emerging. However, these new viruses are relatively few in number, which reflects the constraints placed on viral evolution by the requirement for maintenance of virus structure and function and virus adaptation to restricted ecologic sites. Most "new" viral diseases, such as the hemorrhagic fevers, result from environmental disruptions that increase human contact with animals or insect vectors of old viruses. However, truly novel viruses with lethal potential or capacity for global spread have emerged in animals as a consequence of single-point mutations or genetic recombination between viruses. Given the mutability of viruses and the inevitability of environmental change, we must be prepared for the evolution of new virus diseases.

Acquired Immunodeficiency Syndrome↗
PubMed1986

Influenza B virus PB1 protein; nucleotide sequence of the genome RNA segment predicts a high degree of structural homology with the corresponding influenza A virus polymerase protein.

The complete nucleotide sequence of a cloned cDNA copy of the genome RNA segment encoding the influenza B/Lee/40 virus PB1 polymerase protein has been determined. The genome RNA segment is 2368 nucleotides in length and is capable of encoding a polymerase (PB1) protein of 752 amino acids with a calculated mol mass of 84,407 Da. As expected, the protein is highly basic with a net charge of +20 at pH 7.0. Sequence comparison between the influenza A and B virus PB1 proteins reveals that they share 61% amino acid homology. An internal hydrophobic domain and 90% of the proline residues found within the influenza A virus PB1 protein are conserved in the influenza B virus molecule. The influenza A and B virus PB1 proteins share the highest homology yet seen between proteins encoded by these disparate viruses. This remarkable conservation of primary structure argues for severe functional constraint on the evolution of this influenza virus polymerase protein.

Amino Acid Sequence↗
PubMed1982

Viral src gene products are related to the catalytic chain of mammalian cAMP-dependent protein kinase.

The transforming protein sequences translated from the Rous avian and Moloney murine sarcoma virus src genes are shown to be related to the catalytic chain of bovine cAMP-dependent protein kinase (ATP:protein phosphotransferase, EC 2.7.1.37). The avian transforming protein, also a protein kinase, shows greatest homology with the bovine protein kinase in the carboxyl-terminal half, where the protein kinase activity is localized. Moreover, lysine occurs in the inferred transforming protein sequences at the position homologous with the proposed ATP-binding lysine of the bovine protein kinase. This relationship is consistent with the hypothesis that the src genes originated in the host genomes, in which they are members of a superfamily of distantly related protein kinases that are normal constituents of mammalian cells. In the host, these sequences are much more highly conserved than in the viruses.

Amino Acid Sequence↗
PubMed1990

Evolution of the NS genes of the influenza A viruses. II. Characteristics of the amino acid changes in the NS1 proteins of the influenza A viruses.

We compared the amino acid sequences of the NS1 proteins of human, equine, and avian influenza viruses. The ratios of the amino acid substitutions per nucleotide substitutions in the NS1 proteins were about 27-45%, suggesting the existence of constraints on the amino acid changes of the NS1 protein in evolution. As a measure of constraints exerted on the regions of a protein, a changeability index is proposed. There was a highly conserved region between amino acid residues 30 and 50. The C-terminal region of amino acid residue 165 was a continuously changeable region. We have either introduced several nucleotide substitutions to the NS cDNA of the A/Udorn/72 virus in vitro or constructed the recombinant NS cDNAs between the A/Udorn/72 and A/chick/Japan/24 viruses, and then expressed them in animal cells. We have found that the amino acid substitutions introduced to the low-conserved region of the NS1 protein affected the stability and nuclear localization of the NS1 protein. One of the chimeric proteins between the A/Udorn/72 and A/chick/Japan/24 viruses did not move to the nucleus of the cell and remained in the cytoplasm.

Amino Acid Sequence↗
PubMed2006

Longitudinal analysis of human immunodeficiency virus type 1 nef/long terminal repeat sequences in a cohort of long-term survivors infected from a single source.

