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PubMed2005

Whole-genome analysis of human influenza A virus reveals multiple persistent lineages and reassortment among recent H3N2 viruses.

Understanding the evolution of influenza A viruses in humans is important for surveillance and vaccine strain selection. We performed a phylogenetic analysis of 156 complete genomes of human H3N2 influenza A viruses collected between 1999 and 2004 from New York State, United States, and observed multiple co-circulating clades with different population frequencies. Strikingly, phylogenies inferred for individual gene segments revealed that multiple reassortment events had occurred among these clades, such that one clade of H3N2 viruses present at least since 2000 had provided the hemagglutinin gene for all those H3N2 viruses sampled after the 2002-2003 influenza season. This reassortment event was the likely progenitor of the antigenically variant influenza strains that caused the A/Fujian/411/2002-like epidemic of the 2003-2004 influenza season. However, despite sharing the same hemagglutinin, these phylogenetically distinct lineages of viruses continue to co-circulate in the same population. These data, derived from the first large-scale analysis of H3N2 viruses, convincingly demonstrate that multiple lineages can co-circulate, persist, and reassort in epidemiologically significant ways, and underscore the importance of genomic analyses for future influenza surveillance.

Evolution, Molecular↗
PubMed1999

Human immunodeficiency virus type 1 genetic evolution in patients with prolonged suppression of plasma viremia.

Treatment of human immunodeficiency virus type 1 (HIV-1)-infected patients with combination drug regimens results in a reduction of plasma viral load to levels below the limit of detection. To investigate the genomic fluctuations in HIV-1 populations from long-term responders to antiviral therapies we analyzed the viral sequence evolution of env and pol genes from sequential peripheral blood mononuclear cell (PBMC) DNA samples of three infected patients. Analyses of sequences covering the V3 and flanking env regions obtained from blood samples at the beginning of the therapy and at 14 or 24 months from baseline revealed that HIV-1 quasispecies continue to evolve in the three patients following combination antiretroviral therapy. Minor drug-resistant mutant subpopulations were also searched for and found in one patient. Interestingly, no minor resistant subpopulations were found in the other two patients despite the fact that they showed evidence of ongoing viral replication. Finally, the genetic analysis of the env gene shows a reduction in PBMC env viral population diversity after long-term response to the therapy in all the patients analyzed.

Anti-HIV Agents↗
PubMed1999

Rearrangements in the 5' nontranslated region and phylogenetic analyses of cucumber mosaic virus RNA 3 indicate radial evolution of three subgroups.

Cucumber mosaic virus (CMV) has been divided into two subgroups based on serological data, peptide mapping of the coat protein, nucleic acid hybridization, and nucleotide sequence similarity. Analyses of a number of recently isolated strains suggest a further division of the subgroup I strains. Alignment of the 5' nontranslated regions of RNA 3 for 26 strains of CMV suggests the division of CMV into subgroups IA, IB, and II and suggests that rearrangements, deletions, and insertions in this region may have been the precursors of the subsequent radiation of each subgroup. Phylogeny analyses of CMV using the coat protein open reading frame of 53 strains strongly support the further division of subgroup I into IA and IB. In addition, strains within each subgroup radiate from a single point of origin, indicating that they have evolved from a single common ancestor for each subgroup.

5' Untranslated Regions↗
PubMed1997

Evolution of hepatitis C virus quasispecies in mothers and infants infected through mother-to-infant transmission.

BACKGROUND/AIMS: Two mother-infant pairs (Pair H and P) were studied to determine the evolution of hepatitis C virus (HCV) quasispecies. METHODS: Eight clones of the hypervariable region of HCV cDNA from the infants' sera sampled at the age of 3 months, 1, 2, and 3 years and the time-corresponding maternal sample were also sequenced. The sequences were analyzed by the nucleotide diversity, substitution rate, and phylogenetic studies. RESULTS: HCV quasispecies of the infants were more homogeneous than those of their mothers, particularly at the age of 3 months (nucleotide diversity, pi = 0.18 x 10(-2)/site in infant H, and 0.22 x 10(-2)/site in infant P). The nucleotide substitution rate in infants also increased as they aged, from 1.2 x 10(-2) to 4.46 x 10(-2)/site/year in infant H, and from 0.21 x 10(-2) to 4.88 x 10(-2)/site/year in infant P respectively. The nucleotide sequence differences between infants and mothers increased from 2.63 x 10(-2) to 9.06 x 10(-2)/site in Pair H, and from 1.85 x 10(-2) to 5.33 x 10(-2)/site in Pair P within 3 years. Phylogenetic studies suggest the infants' initial quasispecies were closely related to their mothers', while they evolved differently. HCV RNA titer was stable during follow-up and the infants' titer was similar to their mothers'. The fluctuations in titer did not correlate with nucleotide diversity. CONCLUSIONS: HCV quasispecies evolved differently in each individual, even though they were genetically linked. The sequence in infants was not a complex as in their mothers.

