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At least 1,171 records · Page 65Linked to original sources
PubMed2001

Pathogenicity of a natural recombinant associated with ageratum yellow vein disease: implications for geminivirus evolution and disease aetiology.

Yellow vein disease of Ageratum conyzoides is caused by a viral DNA complex consisting of the genomic component (DNA A) of the monopartite begomovirus Ageratum yellow vein virus (AYVV, family: Geminiviridae) and a small satellite-like DNA beta component. AYVV DNA A is unable to induce symptoms in this host alone but can systemically infect A. conyzoides in which it accumulates to low levels. Here, we demonstrate that the yellow vein phenotype can also be produced by co-inoculating A. conyzoides with AYVV DNA A and recDNA-Abeta17, a naturally occurring recombinant of approximately the same size as DNA beta that contains sequences from both DNA A and DNA beta. Symptoms induced by DNA A and recDNA-Abeta17 in A. conyzoides and Nicotiana glutinosa are qualitatively similar to those associated with DNA A and DNA beta although milder. Recombination between DNA A and DNA beta to produce a chimera resembling recDNA-Abeta17 was observed after whitefly transmission of the disease in A. conyzoides. Hence, such recombination events are likely to occur frequently, implying that recombinants will normally be associated with this type of disease complex in the field. Possible implications of these findings for the evolution of begomoviruses and the aetiology of their diseases are discussed.

Asteraceae↗
PubMed1997

Retroviral oligonucleotide distributions correlate with biased nucleotide compositions of retrovirus sequences, suggesting a duplicative stepwise molecular evolution.

A computer-assisted analysis was made of 24 complete nucleotide sequences selected from the vertebrate retroviruses to represent the ten viral groups. The conclusions of this analysis extend and strengthen the previously made hypothesis on the Moloney murine leukemia virus: The evolution of the nucleotide sequence appears to have occurred mainly through at least three overlapping levels of duplication: (1) The distributions of overrepresented (3-6)-mers are consistent with the universal rule of a trend toward TG/CT excess and with the persistence of a certain degree of symmetry between the two strands of DNA. This suggests one or several original tandemly repeated sequences and some inverted duplications. (2) The existence of two general core consensuses at the level of these (3-6)-mers supports the hypothesis of a common evolutionary origin of vertebrate retroviruses. Consensuses more specific to certain sequences are compatible with phylogenetic trees established independently. The consensuses could correspond to intermediary evolutionary stages. (3) Most of the (3-6)-mers with a significantly higher than average frequency appear to be internally repeated (with monomeric or oligomeric internal iterations) and seem to be at least partly the cause of the bias observed by other researchers at the level of retroviral nucleotide composition. They suggest a third evolutionary stage by slippage-like stepwise local duplications.

Animals↗
PubMed2006

Evolutionary history of the closely related group 2 coronaviruses: porcine hemagglutinating encephalomyelitis virus, bovine coronavirus, and human coronavirus OC43.

The close genetic and antigenic relatedness among the group 2 coronaviruses human coronavirus OC43 (HCoV-OC43), bovine coronavirus (BCoV), and porcine hemagglutinating encephalomyelitis virus (PHEV) suggests that these three viruses with different host specificities diverged fairly recently. In this study, we determined the complete genomic sequence of PHEV (strain PHEV-VW572), revealing the presence of a truncated group 2-specific ns2 gene in PHEV in comparison to other group 2 coronaviruses. Using a relaxed molecular clock approach, we reconstructed the evolutionary relationships between PHEV, BCoV, and HCoV-OC43 in real-time units, which indicated relatively recent common ancestors for these species-specific coronaviruses.

Animals↗
PubMed1997

Genetic analysis of the hepatitis C virus (HCV) genome from HCV-infected human T cells.

