Herpesviruses, latency and cancer: a biochemical approach.
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BLV and HTLV-I: their unique genomic structures and evolutionary relationship.
We have compared the sequences of the entire genomes of bovine leukemia virus (BLV) and human T-cell leukemia virus type I (HTLV-I). Both the gag and pol genes show overall strong homologies between the two retroviruses, indicating their close evolutionary relationship. However, a surface glycoprotein portion of the env gene shows little if any homology, probably reflecting a difference in their host range. These retroviruses appear to harbour a gag precursor-cleaving protease, a not yet experimentally identified viral protein, between their gag and pol genes. Most interestingly, the 3' end portion of the BLV genome (designated pXBL) contains a long open reading frame that has a typical protein-coding property. The product of this open reading frame has now been identified as a protein of 38,000 daltons, which is produced by a spliced mRNA. We note that its amino acid sequence shows appreciable homology, especially in its N-terminal quarter, to that of the HTLV-I counterpart (pX), and we thus suggest that BLV pXBL and HTLV-I pX has diverged from a common ancestral gene. Finally and very importantly, comparisons of the best conserved pol sequences and overall genomic organizations between BLV and several other oncoviruses allow us to propose that BLV and HTLV-I constitute a novel group of Oncovirinae, designated here as type "E."
Biological Evolution↗
Evidence for a model ancestral viroid.
The generation of a phylogenetic tree of viroids and viroid-like plant satellite RNAs via computer analysis, coupled with several conspicuous biochemical characteristics of the rolling circle replication of these RNAs -including both self-cleavage and self-ligation- leads us to propose the peach latent mosaic viroid (PLMVd) as a current "living fossil" dating from a precellular world. Incorporated within this proposal is a revised mechanism of PLMVd rolling circle replication which requires a minimal protein involvement.
Evolution, Molecular↗
Simian immunodeficiency virus (SIV) envelope quasispecies transmission and evolution in infant rhesus macaques after oral challenge with uncloned SIVmac251: increased diversity is associated with neutralizing antibodies and improved survival in previously immunized animals.
BACKGROUND: Oral infection of infant macaques with simian immunodeficiency virus (SIV) is a useful animal model to test interventions to reduce postnatal HIV transmission via breast-feeding. We previously demonstrated that immunization of infant rhesus macaques with either modified vaccinia virus Ankara (MVA) expressing SIV Gag, Pol and Env, or live-attenuated SIVmac1A11 resulted in lower viremia and longer survival compared to unimmunized controls after oral challenge with virulent SIVmac251 (Van Rompay et al., J. Virology 77:179-190, 2003). Here we evaluate the impact of these vaccines on oral transmission and evolution of SIV envelope variants. RESULTS: Limiting dilution analysis of SIV RNA followed by heteroduplex mobility assays of the V1-V2 envelope (env) region revealed two major env variants in the uncloned SIVmac251 inoculum. Plasma sampled from all infants 1 week after challenge contained heterogeneous SIV env populations including one or both of the most common env variants in the virus inoculum; no consistent differences in patterns of env variants were found between vaccinated and unvaccinated infants. However, SIV env variant populations diverged in most vaccinated monkeys 3 to 5 months after challenge, in association with the development of neutralizing antibodies. CONCLUSIONS: These patterns of viral envelope diversity, immune responses and disease course in SIV-infected infant macaques are similar to observations in HIV-infected children, and underscore the relevance of this pediatric animal model. The results also support the concept that neonatal immunization with HIV vaccines might modulate disease progression in infants infected with HIV by breast-feeding.
Animals↗
Evolution of bovine respiratory syncytial virus.
Until now, the analysis of the genetic diversity of bovine respiratory syncytial virus (BRSV) has been based on small numbers of field isolates. In this report, we determined the nucleotide and deduced amino acid sequences of regions of the nucleoprotein (N protein), fusion protein (F protein), and glycoprotein (G protein) of 54 European and North American isolates and compared them with the sequences of 33 isolates of BRSV obtained from the databases, together with those of 2 human respiratory syncytial viruses and 1 ovine respiratory syncytial virus. A clustering of BRSV sequences according to geographical origin was observed. We also set out to show that a continuous evolution of the sequences of the N, G, and F proteins of BRSV has been occurring in isolates since 1967 in countries where vaccination was widely used. The exertion of a strong positive selective pressure on the mucin-like region of the G protein and on particular sites of the N and F proteins is also demonstrated. Furthermore, mutations which are located in the conserved central hydrophobic part of the ectodomain of the G protein and which result in the loss of four Cys residues and in the suppression of two disulfide bridges and an alpha helix critical to the three-dimensional structure of the G protein have been detected in some recent French BRSV isolates. This conserved central region, which is immunodominant in BRSV G protein, thus has been modified in recent isolates. This work demonstrates that the evolution of BRSV should be taken into account in the rational development of future vaccines.