Adult↗
PubMed1996

Consistent risk group-associated differences in human immunodeficiency virus type 1 vpr, vpu and V3 sequences despite independent evolution.

Human immunodeficiency virus 1 type vpr, vpu and V3 sequences from 15 homosexual men and 19 intravenous drug users in the Amsterdam Cohort studies were analysed. Previously, we reported that V3 domains of viruses from drug users are distinguishable from those of homosexual men on the basis of two silent mutations. Phylogenetic analysis of vpr, vpu and V3 shows that differences in all three regions correlate with risk group. Two positions in both vpr and vpu were found to differ significantly between the risk groups. The distinguishing positions were confirmed for sequences from 11 Scottish and four German samples. The three regions show relatively independent evolution patterns; they resulted in different phylogenies, the only stable clustering being that based on the risk group distinction. Pairwise differences between sequences of the genes were moderately correlated (around 0.30). Surprisingly, when only silent changes are counted, the correlations dropped almost to zero, indicating that the evolution towards independence was more advanced in the silent than in the non-silent positions. This suggests that selection at the amino acid level is not the primary driving force for the independent evolutionary behaviour of the genes. Recombination, combined with restrictions on certain amino acids because of epistatic interactions between the genes, could be an alternative explanation of this phenomenon.

Base Sequence↗
PubMed1987

Molecular epizootiology and evolution of vesicular stomatitis virus New Jersey.

Vesicular stomatitis virus (VSV) has been shown previously to be capable of undergoing rapid mutational change during sequential experimental infections in various tissue culture cell systems (J. Holland, K. Spindler, F. Horodyski, E. Grabau, S. Nichol, and S. Vandepol, Science 215:1577-1585, 1982). The present study was undertaken to determine the degree of genetic diversity and evolution of the virus under natural infection conditions and to gain insight into the epizootiology of the disease. Between 1982 and 1985, numerous outbreaks of VSV of the New Jersey serotype were reported throughout regions of the United States and Mexico. A T1 RNase fingerprint analysis was performed on the RNA genomes of 43 virus isolates from areas of epizootic and enzootic virus activity. This indicates that virus populations were genetically relatively homogeneous within successive U.S. virus epizootics. The data included virus isolates from different epizootic stages, geographical locations, host animals, and host lesion sites. In contrast, only distant genome RNA T1 fingerprint similarities were observed among viruses of the different U.S. epizootics. However, Mexican viruses isolated before or concurrent with U.S. epizootics had very similar RNA genome fingerprints, suggesting that Mexico may have been the possible origin of virus initiating recent U.S. VSV New Jersey outbreaks. Comparison of T1 fingerprints of viruses with enzootic disease areas revealed a greater extent of virus genetic diversity in these areas relative to that observed in epizootic areas. The evolutionary significance of these findings and their relationship to experimental data on VSV evolution are discussed.

Animals↗
PubMed2004

Analysis of hepatitis C virus quasispecies transmission and evolution in patients infected through blood transfusion.

BACKGROUND & AIMS: Studies on hepatitis C virus (HCV) quasispecies dynamics in the natural course of infection are rare owing to difficulties in obtaining samples from the early phase of infection. METHODS: We studied 15 patients from the Transfusion-Transmitted Viruses Study who seroconverted to anti-HCV after receiving infected blood. Follow-up serum samples were collected every 2-3 weeks for 6 months, at 10 months, and at 11-16 years. Viral quasispecies in the second envelope hypervariable region 1 (E2/HVR1) and 5' untranslated region (5'UTR) were analyzed with single-strand conformation polymorphism (SSCP) and heteroduplex mobility assay (HMA). RESULTS: Seven patients cleared infection within 7-24 weeks (mean, 14.0 wk) and 3 patients eventually became anti-HCV negative. In 6 patients with resolving hepatitis the SSCP band pattern remained stable, whereas in one patient minor changes appeared before clearance. In contrast, in all 8 patients progressing to chronicity, major changes in the E2/HVR1 quasispecies developed at 8-22 weeks (mean, 13.1 wk). Shannon entropy and medium mobility shift values derived from HMA gels remained stable in patients with resolving hepatitis but changed in those who developed chronic infection. Only 2 patients showed minor changes in 5'UTR. A decrease in E2/HVR1 complexity at the time of transmission (bottleneck) was found in 5 patients altogether. CONCLUSIONS: Changes in E2/HVR1 quasispecies 8-22 weeks after infection, likely caused by mounting immune pressure, were predictive of ensuing chronic infection, whereas stability was associated with resolution. Our study also showed that composition of HCV quasispecies may be preserved during transmission from host to host.