We recently established a cell culture system for the replication of hepatitis C virus (HCV) by using a human T cell leukaemia virus type I-infected cell line, MT-2, and showed that the quasi-species of the hypervariable region 1 observed in the original inoculum became homogeneous in MT-2 cells 10 days after inoculation of HCV. In this study, we obtained HCV cDNA clones covering the whole viral genome by RT-nested PCR using RNA from HCV-infected cloned MT-2C cells, which support viral replication more efficiently, at 12 days after inoculation. A total of 41 distinct HCV cDNA clones covering almost the whole viral genome were also isolated from a cDNA library derived from the original inoculum. Molecular evolutional analyses comparing the sequences of the HCV clones obtained from both sources revealed that the HCV populations became homogeneous in more than half of the compared regions. This finding suggests that limited HCV populations are able to replicate in MT-2C cells. In addition, we isolated cDNA clones containing a 3' X-tail sequence, which was recently identified as a bona fide 3' terminus of the HCV genome, in the HCV-infected MT-2C cells and confirmed that the nucleotide sequence of the 3' X-tail was highly conserved, suggesting its implication in HCV replication. Finally, on the basis of the sequences of HCV cDNA clones obtained from HCV-infected MT-2C cells, we determined the entire nucleotide sequence of the HCV genome containing the 3' X-tail as a candidate for an infectious HCV molecular clone.

Base Sequence↗
PubMed1997

The antiretrovirus drug 3'-azido-3'-deoxythymidine increases the retrovirus mutation rate.

It was previously observed that the nucleoside analog 5-azacytidine increased the spleen necrosis virus (SNV) mutation rate 13-fold in one cycle of retrovirus replication (V. K. Pathak and H. M. Temin, J. Virol. 66:3093-3100, 1992). Based on this observation, we hypothesized that nucleoside analogs used as antiviral drugs may also increase retrovirus mutation rates. We sought to determine if 3'-azido-3'-deoxythymidine (AZT), the primary treatment for human immunodeficiency virus type 1 (HIV-1) infection, increases the retrovirus mutation rate. Two assays were used to determine the effects of AZT on retrovirus mutation rates. The strategy of the first assay involved measuring the in vivo rate of inactivation of the lacZ gene in one replication cycle of SNV- and murine leukemia virus-based retroviral vectors. We observed 7- and 10-fold increases in the SNV mutant frequency following treatment of target cells with 0.1 and 0.5 microM AZT, respectively. The murine leukemia virus mutant frequency increased two- and threefold following treatment of target cells with 0.5 and 1.0 microM AZT, respectively. The second assay used an SNV-based shuttle vector containing the lacZ alpha gene. Proviruses were recovered as plasmids in Escherichia coli, and the rate of inactivation of lacZ alpha was measured. The results indicated that treatment of target cells increased the overall mutation rate two- to threefold. DNA sequence analysis of mutant proviruses indicated that AZT increased both the deletion and substitution rates. These results suggest that AZT treatment of HIV-1 infection may increase the degree of viral variation and alter virus evolution or pathogenesis.

Antiviral Agents↗
PubMed2006

Evolution of SIV envelope in morphine-dependent rhesus macaques with rapid disease progression.

Three morphine-dependent rhesus macaques that developed accelerated AIDS after virus inoculation, along with three control macaques, were followed for evolution of the SIV/17E-Fr envelope. Viral RNA was isolated from plasma samples collected at weeks 6, 12, and 20 postinfection. A 482-nucleotide fragment in the viral env was amplified and cloned into a pCR2.1-TOPO vector. Between 5 and 10 clones were sequenced at each time point from individual monkeys. The sequence analysis showed more mutations in the control animals compared to those seen in the morphine-dependent animals. The virus at different points did not separate completely in phylogenetic analysis. However, the phylogenetic clustering was more apparent in the control animals. Viral diversity and divergence were significantly higher in the control animals. The control animals lost N-glycosylation sites more rapidly. These results suggest that morphine dependence diminished virus evolution in SHIV/SIV-infected rhesus macaques and there was an inverse correlation between virus evolution and onset of clinical disease.