Amino Acid Sequence↗
Etiopathogenetic role of hepatitis C virus in mixed cryoglobulinemia, chronic liver diseases and lymphomas.
Hepatitis C virus (HCV) infection has been found in the majority of patients with mixed cryoglobulinemia (MC) in studies conducted in different countries. In our series of 110 MC patients the frequency of HCV markers was significantly high (91%) compared with other rheumatic diseases (6.4%) and with healthy Italian controls (1.2%). Moreover, HCV RNA was detected in 81% of the peripheral lymphocytes from MC patients. Comparable percentages of HCV infection were detectable in other disorders, i.e. porphyria cutanea tarda (77%) and autoimmune hepatitis type 1 (77%). The HCV infection of peripheral lymphocytes suggests that this virus could be the triggering factor for the lymphoproliferation underlying MC. In a number of patients with MC the evolution from a benign lymphoproliferation to frank B-cell lymphoma was observed. In these subjects HCV RNA in the sera and in fresh and cultured peripheral lymphocytes was constantly detected. The same phenomenon has been observed in patients with long-lasting type C chronic hepatitis. Interestingly, HCV infection has also been recorded in 32% of idiopathic B-cell non-Hodgkin's lymphomas. Taken together, the above findings suggest that HCV can cause benign B-cell proliferation with the consequent production of various autoantibodies, including rheumatoid factor and mixed cryoglobulins. These serological abnormalities characterise different clinical disorders, including the appearance of lymphoma in a not negligible number of individuals.
Cryoglobulinemia↗
A longitudinal analysis of hepatitis C virus replication following liver transplantation.
BACKGROUND & AIMS: The pathogenesis of graft injury in liver transplant recipients with recurrent hepatitis C virus (HCV) infection remains poorly understood. In this study, the relationship between HCV replication, genotype, and the evolution of graft damage was investigated. METHODS: HCV RNA was quantified in 184 protocol sera from 25 patients transplanted for HCV cirrhosis. HCV isolates were genotyped, and hepatic expression of core and NS4 antigens was sought in protocol allograft biopsy specimens. RESULTS: Acute lobular hepatitis was accompanied by a steep increase in HCV RNA levels and the appearance of core and NS4 antigens in the graft. Methylprednisolone treatment for acute rejection led to a 4-100-fold increase in serum HCV RNA. At the end of follow-up, HCV RNA levels were 3-112 times pretransplant levels and were higher in patients with more severe hepatitis. Progressive liver damage developed in 7 of 14 patients with HCV genotype 1b and in 1 of 11 patients infected with other genotypes (P = 0.03). CONCLUSIONS: Peak viremia levels and the initial detection of HCV antigens in hepatocytes suggests increased viral replication at the time of acute HCV hepatitis in the graft. Genotype 1b and higher viremia levels were associated with more severe chronic graft damage.
Adult↗
Infectious molecular clones from a simian immunodeficiency virus-infected rapid-progressor (RP) macaque: evidence of differential selection of RP-specific envelope mutations in vitro and in vivo.
A minor fraction of simian immunodeficiency virus (SIV)-infected macaques progress rapidly to AIDS in the absence of SIV-specific immune responses. Common mutations in conserved residues of env in three SIVsmE543-3-infected rapid-progressor (RP) macaques suggest the evolution of a common viral variant in RP macaques. The goal of the present study was to analyze the biological properties of these variants in vitro and in vivo through the derivation of infectious molecular clones. Virus isolated from a SIVsmE543-3-infected RP macaque, H445 was used to inoculate six naive rhesus macaques. Although RP-specific mutations dominated in H445 tissues, they represented only 10% of the population of the virus stock, suggesting a selective disadvantage in vitro. Only one of these macaques (H635) progressed rapidly to AIDS. Plasma virus during primary infection of H635 was similar to the inoculum. However, RP-specific mutations were apparently rapidly reselected by 4 to 9 weeks postinfection. Terminal plasma from H635 was used as a source of viral RNA to generate seven full-length, infectious molecular clones. With the exception of one clone, which was similar to SIVsmE543-3, clones with RP-specific mutations replicated with delayed kinetics in rhesus peripheral blood mononuclear cells and human T-cell lines. None of the clones replicated in monocyte-derived or alveolar macrophages, and all used CCR5 as their major coreceptor. RP variants appear to be well adapted to replicate in vivo in RP macaques but are at a disadvantage in tissue culture compared to their parent, SIVsmE543-3. Therefore, tissue culture may not provide a good surrogate for replication of RP variants in macaques. These infectious clones will provide a valuable reagent to study the roles of specific viral variants in rapid progression in vivo.
