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PubMed1999

Phylogenetic analysis of H7 avian influenza viruses isolated from the live bird markets of the Northeast United States.

The presence of low-pathogenic H7 avian influenza virus (AIV), which is associated with live-bird markets (LBM) in the Northeast United States, was first detected in 1994 and, despite efforts to eradicate the virus, surveillance of these markets has resulted in numerous isolations of H7 AIVs from several states from 1994 through 1998. The hemagglutinin, nonstructural, and matrix genes from representative H7 isolates from the LBM and elsewhere were sequenced, and the sequences were compared phylogenetically. The hemagglutinin gene of most LBM isolates examined appeared to have been the result of a single introduction of the hemagglutinin gene. Evidence for evolutionary changes were observed with three definable steps. The first isolate from 1994 had the amino acid threonine at the -2 position of the hemagglutinin cleavage site, which is the most commonly observed amino acid at this site for North American H7 AIVs. In January 1995 a new genotype with a proline at the -2 position was detected, and this genotype eventually became the predominant virus isolate. A third viral genotype, detected in November 1996, had an eight-amino-acid deletion within the putative receptor binding site. This viral genotype appeared to be the predominant isolate, although isolates with proline at the -2 position without the deletion were still observed in viruses from the last sampling date. Evidence for reassortment of multiple viral genes was evident. The combination of possible adaptive evolution of the virus and reassortment with different influenza virus genes makes it difficult to determine the risk of pathogenesis of this group of H7 AIVs.

Amino Acid Sequence↗

PubMed1997

Genetic recombination of poliovirus in a cell-free system.

Genetic recombination of plus-strand RNA viruses is an important process for promoting genetic variation. By using genetically marked poliovirus RNAs, we have demonstrated that genetic recombination can occur in a cell-free system that generates infective virus from added poliovirus RNA. Recombinant polioviruses were isolated, and the region of crossing over was roughly mapped. Recombinants could be isolated even under conditions where the yield of viruses from one of the parental RNAs was depressed to levels comparable to or less than the yield of recombinant viruses, an observation suggesting that only one of the recombining RNAs needs to be replication-competent. The generation of poliovirus recombinants in a cell-free system offers new possibilities for studying recombination and evolution of RNA viruses.

Biological Evolution↗

PubMed1995

[Progression of viral infection in twins born from a mother infected with human immunodeficiency virus].

We studied the evolution of HIV-1 infection and immune response during six years in two twins born from an infected mother. The children had a continuous progression of the infection, proved by CD4+ cell count, serum anti-HIV antibodies, cultivable virus and proviral load. Now, both children are on antiviral treatment. The analysis of serum antibodies showed a different immune response in both children. One of them developed higher levels of antibodies directed against viral proteins and synthetic peptides derived from their aminoacid sequence. In this child, the amount of cultivable virus increased less than in his twin. Nucleotide sequencing of a part of viral genoma, showed that the virus belonged to the B subtype, prevalent in America and Europe. The observed differences in viral sequences suggest a different selective pressure in both twins. This phenomenon could be related to the observed differences in immune response.

Acquired Immunodeficiency Syndrome↗

PubMed2005

The role of viruses in cell fusion and its importance to evolution, invasion and metastasis of cancer clones.

The hypothesis described here is a logical extension of two areas of observation: First, it has been discovered that viruses (and perhaps other intracellular parasites) catalyze cell fusion as a means of cell-to-cell transmission. Effective cell-to-cell transmission appears to require: (i) induced expression of adhesion molecules on the cell surface; (ii) suppression of p53-dependent apoptosis; (iii) arrest of the cell cycle that would otherwise lead to cell death by "mitotic catastrophe". Suppression of apoptosis and cell death through "mitotic catastrophe" are important for formation of stable syncytia. Expression of Bcl-2 or a viral analogue of Bcl-2 (vBcl-2) is particularly useful to viruses because Bcl-2 both suppresses (p53-dependent) apoptosis and arrests the cell cycle through p27. Bcl-2 may also block any p53-independent cell death (e.g., mitotic catastrophe) that is initiated at the mitochondria. Second, it has been found that cell fusion plays a role in cancer clone evolution, invasion of normal cells in tissue adjacent to tumors and metastasis to remote normal tissues. Thus, it can be hypothesized that infection of cancer cells with viruses that spread by cell-to-cell transmission may coincidentally contribute to development of aggressive aneuploid clones and facilitate both invasion and metastasis of tumors. Regardless of the role of viruses, suppression of Bcl-2 may be an approach to preventing successful formation of syncytia and limiting the invasion and metastasis of tumors, thus, making surgical removal and radiation treatment more feasible.