Adult↗
PubMedDate not supplied

Molecular evolution of human immunodeficiency virus type 1 subtype A in Senegal: 1988-1997.

OBJECTIVE: Few studies have been able to track the genetic diversity of HIV-1 viruses in human populations over time. We analyzed the molecular evolution of subtype A over a 10-year period, in a cohort of female sex workers with a known time of infection. STUDY DESIGN/METHODS: We amplified and sequenced the C2-V3 region of the surface envelope glycoprotein from 73 HIV-1-infected women, infected between 1987-1997. RESULTS: Fifty-one patients were infected by subtype A viruses. The viruses demonstrated significant diversification (p < 0.001) with mean genetic distance increasing from 8.6% in 1989 to 15.9% in 1997. The slope of the fitted curve suggested a rate of diversification of 0.7% per year. The majority of subtype A viruses clustered with HIV-1 subtype A/G recombinant form (IbNG). CONCLUSION: The genetic diversity of HIV-1 subtype A infections doubled over the first 10 years of this high risk population's epidemic, suggesting that implementation of vaccines early in the epidemic may have a higher likelihood of success based on levels of genetic diversity. The A/G recombinant form (IbNG) has taken epidemic proportions in West Africa. This is of particular importance in understanding the epidemiology of HIV-1 subtypes in Africa and to further dissect the potential phenotypic and biological characteristics of these viruses.

Cohort Studies↗
PubMed2004

Genetic diversity and evolution of hepatitis C virus--15 years on.

In the 15 years since the discovery of hepatitis C virus (HCV), much has been learned about its role as a major causative agent of human liver disease and its ability to persist in the face of host-cell defences and the immune system. This review describes what is known about the diversity of HCV, the current classification of HCV genotypes within the family Flaviviridae and how this genetic diversity contributes to its pathogenesis. On one hand, diversification of HCV has been constrained by its intimate adaptation to its host. Despite the >30 % nucleotide sequence divergence between genotypes, HCV variants nevertheless remain remarkably similar in their transmission dynamics, persistence and disease development. Nowhere is this more evident than in the evolutionary conservation of numerous evasion methods to counteract the cell's innate antiviral defence pathways; this series of highly complex virus-host interactions may represent key components in establishing its 'ecological niche' in the human liver. On the other hand, the mutability and large population size of HCV enables it to respond very rapidly to new selection pressures, manifested by immune-driven changes in T- and B-cell epitopes that are encountered on transmission between individuals with different antigen-recognition repertoires. If human immunodeficiency virus type 1 is a precedent, future therapies that target virus protease or polymerase enzymes may also select very rapidly for antiviral-resistant mutants. These contrasting aspects of conservatism and adaptability provide a fascinating paradigm in which to explore the complex selection pressures that underlie the evolution of HCV and other persistent viruses.

Biological Evolution↗
PubMed2000

[Evolution of hepatitis C virus (HCV) infection acquired at birth]

Objectives Our aim was to analyze the evolution of HCV infection in children infected at birth. Methods Between September 1994 and December 1998 we analyzed in a prospective study 8 children born of anti-HCV and HCV RNA positive women. Each baby was controlled at birth, every 3 months during the first year of life, and then every 6 months searching for anti-HCV antibodies (ELISA 3, RIBA 2-3), HCV RNA (RT PCR), ALT and viral genotype. Results Viral RNA was detectable in the first 3 months of life in all babies (100%) and remained positive during the follow-up. Viral genotypes were the same for mothers and their children. In 6 babies (75%) ALT remained pathologic during follow-up. Conclusions HCV infection in children usually has an asymptomatic outcome; the infection has chronic features in the majority of cases.

Journal Article↗
PubMed2006

Dominant influence of an HLA-B27 restricted CD8+ T cell response in mediating HCV clearance and evolution.

Virus-specific CD8+ T cell responses play an important role in the natural course of infection; however, the impact of certain CD8+ T cell responses in determining clinical outcome has not been fully defined. A well-defined cohort of women inoculated with HCV from a single source showed that HLA-B27 has a strong association with spontaneous clearance. The immunological basis for this association is unknown. However, the finding is especially significant because HLA-B27 has also been shown to have a protective role in HIV infection. We report the identification of an HLA-B27 restricted hepatitis C virus (HCV)-specific CD8+ T cell epitope that is recognized in the majority of recovered HLA-B27 positive women. In chronically HCV-infected individuals, analysis of the corresponding viral sequence showed a strong association between sequence variations within this epitope and expression of HLA-B27, indicating allele-specific selection pressure at the population level. Functional analysis in 3 chronically HCV-infected patients showed that the emerging variant viral epitopes represent escape mutations. In conclusion, our results suggest a dominant role of HLA-B27 in mediating spontaneous viral clearance as well as viral evolution in HCV infection and mechanistically link both associations to a dominant novel CD8+ T cell epitope. These results support the central role of virus-specific CD8+ T cells and the genetically determined restriction of the virus-specific T cell repertoire in HCV infection.

