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At least 541 records · Page 30Linked to original sources
PubMed2000

The importance of the quasispecies nature of hepatitis C virus (HCV) for the evolution of HCV populations in patients: study on a single source outbreak of HCV infection.

The quasispecies populations of hepatitis C virus (HCV) in the infectious source (IS) and in patients of a single source outbreak were characterized. A predominant variant AD78-1 and some minor variants of HCV 5' NCR were identified in IS. Different complex HCV populations emerged rapidly in patients though HCV populations in chronic infection were rather simple and stable. AD78-1 remained predominant in 17/24 chronically infected patients while new predominant variants with distinct nucleotide substitutions persisted in 7 other patients. Thus, only distinct variants are involved in viral persistence and the genetic heterogeneity of HCV does not successively increase with time.

Acute Disease↗
PubMed2002

The structure and evolution of the major capsid protein of a large, lipid-containing DNA virus.

Paramecium bursaria Chlorella virus type 1 (PBCV-1) is a very large, icosahedral virus containing an internal membrane enclosed within a glycoprotein coat consisting of pseudohexagonal arrays of trimeric capsomers. Each capsomer is composed of three molecules of the major capsid protein, Vp54, the 2.0-A resolution structure of which is reported here. Four N-linked and two O-linked glycosylation sites were identified. The N-linked sites are associated with nonstandard amino acid motifs as a result of glycosylation by virus-encoded enzymes. Each monomer of the trimeric structure consists of two eight-stranded, antiparallel beta-barrel, "jelly-roll" domains related by a pseudo-sixfold rotation. The fold of the monomer and the pseudo-sixfold symmetry of the capsomer resembles that of the major coat proteins in the double-stranded DNA bacteriophage PRD1 and the double-stranded DNA human adenoviruses, as well as the viral proteins VP2-VP3 of picornaviruses. The structural similarities among these diverse groups of viruses, whose hosts include bacteria, unicellular eukaryotes, plants, and mammals, make it probable that their capsid proteins have evolved from a common ancestor that had already acquired a pseudo-sixfold organization. The trimeric capsid protein structure was used to produce a quasi-atomic model of the 1,900-A diameter PBCV-1 outer shell, based on fitting of the Vp54 crystal structure into a three-dimensional cryoelectron microscopy image reconstruction of the virus.

Capsid↗
PubMed2003

Genetic evolution of human immunodeficiency virus type 1 in two spouses responding successfully to highly active antiretroviral therapy.

The current case study provided an unusual setting to track the evolution of HIV-1 envelope gene over a maximum period of 6 years in two asymptomatic spouses undergoing suppressive highly active antiretroviral therapy. For this purpose, proviral DNA samples taken from uncultured peripheral blood mononuclear cells and spanning the C2-V5 regions of env were analyzed at three sampling points per subject. Two distinct topological patterns were observed in the phylogenetic reconstructions of the genetically linked sequences of the couple: an intermingled pattern and a sequentially shifting pattern in the virus populations of the male index case and his spouse, respectively. Application of three evolutionary models for the amino acid-encoded sites, using the maximum likelihood approach, indicated the operation of positive selection in the region only at the second time point in the woman, before receiving therapy. These findings reinforce the evidence of a crucial role for host-selective constraints on HIV-1 env evolution in vivo.

Antiretroviral Therapy, Highly Active↗
PubMed2026

Evolution of virulence of a plant RNA virus in developmental stage-structured host populations.

Natural host populations are age-structured, and developmental stages differ in susceptibility and within-host pathogen dynamics, potentially imposing distinct selective pressures on viruses. However, the evolutionary consequences of host age structure remain poorly understood. We experimentally evolved turnip mosaic potyvirus for 5 passages in Arabidopsis thaliana populations spanning 7 demographic regimes, from juvenile- to mature-dominated cohorts. We quantified disease progression, symptom severity, and viral load, cross-inoculated evolved lineages across host stages to construct infection matrices, and performed whole-population sequencing at passages 1 and 5. Disease traits changed markedly with passage, demography, and their interaction. Disease progression evolved faster in older populations, whereas symptom severity was independent of median age, indicating demographic reweighting of virulence components. Viral load increased across passages and positively correlated with severity, linking within-host fitness to symptoms. Cross-inoculation assays revealed a modular infection network: juvenile-evolved lineages specialized on juvenile hosts, whereas lineages from intermediate and older populations were more generalist. Genomically, we detected both parallel and demography-specific adaptations, including recurrent changes in the viral protein VPg (involved in translation, replication, and host interactions) as well as synonymous variants showing consistent or opposing selection across host population stage structures. Overall, host age structure emerges as a major ecological driver of virulence evolution, shaping tradeoffs between disease progression and severity and determining specialization versus generalism. These results integrate phenotypic and genomic responses and suggest that manipulating crop age structure could steer virus evolution toward less damaging outcomes.