Aneuploidy↗

PubMed1988

Rapid selection of genetic and antigenic variants of foot-and-mouth disease virus during persistence in cattle.

Rapid evolution of foot-and-mouth disease virus (FMDV) is documented during persistent infections of cattle. The carrier state was established experimentally with plaque-purified FMDV of serotype C3. Virus was recovered from the esophageal pharyngeal area of the animals up to 539 days postinfection. Analysis of capsid proteins by electrofocusing and by electrophoretic mobility of the genomic poly(C)-rich tract suggested heterogeneity in several isolates and sequential dominance of viral subpopulations. Nucleotide sequences of the VP1-coding region of the parental FMDV C3 clones and of seven isolates from the carrier cattle showed point mutations that represented rates of fixation of mutations of 0.9 X 10(-2) to 7.4 X 10(-2) substitutions per nucleotide per year; 59% of the base changes led to amino acid substitutions, some of which were located within residues 135 to 151, a region involved in neutralization of FMDV. In the esophageal pharyngeal fluid samples, FMDV C3-neutralizing activity was present. Antigenic variation was demonstrated with monoclonal antibodies raised against FMDV C3. Two isolates from carrier cattle differed from the parental virus by 10(2)- or 10(3)-fold decreased reactivity with neutralizing monoclonal antibodies. We suggest that persistent, inapparent infections of ruminants, in addition to being a reservoir of virus, may promote the rapid selection of antigenically variant FMDVs.

Amino Acid Sequence↗

PubMed1954

[The viruses of the 1952-3 influenza epidemic].

The results of antigenic studies of the viruses received at the World Influenza Centre from the 1952-3 influenza epidemic are described. As in 1950-1, two main antigenic groups of influenza A viruses could be distinguished. One group, called Liverpool, contained strains closely related to 1950-1 Liverpool strains. The other, called Scandinavian, contained strains related to but not identical with 1950-1 Scandinavian viruses. Altogether, 175 Scandinavian, 33 Liverpool, and 4 influenza B virus strains were examined.A peculiar relationship between 1950-1 and 1952-3 Scandinavian viruses was investigated by antibody absorption experiments. It was concluded that A/Sweden/3/50 and A/Missouri/303/52 viruses had a rather similar antigenic composition, but that the dominant antigen in the former strain was contained within the virus particle whereas it was a surface constituent of the latter strain. The possible significance of this finding in the antigenic evolution of influenza viruses is discussed.The findings suggest that survival of influenza viruses without much antigenic alteration from one epidemic to the next, two years later, is a demonstrable but uncommon finding. Evidence is presented that this survival was followed by separate spread of each antigenic variety of virus in different countries.

Antibodies↗

PubMed1990

Molecular evolution of human T-cell leukemia virus.

Phylogenetic trees for the human T-cell leukemia virus type I (HTLV-I) and its related viruses were constructed by use of nucleotide sequences of the long terminal repeat (LTR) and the tax gene. The trees showed that the viruses diverged from a common ancestral virus and that they are classified into two groups whose hosts are either primates or bovines. However, the topology of the trees for the viruses differed from that for the hosts. This suggests that HTLV-I and HTLV-I-related viruses evolved independently of host-species divergence and that interspecies transmission between human and monkeys occurred in the past. The nucleotide diversity of the tax genes of HTLV-I was estimated to be 0.025. This value is more than 10 times larger than that of human globin genes, but it is about 20 times smaller than that of hemagglutinin genes of influenza A viruses. Thus, the genetic variability of the HTLV-I genes seems to be higher than that of nuclear genes but much lower than the genes of typical RNA viruses. Furthermore, we examined functional constraints on the overlapping region of the rex and tax genes. The results obtained imply that for the overlapping region, the tax gene has much stronger constraints against amino acid changes than the rex gene.

Animals↗

PubMed2006

Compensatory substitutions restore normal core assembly in simian immunodeficiency virus isolates with Gag epitope cytotoxic T-lymphocyte escape mutations.

