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PubMed1998

[Human immunodeficiency virus and AIDS in terms of reverse transcriptase and molecular evolution].

Human immunodeficiency virus type 1 (HIV-1) evolves rapidly in the host. The computer analysis of the HIV-1 genome has shown that the mutation manner is dependent on oligonucleotide sequences (in particular, six bases long); thus HIV-1 adaptively evolves. The six-base-long interaction between template-primer oligonucleotide and the reverse transcriptase (RT) has been revealed by the crystal structure of RT, in vitro termination assay of plymerization, and hydroxyl radical footprint analysis. It has been thought that AIDS is caused by the large numbers of HIV-1 quasispecies yielded by the adaptive and rapid evolution in the host. However, the slow evolution and the high levels of viral RNA in the progressive HIV-1 infected individuals (progressives) were recently reported; in contrast, the adaptive and rapid evolution and the low viral-RNA levels were reported in the non-progressives. This suggests that the physiological environment, e.g. pH and dNTP balance, in which RT works in the progressives is different from that in the non-progressives.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

Effect of prostaglandin E2 (PGE2) and cyclic adenosine monophosphate (cAMP) upon actin cytoskeleton in human pulmonary fibroblasts (ICP-23) infected by measles virus.

The evolution of the actin cytoskeleton after trypsinization and recultivation as well as the effect of the PGE2 modulator and that of the secondary messenger, the cyclic AMP upon the same cytoskeletal proteins in human pulmonary fibroblasts (ICP-23) were studied. The substances were administered simultaneously and after one hour of viral adsorption. Using epifluorescence for pointing out filamentous actin the modifications occurring in this cytoskeletal protein when contacting trypsin and the virus and when PGE2 and cAMP are administered in the experimental variants are observed. Actin arrangement is obviously modified by the viral infection but the restrictive effect of PGE2 and cAMP upon virus replication is correlated with modifications occurring in the actin cytoskeleton.

Actins↗
PubMed2005

Evolution of human immunodeficiency virus type 2 coreceptor usage, autologous neutralization, envelope sequence and glycosylation.

To investigate why human immunodeficiency virus type 2 (HIV-2) is less virulent than HIV-1, the evolution of coreceptor usage, autologous neutralization, envelope sequence and glycosylation was studied in sequentially obtained virus isolates and sera from four HIV-2-infected individuals. Neutralization of primary HIV-2 isolates was tested by a cell line-based assay and IgG purified from patients' sera. Significant autologous neutralization was observed for the majority (39 of 54) of the HIV-2 serum-virus combinations tested, indicating that neutralization escape is rare in HIV-2 infection. Furthermore, sera from 18 HIV-2 patients displayed extensive heterologous cross-neutralization when tested against a panel of six primary HIV-2 isolates. This indicates that HIV-2 is intrinsically more sensitive to antibody neutralization than HIV-1. In line with earlier reports, HIV-2 isolates could use several alternative receptors in addition to the major coreceptors CCR5 and CXCR4. Intrapatient evolution from CCR5 use to CXCR4 use was documented for the first time. Furthermore, CXCR4 use was linked to the immunological status of the patients. Thus, all CXCR4-using isolates, except one, were obtained from patients with CD4 counts below 200 cells microl(-1). Sequence analysis revealed an association between coreceptor usage and charge of the V3 loop of the HIV-2 envelope, as well as an association between the rate of disease progression and the glycosylation pattern of the envelope protein. Furthermore, HIV-2 isolates had fewer glycosylation sites in the V3 domain than HIV-1 (two to three versus four to five). It is proposed here that HIV-2 has a more open and accessible V3 domain than HIV-1, due to differences in glycan packing, and that this may explain its broader coreceptor usage and greater sensitivity to neutralizing antibodies.

Amino Acid Sequence↗
PubMed1999

Rapid evolution of H5N1 influenza viruses in chickens in Hong Kong.