Amino Acid Sequence↗
[Molecular evolutionary analysis of GB viruses and hepatitis G virus].
Recently, new blood-transfusion transmissible viruses, called hepatitis G virus(HGV) and GB virus-C(GBV-C), have been reported. It was found that two viruses were independent isolates of the same virus, the genomic structure resembled that of flavivirus family, and GBV-C/HGV was closely related to HCV. To elucidate the evolutionary relationship between hepatitis C virus(HCV) and GBV-C/HGV, we constructed the phylogenetic trees for the putative RNA helicase and the RNA-dependent RNA polymerase regions of the Flaviviridae by UPGMA. The tree showed that HCV was closely related to GB virus-B(GBV-B) and HGV was more nearer to GB virus-A(GBV-A) rather than HCV.
Amino Acid Sequence↗
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↗
Evidence for recombination in natural populations of dengue virus type 1 based on the analysis of complete genome sequences.
Recombination events are known to occur in non-segmented RNA viruses like polioviruses or alphaviruses. Analysis of the subgenomic sequences of dengue virus type 1 (DENV-1) structural genes has recently allowed the identification of possible recombination breakpoints. Because DENV is a major human pathogen, this discovery might have important implications for virus pathogenicity, vaccine safety and efficiency, or diagnosis and, therefore, requires clear confirmation. We report the complete sequence determination of one Asian and two African strains of DENV-1 isolated from human patients. Rigorous sequence analysis provided strong evidence for the occurrence of intragenomic recombination events between DENV-1 strains belonging to different lineages. Singapore S275/90 strain appears to be the evolutionary product of a recombination event between viruses belonging to two distinct lineages: one lineage includes an African strain isolated in Abidjan (Ivory Coast) and the other includes isolates from Djibouti and Cambodia. The 'Recombination Detection Program', bootscanning and analysis of diversity plots provided congruent results concerning the existence of a two-switch recombination event and the localization of recombination breakpoints. Thus, the 5' and 3' genomic ends of the Singapore S275/90 strain were inherited from a Djibouti/Cambodia lineage ancestor and an internal fragment located in the envelope/NS1 region originated from an Abidjan lineage ancestor.
Base Sequence↗
Genomic sequence of the structural proteins of louping ill virus: comparative analysis with tick-borne encephalitis virus.
The genomic RNA of louping ill virus coding for capsid, premembrane, membrane, and envelope proteins was cloned and sequenced. Hydrophilicity profiles of the deduced amino acid sequence shared homologous functional domains with other flaviviruses. The premembrane and envelope proteins contain N-glycosylation sites and conserved cysteine residues which are important for maintaining the secondary structures of the proteins. Sequence comparisons of louping ill envelope protein showed greater homology with tick-borne than mosquito-borne flaviviruses and greater homology with the western than the far eastern subtype of tick-borne encephalitis virus. With the capsid and membrane proteins, the degree of homology between louping ill and the western subtype was greater than that between the two subtypes, indicating very close evolutionary relationships between louping ill and the western subtype of tick-borne encephalitis. Thus, louping ill and tick-borne encephalitis may be varieties of a common tick-borne ancestral virus. The average amino acid sequence diversity between members of the tick-borne serogroup was significantly lower than that of mosquito-borne serogroups, suggesting that tick-borne flaviviruses have been subjected to different evolutionary immune selection pressure from the mosquito-borne viruses. Using the published model of tick-borne encephalitis envelope protein and our sequence data on louping ill virus, we have identified three discontinuous peptides (amino acids 81-88, 207-212, and 230-234) which may represent critical molecular determinants within the receptor binding site of tick-borne flaviviruses and may provide a specific genetic marker for these viruses.
Amino Acid Sequence↗
Evidence of recombination in the norovirus capsid gene.
Noroviruses are single-stranded RNA viruses with high genomic variability. They have emerged in the last decade as a major cause of acute gastroenteritis. It remains so far unclear whether norovirus evolution is driven by sequence mutation and/or recombination. In this study, we have assessed the occurrence of recombination in the norovirus capsid gene. For this purpose, 69 complete capsid sequences of norovirus strains accessible in GenBank as well as 25 complete capsid sequences generated from norovirus-positive clinical samples were examined. Unreported recombination was detected in about 8% of norovirus strains belonging to genetic clusters I/1 (n = 1), II/1 (n = 1), II/3 (n = 1), II/4 (n = 3), and II/5 (n = 1). Recombination breakpoints were mainly located at the interface of the putative P1-1 and P2 domains of the capsid protein and/or within the P2 domain. The recombination region displayed features such as length, sequence composition (upstream and downstream GC- and AU-rich sequences, respectively), and predicted RNA secondary structure that are characteristic of homologous recombination activators. Our results suggest that recombination in the norovirus capsid gene may naturally occur, involving capsid domains presumably exposed to immunological pressure.