Adult↗
PubMed1994

Evolution of feline leukemia virus variant genomes with insertions, deletions, and defective envelope genes in infected cats with tumors.

In order to study retroviral variation, selection, and viral correlates of in vivo pathogenicity, we documented the evolution of feline leukemia virus (FeLV) variants in cats that died with thymic lymphoma after infection with molecularly cloned subgroup A FeLV. Using genomic DNA from cat necropsy samples, we employed PCR to amplify and clone the envelope gene, which is a major determinant of the specific pathogenicity of different FeLV variants. In the envelope gene, mutations encoded scattered amino acid changes that did not cluster into clearly definable variable regions; however, characterization of these terminal variant sequences revealed a predominance of G-to-A and A-to-G nucleotide substitutions. Additionally, some cats harbored variants with recombinant subgroup B-like envelope genes, while the major variant from one cat had a 12-bp insertion in a region previously characterized as an immunodeficiency-inducing determinant. Finally, proviruses from tumor DNA frequently possessed envelope genes predicted to encode a protein truncated in the N-terminal half because of either premature termination codons or deletions ranging from 29 to 1,666 bp. In contrast, all envelope genes cloned from the bone marrow of one cat were predicted to encode full-length envelope product, and only a minority of proviral clones from a cat that did not develop a tumor had defective envelope genes. Thus, in the cat, viruses evolved from subgroup A FeLV that had point mutations, insertions, deletions, or recombinant envelope genes. Furthermore, defective variants were particularly prominent in T-cell tumors.

Amino Acid Sequence↗
PubMed2000

Iridovirus homologues of cellular genes--implications for the molecular evolution of large DNA viruses.

Iridoviruses belong to the group of large cytoplasmic deoxyriboviruses and infect either insects or vertebrates. In analogy to other large DNA viruses of eucaryotes it was found that iridoviruses encode a number of cellular protein homologues. The majority of these proteins represent orthologues of cellular enzymes involved in transcription, replication, and nucleotide metabolism. Others may have the potential to interfere with cell cycle regulation or immune defence mechanisms of the host. This raises the question about the phylogenetic origin of the corresponding viral genes. During the evolution of large cytoplasmic DNA viruses such as iridoviruses, poxviruses, and African swine fever virus the acquirement of cellular genes appears to be a crucial event. Each member of this group of viruses encodes a DNA polymerase, two subunits of the DNA-dependent RNA polymerase, and two subunits of the ribonucleotide reductase. It is important to note that all of these viral proteins show a high level of multidomain structure conservation as compared to their cellular orthologues. As a consequence the large cytoplasmic DNAviruses have the ability to replicate independently of the cellular nucleus in the cytoplasm of the infected cell. Assuming a common cellular origin of viral DNA polymerase genes the corresponding amino acid sequences were chosen to construct a phylogenetic tree showing the relatedness among large DNA viruses of eucaryotes.

Animals↗
PubMed1991

Evolution of human immunodeficiency virus type 1 nef and long terminal repeat sequences over 4 years in vivo and in vitro.

The evolution of an 851-bp segment of the human immunodeficiency virus type 1 (HIV-1) genome encoding the nef open reading frame and U3/R elements of the long terminal repeat has been followed over a 4-year period in vivo and in vitro. The population of viral sequences at any given time was established by sequencing cloned polymerase chain reaction products. The samples studied were derived from the same man for whom a detailed analysis of the tat gene was previously described (A. Meyerhans, R. Cheynier, J. Albert, M. Seth, S. Kwok, J. Sninsky, L. Morfeldt-Manson, B. Asjö, and S. Wain-Hobson, Cell 58:901-910, 1989). Once again in vitro culture resulted in the selection of minor forms. Over a 4-year period in vivo, there was no obvious selection for, or outgrowth of, any particular nef or U3/R sequence. Few defective nef protein sequences were observed, which argues against nef acting as a negative regulatory factor. Although no functionally defective promoter/trans-activation-responsive elements were identified, the transactivation efficiencies varied between 0.2 and 2 times that of the control. The sequence encoding the most efficient trans-activation-responsive region did not outgrow others. The extreme genetic heterogeneity of the different samples of the locus, either in vivo or in vitro, indicates that there is no such thing as a single, distinct HIV sequence. It is suggested that different HIV-1 loci evolve independently, recombination being responsible for their uncoupling.

Base Sequence↗