The H5N1 avian influenza virus that killed 6 of 18 persons infected in Hong Kong in 1997 was transmitted directly from poultry to humans. Viral isolates from this outbreak may provide molecular clues to zoonotic transfer. Here we demonstrate that the H5N1 viruses circulating in poultry comprised two distinguishable phylogenetic lineages in all genes that were in very rapid evolution. When introduced into new hosts, influenza viruses usually undergo rapid alteration of their surface glycoproteins, especially in the hemagglutinin (HA). Surprisingly, these H5N1 isolates had a large proportion of amino acid changes in all gene products except in the HA. These viruses maybe reassortants each of whose HA gene is well adapted to domestic poultry while the rest of the genome arises from a different source. The consensus amino acid sequences of "internal" virion proteins reveal amino acids previously found in human strains. These human-specific amino acids may be important factors in zoonotic transmission.

Amino Acid Sequence↗
PubMed2003

Selection-driven evolution of emergent dengue virus.

In the last four decades the incidence of dengue fever has increased 30-fold worldwide, and over half the world's population is now threatened with infection from one or more of four co-circulating viral serotypes (DEN-1 through DEN-4). To determine the role of viral molecular evolution in emergent disease dynamics, we sequenced 40% of the genome of 82 DEN-4 isolates collected from Puerto Rico over the 20 years since the onset of endemic dengue on the island. Isolates were derived from years with varying levels of DEN-4 prevalence. Over our sampling period there were marked evolutionary shifts in DEN-4 viral populations circulating in Puerto Rico; viral lineages were temporally clustered and the most common genotype at a particular sampling time often arose from a previously rare lineage. Expressed changes in structural genes did not appear to drive this lineage turnover, even though these regions include primary determinants of viral antigenic properties. Instead, recent dengue evolution can be attributed in part to positive selection on the nonstructural gene 2A (NS2A), whose functions may include replication efficiency and antigenicity. During the latest and most severe DEN-4 epidemic in Puerto Rico, in 1998, viruses were distinguished by three amino acid changes in NS2A that were fixed far faster than expected by drift alone. Our study therefore demonstrates viral genetic turnover within a focal population and the potential importance of adaptive evolution in viral epidemic expansion.

Communicable Diseases, Emerging↗
PubMed1992

Evolving views of viral evolution: towards an evolutionary biology of viruses.

Despite considerable interest in viral evolution, at least among virologists, viruses are rarely considered from the same evolutionary vantage point as other organisms. Early work of necessity emphasized phenotype and phenotypic variation (and therefore arguably was more oriented towards the broader biological and ecological perspectives). More recent work (essentially since the development of molecular evolution in the 1960's but beginning earlier) has concentrated on genotypic variation, with less clarity about the significance of such variations. Other aspects of evolutionary theory, especially considerations of natural selection and of evolutionary constraints, have not widely been applied to viruses, and an evolutionary framework for virology has long been lacking. This becomes apparent in considering 'emerging' viruses, which have often been treated on an ad hoc basis. It was often felt that, because previously unrecognized viruses are involved, mechanisms of viral emergence must mirror the unpredictability of mutations in the viral genome. However, most examples of viral emergence are independent of mutation, at least initially, and are often pre-existing viruses in changed circumstances ('viral traffic'). This conclusion also readily follows from ordinary Darwinian premises, which would require that, like other living species, 'new' organisms are descended only from existing species. In this respect, from a Darwinian perspective, viruses would appear to resemble other organisms.

Biological Evolution↗
PubMed2004

Evolution of hepatitis B virus precore/basal core promoter gene in HBeAg-positive chronic hepatitis B patients receiving lamivudine therapy.