Amino Acid Sequence↗
Inhibition of ribozymes by deoxyribonucleotides and the origin of DNA.
Two catalytic functions were required, minimally, for the appearance of DNA in evolution: a ribonucleotide reductase (RNR) and a reverse transcriptase (RT). If one accepts the explanatory strength of the RNA world model, it is clear that DNA molecules arose in the RNA world at some stage during the early evolution of cells. I suggest that competition for limited and valuable resources such as nucleotides, amino acids, and sugars made an early appearance among RNA cells, RNA viruses, viroids, and RNA plasmids. Structural and functional similarities between the different types of polymerases favor the simple hypothesis that the first RTs were RNA polymerase mutants that preferentially joined together preexisting deoxyribonucleotide triphosphates (dNTPs) using RNA templates. What was the role of dNTPs inside cells before DNA was synthesized and tested by natural selection? The oxygen atom that is removed by the reductase is of crucial importance to many ribozyme functions, since the 2'-OH is a strong nucleophile that forms transitional states during catalysis. Consequently, a RNR may have been used by cellular parasites to inhibit ribozyme action. Thus, DNA may have been, initially, an inert by-product of retrotranscription in lineages that acquired RTs and could synthesize DNA molecules using cellular RNA templates to detoxify the intracellular environment. DNA was useless as template until a transcriptase (DNA-dependent RNA polymerase) evolved that could copy (-)DNA to reconstitute the (+)RNA genome, indeed a successful way of confronting ribonuclease threats in the RNA world.
DNA↗
[Genome of influenza virus: organization, function, evolution].
Basic features of influenza virus genome structure, replication and evolution are reviewed with a special emphasis upon the segmentary structure of the genome and the use of cell mRNA as primer in virus-specific transcription. The structural and functional autonomy of virus genomic segments and the selection of the segments in the process of viral genome assembly is considered to be the basis for the gene reassortment and the appearance of recombinants. The reassortment of genes is discussed in relation to the nature of "new" antigenic subtypes of human influenza A virus, that is, to the orivin of antigenic shifts and pandemic strains. Another kind of antigenic variation (antigenic drift) is produced by the accumulation of mutations under the conditions of selection pressure in an immune population. Together with the conservation of earlier antigenic subtypes in animal populations these two types of evolutionary changes produce a complex pattern of influenza virus evolution. The prospects of influenza control are briefly discussed in connection with the characteristics of influenza virus genome structure and evolution.
Antigens, Viral↗
Comparison of Colombian and Costa Rican strains of rice hoja blanca tenuivirus.
The sequences of RNA-3 and RNA-4 of rice hoja blanca tenuivirus isolates from Colombia and from Costa Rica were determined and analyzed. These isolates were 98.9% and 98.6% identical in the coding and non-coding regions of RNA-3, and 96.9 and 91.5% identical in the coding and non-coding regions of RNA-4, and are therefore strains of the same virus. There is about three times as much variation between isolates (based on consensus sequences) as there is within isolates (based on sequences of individual clones). There is also considerably more variation for RNA-4 (both between and within isolates) than there is for RNA-3, even though between tenivirus species RNA-3 has diverged more than RNA-4, implying that the evolution of the tenuivirus RNAs is not necessarily dependent on the amount of variation found for these RNAs.
Colombia↗
A genomewide search for ribozymes reveals an HDV-like sequence in the human CPEB3 gene.
Ribozymes are thought to have played a pivotal role in the early evolution of life, but relatively few have been identified in modern organisms. We performed an in vitro selection aimed at isolating self-cleaving RNAs from the human genome. The selection yielded several ribozymes, one of which is a conserved mammalian sequence that resides in an intron of the CPEB3 gene, which belongs to a family of genes regulating messenger RNA polyadenylation. The CPEB3 ribozyme is structurally and biochemically related to the human hepatitis delta virus (HDV) ribozymes. The occurrence of this ribozyme exclusively in mammals suggests that it may have evolved as recently as 200 million years ago. We postulate that HDV arose from the human transcriptome.
Base Pairing↗
Phylogenetic evidence for the rapid evolution of human B19 erythrovirus.
Human B19 erythrovirus is a ubiquitous viral pathogen, commonly infecting individuals before adulthood. As with all autonomous parvoviruses, its small single-stranded DNA genome is replicated with host cell machinery. While the mechanism of parvovirus genome replication has been studied in detail, the rate at which B19 virus evolves is unknown. By inferring the phylogenetic history and evolutionary dynamics of temporally sampled B19 sequences, we observed a surprisingly high rate of evolutionary change, at approximately 10(-4) nucleotide substitutions per site per year. This rate is more typical of RNA viruses and suggests that high mutation rates are characteristic of the Parvoviridae.
Base Sequence↗