Amino Acid Sequence↗
PubMed2005

Molecular analysis of the NS3/NS3A gene of Bluetongue virus isolates from the 1979 and 1998-2001 epizootics in Greece and their segregation into two distinct groups.

The sequence of the genome segment 10 (Seg-10) encoding NS3/NS3A was determined for 19 field isolates of Bluetongue virus (BTV) of serotypes BTV-1, BTV-4, BTV-9 and BTV-16, derived from epizootics in Greece in the years 1979 and 1998-2001. The aim of the study was to define the molecular epidemiology of the virus in this part of the Mediterranean basin. On the basis of the Seg-10 sequences, the isolates grouped into two distinct phylogenetic clusters. These were Greek group I of solely serotype BTV-4 viruses, and Greek group II of serotypes BTV-1, BTV-9 and BTV-16 viruses. The isolates in Greek group I clustered with the Corsican and Tunisian BTV-2 serotypes and US group II strains of BTV-10 and BTV-13 serotypes, while those in Greek group II with Chinese, Indian and Australian viruses of different serotypes suggesting that viruses derived from two distinct ecosystems have caused BT incursions in Greece over the last 25 years. The NS3/NS3A sequences of most of the BTV-4 isolates were identical, irrespective of the year of isolation, geographical location and host species or tissue origin. Maximum of 15-16% nucleic acid sequence variation, but only 4% deduced amino acid substitution, were observed between groups I and II. Furthermore, the clustering of the NS3/NS3A sequences was independent of the viral serotype, indicating the occurrence of genome segment reassortment during the course of evolution of the viruses.

Amino Acid Sequence↗
PubMed2004

[Treatment of chronic hepatitis B virus infection].

The treatment of the patient with chronic hepatitis B virus infection (HBV) must be carried out with the knowledge that the percentage of patients infected with the B virus that develop chronic hepatitis remains between 5-10%. Of these, 10-30% will present chronic infection with active viral replication, necroinflammatory hepatic lesion, evolution to hepatic cirrhosis and the risk of developing hepatocarcinoma. For this reason, the aim of treatment is to achieve negativisation of the HBeAg, seroconversion to anti-HBe and a reduction of viral replication to undetectable values (estimated by level of DNA-HBV), for protracted periods of time. When a sustained loss of HBeAg and a reduction of viral replication are obtained, a biochemical, clinical and histological remission is achieved. Up until now the therapeutic alternatives in chronic infection by the B virus have been immunomodulation with Interferon alpha and the blocking of viral replication with lamivudine or adefovir dipivoxil. A difference must be drawn between the biochemical response, defined as a fall in the transaminases to normal values, and the virological response, which refers to a fall in the levels of DNA-HBV below 10(5) copies/ml. Finally, the complete response is defined as the virological and biochemical response with negativisation of the HBsAg. If a sustained response is obtained for several months, a histological response can be predicted with reduction in the intensity of the hepatic lesion and an absence or stabilisation in the process of fibrosis. The sustained response should last for no less than 6 to 12 months following the end of treatment.

Adenine↗
PubMed2004

Genotypic analysis of HIV-1 drug resistance at the limit of detection: virus production without evolution in treated adults with undetectable HIV loads.

Human immunodeficiency virus (HIV) production continues in patients receiving highly active antiretroviral therapy (HAART) with undetectable (<50 copies/mL) virus loads. Our initial cross-sectional study showed that this viremia is composed of viruses that lack new resistance mutations to the HAART regimen. Here we describe a longitudinal, clonal genotypic analysis of plasma virus loads in treated adults who had undetectable virus loads. We document a continuous production of virus in 8 HIV-1-infected adults who maintained suppression of viremia for up to 15 months. Using analytical approaches for distinguishing selected resistance mutations from nonselected mutations and polymerase chain reaction errors, we detected no evolution of resistance in the reverse-transcriptase and protease genes. Sporadic resistance mutations were detected in some viral clones that were not selected for subsequently. Thus, in some patients, HAART suppresses replication to a level that does not allow the evolution of drug resistance over a time frame of years.