AIM: Lamivudine is effective in hepatitis B e antigen (HBeAg)-positive chronic hepatitis B, but the relapse rate after cessation of treatment is high. The evolution of viral genome may contribute to the viral replication under antiviral pressure of lamivudine. We therefore determined the evolution of hepatitis B virus (HBV) precore/basal core promoter and polymerase genes in HBeAg-positive chronic hepatitis B patient during lamivudine therapy. METHOD: Thirteen patients with HBeAg-positive chronic hepatitis who had received short-term lamivudine therapy (mean, 30 weeks) during 1999-2001 were enrolled. The precore/basal core promoter region and polymerase gene were amplified and directly sequenced before, during and post lamivudine treatment. RESULT: HBeAg loss or seroconversion occurred in 11, but eight relapsed after stopping therapy and five had reversion of HBeAg. Before treatment, basal core promoter mutation was found in 1. In the first 3 months of therapy, a rapid decline of serum HBV DNA level accompanied with basal core promoter mutation appeared in 11 of 13 patients (vs. before therapy; P=0.003). However, this mutant was replaced by wild-type virus in four of eight patients who relapsed after treatment. There was no significant change of precore sequences before and during therapy. CONCLUSIONS: Lamivudine therapy may result in the rapid development of basal core promoter mutation of HBV, but this mutation may revert to wild type gradually after cessation of therapy.

Adult↗
PubMed2001

Differential evolution of eastern equine encephalitis virus populations in response to host cell type.

Arthropod-borne viruses (arboviruses) cycle between hosts in two widely separated taxonomic groups, vertebrate amplifying hosts and invertebrate vectors, both of which may separately or in concert shape the course of arbovirus evolution. To elucidate the selective pressures associated with virus replication within each portion of this two-host life cycle, the effects of host type on the growth characteristics of the New World alphavirus, eastern equine encephalitis (EEE) virus, were investigated. Multiple lineages of an ancestral EEE virus stock were repeatedly transferred through either mosquito or avian cells or in alternating passages between these two cell types. When assayed in both cell types, derived single host lineages exhibited significant differences in infectivity, growth pattern, plaque morphology, and total virus yield, demonstrating that this virus is capable of host-specific evolution. Virus lineages grown in alternation between the two cell types expressed intermediate phenotypes consistent with dual adaptation to both cellular environments. Both insect-adapted and alternated lineages greatly increased in their ability to infect insect cells. These results indicate that different selective pressures exist for virus replication within each portion of the two-host life cycle, and that alternation of hosts selects for virus populations well adapted for replication in both host systems.

Animals↗
PubMed1991

Positive Darwinian evolution in human influenza A viruses.

We earlier suggested that type A human influenza virus genes undergo positive Darwinian selection through immune surveillance. This requires more favorable amino acid replacements fixed in antigenic sites among the surviving lineages than among the extinct lineages. We now show that viral hemagglutinins fix proportionately more amino acid replacements in antigenic sites in the trunk of the evolutionary tree (survivors) than in the branches (nonsurvivors), demonstrating that type A human influenza virus is undergoing positive Darwinian evolution. The hemagglutinin gene is evolving 3 times faster than the nonstructural gene and the average age of the sampled nonsurvivors is only 1.6 years, so that extinction is not only common but rapid.

Amino Acid Sequence↗
PubMed1997

Human immunodeficiency virus type 1 genetic evolution in children with different rates of development of disease.

The rate of development of disease varies considerably among human immunodeficiency virus type 1 (HIV-1)-infected children. The reasons for these observed differences are not clearly understood but most probably depend on the dynamic interplay between the HIV-1 quasispecies virus population and the immune constraints imposed by the host. To study the relationship between disease progression and genetic diversity, we analyzed the evolution of viral sequences within six perinatally infected children by examining proviral sequences spanning the C2 through V5 regions of the viral envelope gene by PCR of blood samples obtained at sequential visits. PCR product DNAs from four sample time points per child were cloned, and 10 to 13 clones from each sample were sequenced. Greater genetic distances relative to the time of infection were found for children with low virion-associated RNA burdens and slow progression to disease relative to those found for children with high virion-associated RNA burdens and rapid progression to disease. The greater branch lengths observed in the phylogenetic reconstructions correlated with a higher accumulation rate of nonsynonymous base substitutions per potential nonsynonymous site, consistent with positive selection for change rather than a difference in replication kinetics. Viral sequences from children with slow progression to disease also showed a tendency to form clusters that associated with different sampling times. These progressive shifts in the viral population were not found in viral sequences from children with rapid progression to disease. Therefore, despite the HIV-1 quasispecies being a diverse, rapidly evolving, and competing population of genetic variants, different rates of genetic evolution could be found under different selective constraints. These data suggest that the evolutionary dynamics exhibited by the HIV-1 quasispecies virus populations are compatible with a Darwinian system evolving under the constraints of natural selection.