We studied the evolution of human immunodeficiency virus type 1 (HIV-1) in a cohort of long-term survivors infected with an attenuated strain of HIV-1 acquired from a single source. Although the cohort members experienced differing clinical courses, we demonstrate similar evolution of HIV-1 nef/long-terminal repeat (LTR) sequences, characterized by progressive sequence deletions tending toward a minimal nef/LTR structure that retains only sequence elements required for viral replication. The in vivo pathogenicity of attenuated HIV-1 is therefore dictated by viral and/or host factors other than those that impose a unidirectional selection pressure on the nef/LTR region of the HIV-1 genome.

Adaptation, Physiological↗
PubMed2000

Rapid in vivo evolution of a beta-lactamase using phagemids.

RNA viruses are capable of undergoing extremely rapid evolution due to their high rates of reproduction, small genome size, and a high frequency of spontaneous mutagenesis. Here we demonstrate that a virus-like, evolutionary state can be created by propagating a phagemid population in a hypermutator strain of Escherichia coli in the presence of a helper phage. This enables one to subject individual phagemid-encoded genes to rapid in vivo evolution. We applied this approach to TEM-1 beta-lactamase which confers resistance to 0.05 mg/L of the antibiotic cefotaxime. After 3 weeks of in vivo evolution we were able to isolate a double mutant, E104K/G238S, of the enzyme which confers a 500-fold increased level of resistance to cefotaxime compared to the starting enzyme. In two independent experiments we obtained a triple mutant, E104K/G238S/T263M, which confers a 1000-fold increase in resistance compared to the wild type enzyme. The same three mutations have been previously observed in TEM-4 beta-lactamase which was discovered in a highly cefotaxime-resistant clinical isolate. The probability of randomly obtaining a beta-lactamase carrying three identical point mutations is less than 10(-10). This indicates that phagemid evolution can rapidly reproduce evolution occurring in nature.

Bacteriophages↗
PubMed2000

Detection of hepatitis G virus (HGV) RNA and antibodies to the HGV envelope protein E2 in a cohort of hemodialysis patients.

An analysis of the evolution of hepatitis G virus (HGV) infection markers was performed for a cohort of 58 hemodialyzed patients. During follow-up (4.88 +/- 0.42 years), a group of these patients cleared their antibodies against the envelope protein E2 with (4 of 29 cases; 13.8%) or without (9 of 29 cases; 31%) the reappearance of viremia. This finding implies a temporally limited protection in patients previously infected with HGV.

Adult↗
PubMed2006

Evolutionary influences in arboviral disease.

Arthropod-borne viruses (arboviruses) generally require horizontal transmission by arthropod vectors among vertebrate hosts for their natural maintenance. This requirement for alternate replication in disparate hosts places unusual evolutionary constraints on these viruses, which have probably limited the evolution of arboviruses to only a few families of RNA viruses (Togaviridae, Flaviviridae, Bunyaviridae, Rhabdoviridae, Reoviridae, and Orthomyxoviridae) and a single DNA virus. Phylogenetic studies have suggested the dominance of purifying selection in the evolution of arboviruses, consistent with constraints imposed by differing replication environments and requirements in arthropod and vertebrate hosts. Molecular genetic studies of alphaviruses and flaviviruses have also identified several mutations that effect differentially the replication in vertebrate and mosquito cells, consistent with the view that arboviruses must adopt compromise fitness characteristics for each host. More recently, evidence of positive selection has also been obtained from these studies. However, experimental model systems employing arthropod and vertebrate cell cultures have yielded conflicting conclusions on the effect of alternating host infections, with host specialization inconsistently resulting in fitness gains or losses in the bypassed host cells. Further studies using in vivo systems to study experimental arbovirus evolution are critical to understanding and predicting disease emergence, which often results from virus adaptation to new vectors or amplification hosts. Reverse genetic technologies that are now available for most arbovirus groups should be exploited to test assumptions and hypotheses derived from retrospective phylogenetic approaches.

Adaptation, Physiological↗