The evolution of human immunodeficiency virus type 1 (HIV-1) and simian immunodeficiency virus (SIV) as they replicate in infected individuals reflects a balance between the pressure on the virus to mutate away from recognition by dominant epitope-specific cytotoxic T lymphocytes (CTL) and the structural constraints on the virus' ability to mutate. To gain a further understanding of the strategies employed by these viruses to maintain replication competency in the face of the intense selection pressure exerted by CTL, we have examined the replication fitness and morphological ramifications of a dominant epitope mutation and associated flanking amino acid substitutions on the capsid protein (CA) of SIV/simian-human immunodeficiency virus (SHIV). We show that a residue 2 mutation in the immunodominant p11C, C-M epitope (T47I) of SIV/SHIV not only decreased CA protein expression and viral replication, but it also blocked CA assembly in vitro and virion core condensation in vivo. However, these defects were restored by the introduction of upstream I26V and/or downstream I71V substitutions in CA. These findings demonstrate how flanking compensatory amino acid substitutions can facilitate viral escape from a dominant epitope-specific CTL response through the effects of these associated mutations on the structural integrity of SIV/SHIV.

Amino Acid Sequence↗

PubMed2000

Pretransplantation hepatitis C virus quasispecies may be predictive of outcome after liver transplantation.

The evolution of hepatitis C virus (HCV) envelope variation was studied using a liver-transplant model to evaluate the role of HCV quasispecies for hepatocyte infection. Twelve HCV polymerase chain reaction (PCR)-positive liver-transplant recipients (6 with posttransplantation biochemical hepatitis and 6 without hepatitis [controls]) were prospectively evaluated and underwent detailed quasispecies analysis of pre- and postoperative serum samples. HCV amino acid sequence diversity and complexity at the first hypervariable region (HVR1) of the second envelope protein (E2) was correlated with outcome. Recurrence of HCV-induced allograft injury was defined by persistently elevated serum alanine transaminase (ALT) levels. The major variant (sequences >10% of all clones) of recipients with hepatitis accounted for a significantly smaller percent of all preoperative clones compared with controls (41% +/- 6% vs. 69% +/- 8%; P <.015). Recipients with hepatitis had an increased number of pretransplantation major variants (2.5 +/- 0.3 vs. 1.1 +/- 0.2; P <.006). Eighty-three percent of controls had a predominant variant (accounting for >50% of clones) compared with 17% of those with recurrence (P <.05). These differences did not persist postoperatively. In addition, recipients without a pretransplantation predominant variant demonstrated an increased allograft fibrosis score (2.3 +/- 0.3 vs. 0.5 +/- 0.3; P <.015) at 181 to 360 days posttransplantation compared with those in whom a predominant variant was present. Increased HCV envelope complexity may act as a stronger antigenic stimulus or improve hepatocyte receptor binding and lead to allograft hepatitis and fibrosis. Although pretransplantation differences in HCV quasispecies did not persist postoperatively, pretransplantation quasispecies may be a predictor of HCV-induced hepatitis and graft fibrosis after liver transplantation.

Adult↗

PubMed2006

Evolutionary basis of codon usage and nucleotide composition bias in vertebrate DNA viruses.

Understanding the extent and causes of biases in codon usage and nucleotide composition is essential to the study of viral evolution, particularly the interplay between viruses and host cells or immune responses. To understand the common features and differences among viruses we analyzed the genomic characteristics of a representative collection of all sequenced vertebrate-infecting DNA viruses. This revealed that patterns of codon usage bias are strongly correlated with overall genomic GC content, suggesting that genome-wide mutational pressure, rather than natural selection for specific coding triplets, is the main determinant of codon usage. Further, we observed a striking difference in CpG content between DNA viruses with large and small genomes. While the majority of large genome viruses show the expected frequency of CpG, most small genome viruses had CpG contents far below expected values. The exceptions to this generalization, the large gammaherpesviruses and iridoviruses and the small dependoviruses, have sufficiently different life-cycle characteristics that they may help reveal some of the factors shaping the evolution of CpG usage in viruses.

Animals↗

PubMed2000

Sequence and functional analysis of a homolog of interleukin-10 encoded by the parapoxvirus orf virus.