Amino Acid Sequence↗
PubMed1998

Genetic evolution of hepatitis G virus in chronically infected individual patients.

Comparative sequence analysis of different isolates of hepatitis G virus (HGV) has demonstrated significant intersubject genetic heterogeneity, but few data on intrasubject genetic evolution have been reported. To further investigate the genetic diversification of the HGV genome, 36 plasma samples from eleven patients chronically infected with HGV serially obtained 2-4 years apart were analysed. We determined the viral nucleotide sequence of the 5' non-coding (NC) and the NS3 regions by directly sequencing the RT-PCR amplified products obtained from the viral RNAs. Intrasubject sequence variation was found to be 1.3-2.4 x 10(-3) base substitutions per genome site per year within the 5' NC region and 1.3-9.4 x 10(-3) base substitutions per genome site per year within the NS3 region. Depending on the genomic region analysed (i.e. 5' NC or NS3 region), pairwise comparisons and phylogenetic reconstructions showed that intersubject genetic distances were 17.5- to 20.8-fold greater than intrasubject ones. Overall, the evolution rate of HGV in the regions analysed is not significantly different from that found in hepatitis C virus.

Chronic Disease↗
PubMed1997

Secondary structure-dependent evolution of Cymbidium ringspot virus defective interfering RNA.

Mutational analysis of defective interfering (DI) RNAs of Cymbidium ringspot virus (CymRSV) was used to study the mechanism of DI RNA evolution. It was shown that a highly base-paired structure in the 3' region of the longer DI RNA directed the formation of smaller DI RNA molecules. Mutations which increased the stability of the computer-predicted, highly structured 3' region of the longest DI RNA of CymRSV significantly enhanced the generation and accumulation of the smaller derivatives. Sequence analysis of smaller progeny molecules revealed that the highly base-paired region was deleted from the precursor DI RNA. Moreover, sites of recombination were found in other regions of the DI RNA progenies due to transposition of the highly base-paired structure. It is likely that the deletion event was structure- and not sequence-specific, and operated when a foreign sequence containing a 37-nt-long base-paired stem was inserted at the appropriate position of DI RNA.

Base Sequence↗
PubMed2006

Distinct patterns of evolution between respiratory syncytial virus subgroups A and B from New Zealand isolates collected over thirty-seven years.

Respiratory syncytial virus (RSV) is the most important cause of viral lower respiratory tract infections in infants and children worldwide. In New Zealand, infants with RSV disease are hospitalized at a higher rate than other industrialized countries, without a proportionate increase in known risk factors. The molecular epidemiology of RSV in New Zealand has never been described. Therefore, we analyzed viral attachment glycoprotein (G) gene sequences from 106 RSV subgroup A isolates collected in New Zealand between 1967 and 2003, and 38 subgroup B viruses collected between 1984 and 2004. Subgroup A and B sequences were aligned separately, and compared to sequences of viruses isolated from other countries during a similar period. Genotyping and clustering analyses showed RSV in New Zealand is similar and temporally related to viruses found in other countries. By quantifying temporal clustering, we found subgroup B viruses clustered more strongly than subgroup A viruses. RSV B sequences displayed more variability in stop codon usage and predicted protein length, and had a higher degree of predicted O-glycosylation site changes than RSV A. The mutation rate calculated for the RSV B G gene was significantly higher than for RSV A. Together, these data reveal that RSV subgroups exhibit different patterns of evolution, with subgroup B viruses evolving faster than A.

Biological Evolution↗