Virulence↗
PubMed1997

Characteristic in vitro evolution pattern of foot and mouth disease virus A81/Castellanos/Arg/87.

The in vitro evolution of Foot and mouth disease virus (FMDV) A/81/Castellanos/Arg/87 (A/Castellanos/87) was studied by partial biological and biochemical characterization of viral populations selected after 25 passages on secondary fetal bovine kidney cell monolayers. These passages were performed in the presence or absence of immune pressure exerted in the form of antiviral polyclonal serum. While the viral populations passaged in the absence of immune pressure acquired characteristics such as antigenic heterogeneity, VP1 amino acid modification and plaque size reduction, the populations selected after immune pressure also presented both neutralizing resistance and attenuation for suckling mice. The comparison with other previously studied FMDV strains suggests that FMDV A/Castellanos/87 adopts a differential response to immunological pressure and other selective forces. In addition, the sequencing analysis of viral selected populations shows a restriction in the number and type of amino acid replacements tolerated by FMDV capsid proteins.

Amino Acid Sequence↗
PubMed1987

The evolution of multicompartmental genomes in viruses.

The genetic information of many viruses is divided between separately encapsidated nucleic acid molecules. A simple evolutionary model is constructed to explain this phenomenon. All multicompartmental viruses infect plants, and most are RNA viruses. The former fact may be due to the high transmission multiplicities enjoyed by plant viruses. The latter may be due to the low replication fidelity of RNA, although another explanation is also offered. The logic of the analysis is contrasted with that of previous explanations. In particular, this paper proceeds from a "selfish DNA" viewpoint. It is not necessary to suppose that the division of the genome fills any adaptive function for the virus. The theory makes testable predictions about the parameters of multicompartmental viruses.

Biological Evolution↗
PubMed2005

Neutralizing antibody responses drive the evolution of human immunodeficiency virus type 1 envelope during recent HIV infection.

HIV type 1 (HIV-1) can rapidly escape from neutralizing antibody responses. The genetic basis of this escape in vivo is poorly understood. We compared the pattern of evolution of the HIV-1 env gene between individuals with recent HIV infection whose virus exhibited either a low or a high rate of escape from neutralizing antibody responses. We demonstrate that the rate of viral escape at a phenotypic level is highly variable among individuals, and is strongly correlated with the rate of amino acid substitutions. We show that dramatic escape from neutralizing antibodies can occur in the relative absence of changes in glycosylation or insertions and deletions ("indels") in the envelope; conversely, changes in glycosylation and indels occur even in the absence of neutralizing antibody responses. Comparison of our data with the predictions of a mathematical model support a mechanism in which escape from neutralizing antibodies occurs via many amino acid substitutions, with low cross-neutralization between closely related viral strains. Our results suggest that autologous neutralizing antibody responses may play a pivotal role in the diversification of HIV-1 envelope during the early stages of infection.

Adult↗
PubMed2004

Evolution of hepatitis C virus quasispecies immediately following liver transplantation.

Liver cirrhosis caused by chronic hepatitis C virus (HCV) infection is the main indication for liver transplantation (LT). There is little information on HCV genetic evolution following transplantation. The aim of this study was to carefully assess early evolution of HCV quasispecies in a cohort of 18 liver transplant recipients followed prospectively. Quasispecies analysis was performed by sequence analysis of the hypervariable region 1 (HVR1) before transplantation and at day 4 and week 4 following LT. A predominant variant was present in 12 (67%) of the 18 patients before transplantation and the same variant was propagated and remained predominant after LT in 6 (50%) of these patients. In the remaining individuals, there were major changes in the quasispecies composition, mostly occurring during the first days after LT. There was a progressive decrease in the nonsynonymous (dN)/synonymous (dS) ratios from baseline (1.2) to day 4 (.6) (P = .08) and to week 4 after LT (.3) (P = .015). Similarly, genetic distance (GD) declined from baseline (.1) to day 4 (.03) (P = .07) and to week 4 (.04) (P = .04). We did not find any differences in HCV genetic evolution between patients with mild (n = 10) or severe (n = 8) disease recurrence. In conclusion, during the first days following transplantation, HCV quasispecies becomes more homogenous, even after major changes in its composition. Importantly, these changes persist and even increase during the 1st month after transplantation. The "bottleneck" effect caused by the implantation of a new graft and the lack of selective pressure due to the strong immunosuppression most likely explain this particular pattern of genetic evolution.

Adult↗
PubMed1995

A deletion mutant of the LMP1 oncogene of Epstein-Barr virus is associated with evolution of angioimmunoblastic lymphadenopathy into B immunoblastic lymphoma.