Adult↗
PubMed2006

Genome sequence diversity and clues to the evolution of variola (smallpox) virus.

Comparative genomics of 45 epidemiologically varied variola virus isolates from the past 30 years of the smallpox era indicate low sequence diversity, suggesting that there is probably little difference in the isolates' functional gene content. Phylogenetic clustering inferred three clades coincident with their geographical origin and case-fatality rate; the latter implicated putative proteins that mediate viral virulence differences. Analysis of the viral linear DNA genome suggests that its evolution involved direct descent and DNA end-region recombination events. Knowing the sequences will help understand the viral proteome and improve diagnostic test precision, therapeutics, and systems for their assessment.

DNA, Viral↗
PubMed1993

Origin of the pandemic 1957 H2 influenza A virus and the persistence of its possible progenitors in the avian reservoir.

H2N2 influenza A viruses caused the Asian pandemic of 1957 and then disappeared from the human population 10 years later. To assess the potential for similar outbreaks in the future, we determined the antigenicity of H2 hemagglutinins (HAs) from representative human and avian H2 viruses and then analyzed the nucleotide and amino acid sequences to determine their evolutionary characteristics in different hosts. The results of longitudinal virus surveillance studies were also examined to estimate the prevalence of avian H2 isolates among samples collected from wild ducks and domestic poultry. Reactivity patterns obtained with a large panel of monoclonal antibodies indicated antigenic drift in the HA of human H2 influenza viruses, beginning in 1962. Amino acid changes were clustered in two regions of HA1 that correspond to antigenic sites A and D of the H3 HA. By contrast, the antigenic profiles of the majority of avian H2 HAs were remarkably conserved through 1991, resembling the prototype Japan 57 (H2N2) strain. Amino acid changes were distributed throughout HA1, indicating that antibodies do not play a major role in the selection of avian H2 viruses. Phylogenetic analysis revealed two geographic site-specific lineages of avian H2 HAs: North American and Eurasian. Evidence is presented to support interregion transmission of gull H2 viruses. The human H2 HAs that circulated in 1957-1968 form a separate phylogenetic lineage, most closely related to the Eurasian avian H2 HAs. There was an increased prevalence of H2 influenza viruses among wild ducks in 1988 in North America, preceding the appearance of H2N2 viruses in domestic fowl. As the prevalence of avian H2N2 influenza viruses increased on turkey farms and in live bird markets in New York City and elsewhere, greater numbers of these viruses have come into direct contact with susceptible humans. We conclude that antigenically conserved counterparts of the human Asian pandemic strain of 1957 continue to circulate in the avian reservoir and are coming into closer proximity to susceptible human populations.

Americas↗
PubMed1997

The type IC hsd loci of the enterobacteria are flanked by DNA with high homology to the phage P1 genome: implications for the evolution and spread of DNA restriction systems.

EcoR124l, EcoDXXl and Ecoprrl are the known members of the type IC family of DNA restriction and modification systems. The first three are carried on large, conjugative plasmids, while Ecoprrl is chromosomally encoded. The enzymes are coded by three genes, hsdR, hsdM and hsdS. Analysis of the DNA sequences upstream and downstream of the type IC hsd loci shows that all are highly homologous to each other and also to sequences present in the bacteriophage P1 genome. The upstream sequences include functional phd and doc genes, which encode an addiction system that stabilizes the P1 prophage state, and extend to and beyond pac, the site at which phage DNA packaging begins. Downstream of the hsd loci, P1 DNA sequences begin at exactly the same place for all of the systems. For EcoDXXl and Ecoprrl the P1 homology extends for thousands of base pairs while for EcoR124l and IS1 insertion and an associated deletion have removed most of the P1-homologous sequences. The significance of these results for the evolution of DNA restriction and modification systems is discussed.