Orf virus is a large DNA virus and is the type species of the Parapoxvirus genus of the family Poxviridae. Orf virus infects the epithelium of sheep and goats and is transmissible to humans. Recently we discovered a gene in orf virus that encodes a polypeptide with remarkable homology to mammalian interleukin (IL-10) and viral encoded IL-10s of herpes viruses. The predicted polypeptide sequence shows high levels of amino acid identity to IL-10 of sheep (80%), cattle (75%), humans (67%) and mice (64%), as well as IL-10-like proteins of Epstein-Barr virus (63%) and equine herpes virus (67%). The C-terminal region, comprising two-thirds of the orf virus protein, is identical to ovine IL-10 which suggests that this gene has been captured from its host sheep during the evolution of orf virus. In contrast the N-terminal region shows little homology with cellular IL10s and in this respect resembles other viral IL-10s. IL-10 is a pleiotrophic cytokine that can exert either immunostimulatory or immunosuppressive effects on many cell types. IL-10 is a potent anti-inflammatory cytokine with inhibitory effects on non-specific immunity in particular macrophage function and Thl effector function. Our studies so far, indicate, that the functional activities of orf virus IL-10 are the same as ovine IL-10. Orf virus IL-10 stimulates mouse thymocyte proliferation and inhibits cytokine synthesis in lipopolysaccharide-activated ovine macrophages, peripheral blood monocytes and keratinocytes. Infection of sheep with an IL-10 deletion mutant of orf virus has shown that interferon-gamma levels are higher in tissue infected with the mutant virus than the parent virus. The functional activities of IL-10 and our data on orf virus IL-10 suggest a role in immune evasion.

Amino Acid Sequence↗

PubMed2001

The immune response to ocular herpes simplex virus type 1 infection.

Herpes simplex virus type 1 (HSV-1) is a prevalent microbial pathogen infecting 60% to 90% of the adult world population. The co-evolution of the virus with humans is due, in part, to adaptations that the virus has evolved to aid it in escaping immune surveillance, including the establishment of a latent infection in its human host. A latent infection allows the virus to remain in the host without inducing tissue pathology or eliciting an immune response. During the acute infection or reactivation of latent virus, the immune response is significant, which can ultimately result in corneal blindness or fatal sporadic encephalitis. In fact, HSV-1 is one of the leading causes of infectious corneal blindness in the world as a result of chronic episodes of viral reactivation leading to stromal keratitis and scarring. Significant inroads have been made in identifying key immune mediators that control ocular HSV-1 infection and potentially viral reactivation. Likewise, viral mechanisms associated with immune evasion have also been identified and will be discussed. Lastly, novel therapeutic strategies that are currently under development show promise and will be included in this review. Most investigators have taken full advantage of the murine host as a viable working in vivo model of HSV-1 due to the sensitivity and susceptibility to viral infection, ease of manipulation, and a multitude of developed probes to study changes at the cellular and molecular levels. Therefore, comments in this review will primarily be restricted to those observations pertaining to the mouse model and the assumption (however great) that similar events occur in the human condition.

Animals↗

PubMed2001

Characterization of a novel simian immunodeficiency virus from guereza colobus monkeys (Colobus guereza) in Cameroon: a new lineage in the nonhuman primate lentivirus family.

Exploration of the diversity among primate lentiviruses is necessary to elucidate the origins and evolution of immunodeficiency viruses. During a serological survey in Cameroon, we screened 25 wild-born guereza colobus monkeys (Colobus guereza) and identified 7 with HIV/SIV cross-reactive antibodies. In this study, we describe a novel lentivirus, named SIVcol, prevalent in guereza colobus monkeys. Genetic analysis revealed that SIVcol was very distinct from all other known SIV/HIV isolates, with average amino acid identities of 40% for Gag, 50% for Pol, 28% for Env, and around 25% for proteins encoded by five other genes. Phylogenetic analyses confirmed that SIVcol is genetically distinct from other previously characterized primate lentiviruses and clusters independently, forming a novel lineage, the sixth in the current classification. Cercopithecidae monkeys (Old World monkeys) are subdivided into two subfamilies, the Colobinae and the Cercopithecinae, and, so far, all Cercopithecidae monkeys from which lentiviruses have been isolated belong to the Cercopithecinae subfamily. Therefore, SIVcol from guereza colobus monkeys (C. guereza) is the first primate lentivirus identified in the Colobinae subfamily and the divergence of SIVcol may reflect divergence of the host lineage.

Amino Acid Sequence↗

PubMed2002

Polymorphism in the infectious salmon anemia virus hemagglutinin gene: importance and possible implications for evolution and ecology of infectious salmon anemia disease.

Infectious salmon anemia (ISA) is an emerging disease in farmed Atlantic salmon with important commercial consequences. The pathogenicity of the ISA virus (ISAV; an orthomyxovirus) varies, observed as differences in disease development and clinical signs. A small polymorphic region (PR) in the ISAV genomic segment encoding the hemagglutinin (HA) has been described. An analysis of 33 HA gene sequences from historical and recent ISA outbreaks was performed, added to a selection of previously published HA sequences. A differential deletion model explaining the generation of HA polymorphism is proposed. The European ISAV sequences could be grouped according to deletion patterns in PR. Cell-culture replication and cytopathic effect varied between viruses from different PR groups. A rather complex epidemiology is suggested, as (a) HA sequences representing several PR variants were detected in three samples; (b) identical mutations occurred in different genetic lineages; and (c) large genetic differences were present in closely related viruses.