The latent membrane protein 1 (LMP1) oncogene is one of the major proteins synthesized by the Epstein-Barr virus (EBV). It is expressed in Reed-Sternberg cells of Hodgkin's disease (HD), tumor cells of nasopharyngeal carcinoma (NPC), and immunoblasts of angioimmunoblastic lymphadenopathy (AILD). A particular LMP1 deletion mutant was recently identified in NPC and clinically and histologically aggressive HD. We studied two patients with AILD that subsequently progressed into immunoblastic lymphoma (IBL) in order to investigate whether the LMP1 deletion mutant was implicated in progression of AILD into IBL. Immunohistology and in situ hybridization were performed on diagnostic biopsies. DNA extracted from fresh frozen material was used for rearrangement studies and polymerase chain reaction (PCR) based amplification and sequencing of portions of the LMP1 gene. Immunohistochemistry revealed B cell origin of both cases of IBL. In the first patient clonal rearrangement of the immunoglobulin heavy-chain gene was present in IBL but not in AILD. In this patient, scattered immunoblasts of AILD and numerous tumor cells of B-IBL were shown to contain EBV transcripts (EBER1) and to express LMP1. Sequence analysis of the LMP1 gene from AILD and IBL in the first, and from IBL in the second patient, revealed identical deletions and point mutations. This LMP1 deletion mutant is identical to those which have been reported in HD and NPC. Its association with evolution of AILD into B-IBL, aggressive HD and NPC, suggests that this particular mutant is more widespread than originally thought and is clinically relevant.

Adult↗
PubMed1992

Evolution of hepatitis delta virus RNA during chronic infection.

The complete RNA sequences of hepatitis delta virus (HDV) isolated at three different time points from a chronic delta hepatitis patient were determined. These time points represented three different periods of clinical flare-ups. The sequence analysis showed that these three different HDV isolates evolved at a rate ranging from 3.0 x 10(-2) to 3.0 x 10(-3) substitutions/nucleotide/year, depending on the period of infection. The evolution rates appeared to correlate with the changes of clinical pictures of hepatitis, i.e., the more drastic the change in the symptom of hepatitis was, the more nucleotide changes were detected. Except during the transition from the acute phase to chronic phase of delta hepatitis, when there was a much larger number of changes in HDV RNA sequence, the overall evolution rate of HDV RNA in the chronic phase appeared to be similar to those of other RNA viruses. Sequence relationship of these HDV RNAs suggested that acute exacerbations in chronic delta hepatitis were associated with the evolution of the persistently infected HDV, rather than resulting from new viral infections. However, some of the mutations were not cumulative, suggesting that HDV isolated at a later time was not directly evolved from the immediately previous one. Thus, HDV at any time point was a mixture of viruses with slight sequence variations, and a specific HDV RNA species was selected from this virus population under different environments. These findings indicate that HDV RNA is heterogeneous and evolves at a fast rate. The evolution rates in different parts of HDV RNA also varied. The evolution rate of HDV RNA determined here was higher than the ones determined previously from partial RNA sequences of two Japanese HDV isolates.

Adult↗
PubMed2005

Evolution of H9N2 influenza viruses from domestic poultry in Mainland China.

H9N2 viruses have circulated in domestic poultry in Mainland China since 1994, and an inactivated vaccine has been used in chickens to control the disease since 1998. The present study analyzed 27 H9N2 avian influenza viruses that were isolated from chickens and ducks from 1996 to 2002. Infection studies indicated that most of the viruses replicate efficiently but none of them is lethal for SPF chickens. However, these viruses exhibit different phenotypes of replication in a mouse model. Five viruses, including 4 early isolates and one 2000 isolate, are not able to replicate in mice; 14 viruses replicate to moderate titers in mouse lungs and cause less than 5% weight loss, while other 8 viruses could replicate to high titers in the lungs and 7 of them induce 10-20% weight loss of the mice on day 5 after inoculation. Most of the viruses isolated after 1996 are antigenically different from the vaccine strain that is currently used in China. Three viruses isolated in central China in 1998 are resistant to adamantanes. Phylogenetic analysis revealed that all of the viruses originated from CK/BJ/1/94-like virus and formed multiple genotypes through complicated reassortment with QA/HK/G1/97-, CK/HK/G9/97-, CK/SH/F/98-, and TY/WI/66-like viruses. This study is a description of the previously uncharacterized H9N2 avian influenza viruses recently circulating in chickens and ducks in Mainland China. Our findings suggest that urgent attention should be paid to the control of H9N2 influenza viruses in animals and to the human's influenza pandemic preparedness.

Animals↗
PubMed2001

Subversion and piracy: DNA viruses and immune evasion.