Bacteriophage P1↗
PubMed2001

Emergence of rotavirus G4P8 strain among children suffering from watery diarrhea in Calcutta, India.

Rotavirus RNAs from the fecal samples were hybridized with cDNAs specific for G1 and G2 genotypes. 59 out of 138 samples (42.7%) did not hybridize with either probe. The cDNAs coding for VP7 and VP4 from one such sample, SC134, were synthesized by combined reverse transcriptase/polymerase chain reaction (PCR) using specific oligonucleotide primers and were used as probes to screen those local isolates which did not hybridize with either G1 or G2. 26/59 (44%) of fecal RNA hybridized with these cDNAs indicating a possible emergence of this strain in this part of India. The VP7 and VP4 genotype specificity of SC134 was found to be G4P8 by multiplex PCR. The VP7 gene of SC134 was cloned and characterized in detail by restriction enzyme digestion and DNA sequence analysis. Comparison of nucleotide and predicted amino acid sequence of the VP7 gene of SC134 with other serotypes revealed that the VP7 gene of SC134 was closely related to G4. However, amio acids within the VP7 sequence differed in seven positions with that of both the subtype 'A' and 'B' of the G4 serotype. To establish the relation of this emerging strain with the other reported G4 strains, a phylogenetic tree was constructed and SC134 was found to be more closely related to the ST3 strain isolated in England and included in the tetravalent vaccine formulation along with two Japanese strains, although all four were distinct and did not form any cluster as was evident by the horizontal distance separating them. The VP7 gene sequence of SC134 was submitted to EMBL and was assigned the accession number AJ278217.

Antigens, Viral↗
PubMed1998

Sequence variation of EBNA2 of Epstein-Barr virus isolates from Korea.

To reveal sequence variations in the Epstein-Barr virus nuclear antigen 2 (EBNA2) genes of Epstein-Barr virus (EBV) strains circulating in the Korean population, the EBNA2 divergent region was amplified and sequenced from 13 EBV-1 isolates, 2 EBNA2 type 1 intertypic EBV isolates, and two EBV-2 isolates, all derived from Korean cancer patients. Comparative sequence analysis revealed that type 1 and type 2 EBNA2 divergent regions of Korean EBV isolates were almost identical to the respective regions of the B95-8 EBV-1 and AG876 EBV-2 strains. Two of the nucleotide changes found in the type 1 divergent regions of all Korean isolates, G-to-T and C-to-A at B95-8 EBV positions 48,991 and 48,998, respectively, are also present in all EBV-1 strains of non-Asian origins, indicating that these two sites might be mutational hot sites. Besides these two mutations, EBV-1 strains from Papua New Guinea or European Caucasians and Africa show unique patterns of identical sequence variations from B95-8, which were not found in type 1 isolates from Korea, suggesting that Korean type 1 are evolving as a lineage distinct from isolates from Papua New Guinea or European Caucasian and Africa.

Africa↗
PubMed1999

Determinants of the natural history of human immunodeficiency virus type 1 infection.

Variation in the time to AIDS and duration of survival of human immunodeficiency virus (HIV)-1-infected persons was recognized early in the epidemic. Recent studies have indicated that the rate of viral replication, as manifest by the number of copies of HIV RNA per milliliter of plasma, is a major determinant of outcome in an infected person. The predictive power of the measurement of plasma HIV RNA copy number is enhanced by combining this result with the CD4 lymphocyte number. The determinants of the rate of viral replication are less clearly defined. Recent studies suggest that polymorphism of the chemokine receptors, required for cellular infection, plays a role in regulating the rate of viral replication. The subsequent adaptive evolution of HIV-1 to the host's immune response is a consequence of this dynamic of the virus. Complicating opportunistic infections also appear to enhance HIV-1 replication, while antiviral therapy, in contrast, can and does suppress viral replication.

Acquired Immunodeficiency Syndrome↗