Amino Acid Sequence↗

PubMed1999

Recombination of hepatitis D virus RNA sequences and its implications.

Recombination between RNA sequences plays a role in the fast evolution of a few viruses. There has been no report on hepatitis D virus (HDV) recombination. In this study, we analyzed genetic recombination of HDV and its possible impact on evolution and clinical course. The aligned HDV sequences allowed us to construct a phylogenetic tree which supported the notion of distinct lineages of HDV. The tree was also used in the analysis of recombination using partial likelihoods assessed through optimization. Nine segments of the HDV genome with significant levels of genetic recombination were detected. Five segments were in the hypervariable region, and four were in the delta-antigen- coding region. None could be found in the well-conserved autocleavage region that is essential for replication. Recombination occurred both between and within types. The results of this study indicated that the remarkable variation in HDV genomic sequences, particularly in the hypervariable region, among different genotypes may at least partly result from multiple episodes of genetic recombination during evolution. Genetic recombination may play a significant role in increasing genetic diversity. Importantly, a genetic recombination (nt 1082-1093) occurred in one of the immunogenic domains of hepatitis delta virus antigen recognized by human and woodchuck antibodies (amino acids 174-195). Genetic recombination also occurred at another segment between nt 1517 and 1535, which was close to one of the predicted T-cell epitopes (amino acids 26-41). In longitudinal analysis of HDV genomes at different time points during chronic infection, novel dominant HDV strains with amino acid changes at these epitopes usually emerged after severe hepatitis attacks. In the comparison of HDV clones during or shortly after flare-up of liver disease, Ka/Ks ratios of > 1 were frequently found, suggesting Darwinian positive selection. Therefore, recombination in these two segments may play an important role for HDV in the evasion of immunity.

Amino Acid Sequence↗

PubMed1995

Blood-feeding behavior of dengue-2 virus-infected Aedes aegypti.

This study was designed to determine if infection of Aedes aegypti with dengue-2 virus affects the ability of the mosquito to efficiently locate and imbibe blood from an uninfected host. Previous studies suggest that some parasites manipulate their arthropod host to increase the probability of transmission by interfering with blood-feeding efficiency. We found no evidence that dengue-2 virus infection by intrathoracic inoculation impaired the blood-feeding efficiency of Ae. aegypti. We speculate that natural selection has not favored the evolution of dengue viruses that increase vector probing time because uninfected Ae. aegypti take multiple blood meals during each gonotrophic cycle and further increases in vector probing would not significantly increase virus fitness.

Aedes↗

PubMed1995

Repair and evolution of nef in vivo modulates simian immunodeficiency virus virulence.

Experimental evidence from the simian immunodeficiency virus (SIV) model of AIDS has shown that the nef gene is critical in the pathogenesis of AIDS. Consequently, nef is of considerable interest in both antiviral drug and vaccine development. Preliminary findings in two rhesus macaques indicated that a deletion of only 12 bp found in the overlapping nef/3' long terminal repeat (LTR) region (9501 to 9512) of the SIVmacC8 molecular clone was associated with reduced virus isolation frequency. We show that this deletion can be repaired in vivo by a sequence duplication event and that sequence evolution continues until the predicted amino acid sequence of the repair is virtually indistinguishable from that of the virulent wild type. These changes occurred concomitantly with reversion to virulence, evidenced by a high virus isolation frequency and load, decline in anti-p27 antibody, substantial reduction in the CD4/CD8 ratio, and development of opportunistic infections associated with AIDS. These findings clearly illustrate the capacity for repair of small attenuating deletions in primate lentiviruses and also strongly suggest that the region from 9501 to 9512 in the SIV nef/3' LTR region is of biological relevance. In addition, the ability of attenuated virus to revert to virulence raises fundamental questions regarding the nature of superinfection immunity.

Amino Acid Sequence↗

PubMed1982

Rapid evolution of RNA genomes.

RNA viruses show high mutation frequencies partly because of a lack of the proofreading enzymes that assure fidelity of DNA replication. This high mutation frequency is coupled with high rates of replication reflected in rates of RNA genome evolution which can be more than a millionfold greater than the rates of the DNA chromosome evolution of their hosts. There are some disease implications for the DNA-based biosphere of this rapidly evolving RNA biosphere.

Animals↗