During the co-evolution of viruses with their vertebrate hosts, the DNA viruses have acquired an impressive array of immunomodulatory genes to combat host immune responses and their hosts have developed a sophisticated immune system to contain virus infections. In order to replicate, the viruses have evolved mechanisms to inhibit key host anti-virus responses that include apoptosis, interferon production, chemokine production, inflammatory cytokine production, and the activity of cytotoxic T-cells, natural killer cells and antibody. In addition, some of the viruses encode cytokine or chemokine homologues that recruit or expand cell numbers for infection or that subvert the host cellular response from a protective response to a benign one. The specificity of the viral immunomodulatory molecules reflects the life cycle and the pathogenesis of the viruses. Herpesviruses achieve latency in host cells by inducing cell survival and protecting infected cells from immune recognition. This involves interference with cell signal transduction pathways. Many of the viral immunomodulatory proteins are homologues of host proteins that appear to have been pirated from the host and reassorted in the virus genomes. Some of these have unique functions and indicate novel or important aspects of both viral pathogenesis and host immunity to viruses. The specific example of orf virus infection of sheep is described.

Animals↗
PubMed2001

Molecular evolution of influenza A/H3N2 viruses in the province of Québec (Canada) during the 1997-2000 period.

In this study, we compared antigenic (hemagglutination inhibition (HI) assay) and molecular (sequencing of the hemagglutinin (HA1) gene) characterization of influenza isolates collected in the Province of Québec (Canada) during the last three flu seasons (1997-2000). Twenty-three isolates were tested by a standard HI assay and 37 by sequencing of the HA1 gene for their homology to the A/H3N2 vaccine strains A/Wuhan/359/95 (1997-1998) and A/Sydney/5/97 (1998-1999 and 1999-2000). By HI, two isolates were antigenically similar to A/Wuhan/359/95 (both from 1997 to 1998), 16 were similar to A/Sydney/5/97 (1997-2000) and no conclusions could be inferred for the other five isolates due to identical HI titers for the two vaccine strains (n=4) or insufficient viral titer (n=1). Sequence analysis revealed that four isolates from 1997 to 1998 were related to A/Wuhan/359/95 whereas the others (n=4) from 1997 to 1998, as well as all isolates from 1998 to 1999 (n=18) and 1999 to 2000 (n=11) were closer to A/Sydney/5/97. The mean number of amino acid differences for the 33 A/Sydney/5/97-like isolates compared with the homologous vaccine strain was 6.3 (1.9%), 9.2 (2.8%) and 13.6 (4.1%) for those collected in 1997-1998, 1998-1999, and 1999-2000, respectively. Phylogenetic analysis confirmed that a progressive drift occurred among our A/H3N2 influenza isolates over the last three flu seasons. Furthermore, it revealed that isolates collected during the last two flu seasons were in fact more related to A/Panama/2007/99 (2000-2001 vaccine strain) than to A/Sydney/5/97. Our studies suggest that molecular analysis of the HA1 gene should complement the HI assay for a more accurate analysis of influenza A virus drift.

Antigens, Viral↗
PubMed1986

Diverse virological, histopathological and prognostic implications of seroconversion from hepatitis B e antigen to anti-HBe in chronic hepatitis B virus infection.

The evolutions of serum hepatitis B virus (HBV)-DNA, liver histology and intrahepatic expressions of HBV antigens were longitudinally investigated in 24 serum HBeAg+/HBV-DNA+ chronic hepatitis B patients who subsequently seroconverted to anti-HBe. After HBeAg conversion, serum HBV-DNA still persisted in 10 patients, and liver HBcAg in 7 of them. Of the 24 patients, 3 subgroups with diverse prognoses were identified. Ten patients progressed from chronic active hepatitis to cirrhosis, and in 7 of them HBV-DNA and/or HBcAg persisted. Eight patients with undetectable HBV-DNA and HBcAg recovered. In the remaining 6 patients, chronic liver diseases persisted; in 3 of them, HBV-DNA and in one HBcAg. These findings indicate that continued viral replication is present in a significant number of patients after HBeAg seroconversion in Taiwan, and is responsible for disease progression. In addition to HBcAg and HBV-DNA, the severity of underlying liver histology, when HBeAg seroconversion occurred, was critical for the outcome of the disease. Another remarkable finding was that clusters of ground-glass hepatocytes, well correlated with the marginal expression of HBsAg, were demonstrated in 14 of 16 biopsies with serum anti-HBe+/HBV-DNA-, but found in only 4 of 44 biopsies with positive serum HBV-DNA, indicating a strong association of the expressions of liver histology and hepatocyte HBsAg with the status of viral replication.

Chronic Disease↗