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PubMed1996

Different hemagglutinin cleavage site variants of H7N7 in an influenza outbreak in chickens in Leipzig, Germany.

The hemagglutinin (HA) genes from four avian H7N7 influenza A isolates, from a single outbreak, were shown to possess different cleavage sites that contain varying numbers of basic amino acid residues (KKKKR, KRKKR, KKRKKR, KKKKKKR). All four variants are highly pathogenic in chickens and share an immediate common ancestral HA with A/tern/Potsdam/342-6/79 (H7N7) and A/swan/Potsdam/63-6/81 (H7N7). These viruses are nonpathogenic and contain no extra basic amino acids at the cleavage site of their HA. During evolution a common precursor virus acquired different sequences at the cleavage site of the HA and became highly pathogenic in chickens. In vitro assays revealed that the HA from A/chicken/Leipzig/79 with KKKKR at the cleavage site was only partially cleaved (41%), compared to 93-100% cleavage of the other HAs. Since all four viruses were highly pathogenic in chickens, these findings confirm that the degree of pathogenicity in vivo is not exclusively determined by the degree of HA cleavability.

Amino Acid Sequence↗
PubMed1990

Evolutionary relationships among California serogroup viruses (Bunyaviridae) and Aedes mosquitoes (Diptera: Culicidae)

More than 100 published and four unpublished papers recording virus isolations of California (CAL) serogroup viruses from mosquitoes and other arthropods were analyzed, followed by a comparison of a contemporary classification of mosquitoes of the genus Aedes with a contemporary classification of CAL serogroup viruses. Using criteria of five or more total isolations of a given virus from a given species of mosquito, and a minimum infection rate of 1:10,000 or greater (more frequent), Aedes, and to a lesser extent Culiseta, species were found to be the arthropods most frequently involved as vectors. Such a comparison could not explain all virus-vector associations on the basis of coevolution of viruses in Aedes mosquito species, probably because of the crossing over of viruses to other mosquito species through horizontal transmission and because of deficiencies in currently available classifications. Coevolution of host-parasite systems is discussed, as are the inadequacies of contemporary taxonomic treatments of viruses and Aedes mosquitoes. The paper ends with hypothetical reconstructions of virus-mosquito relationships over time and possible routes of dispersal of California serogroup viruses to their present geographical distributions.

Aedes↗
PubMed2001

Pathogenicity determinants in the complex virus population of a Plum pox virus isolate.

Several subisolates were separated from a single Plum pox virus (PPV) isolate, PPV-PS. In spite of an extremely high sequence conservation (more than 99.9% similarity), different subisolates differed largely in pathogenicity in herbaceous hosts and infectivity in woody plants. The severity of symptomatology did not seem to correlate with virus accumulation. Sequence analysis and site-directed mutagenesis demonstrated that single amino acid changes in the helper component (HC) protein caused a drastic effect on virus symptoms in herbaceous hosts and notably modified virus infectivity in peach seedlings. These results indicate that HC variation might play an important role in virulence evolution of natural plant virus infections. Moreover, the analysis of Potato virus X (PVX)-HC chimeras showed that the identified HC amino acid changes had parallel effects on the severity of symptoms caused by PPV and on HC-induced enhancement of PVX pathogenicity, indicating that HC functions in potyvirus symptomatology and in synergism with other viruses have overlapping determinants.

Amino Acid Substitution↗
PubMed1988

Evolution of hepatocellular carcinoma associated with chronic hepatitis B virus infection in Alaskan Eskimos.

Hepatocellular carcinoma (HCC) associated with chronic hepatitis B virus (HBV) infection in Yupik Eskimos in southwestern Alaska, detected in early stages as a result of screening, appears to be more frequently associated with variants of chronic portal inflammation in the noninvolved liver than with fully developed cirrhosis, otherwise common in HBV-associated HCC from other geographic areas. Of 38 patients diagnosed with HCC since 1969, adequate tissue was available from both the tumor and nontumorous liver in 17. Of the 17 specimens, 14 had chronic portal inflammation and three had advanced cirrhosis; 12 of the 14 were from hepatitis B surface antigen carriers. These 12 cases were studied in detail to examine the features accompanying the development of HCC unobscured by cirrhotic transformation. In the noninvolved parenchyma they included hepatocytic nodules as apparent precursors to HCC and, as markers of phenotypic alterations, dysplastic hepatocytes and hepatitis B surface antigen-laden ground-glass hepatocytes. The latter were observed in eight instances and often accumulated in nodules. Parenchyma within 1 mm of the HCC exhibited increased confluent hyperplasia and frequently conspicuous necroinflammation associated with pericellular and periductular fibrosis, which contributed, in addition to fibrous connections between displaced and heavily inflamed portal tracts, to the capsule that was forming in all cases to varying degrees in the pericarcinomatous region. The HCC was uniformly trabecular and in a few specimens, a continuous transition from hyperplasia and dysplasia near the periphery of the tumor to increasing anaplasia in the center could be made out in addition to pressure effects of the HCC. The pericarcinomatous changes, including hyperplasia progressing to neoplasia and necroinflammation, are also observed in experimental models, particularly the woodchuck HCC induced by a hepadna virus related to HBV. Coordinated morphologic and molecular biologic studies on such animal models and on human HCC detected by screening, as for instance in Eskimos, neither complicated by cirrhosis, should elucidate the direction of the evolution of the HCC and the postulated promoting role of the inflammation.

Adolescent↗
PubMed1994

In vitro evolution of a neutralizing human antibody to human immunodeficiency virus type 1 to enhance affinity and broaden strain cross-reactivity.

A method is described that allows for the improvement of antibody affinity. This method, termed complementary-determining region (CDR) walking, does not require structural information on either antibody or antigen. Complementary-determining regions are targeted for random mutagenesis followed by selection for fitness, in this case increased binding affinity, by the phage-display approach. The current study targets a human CD4-binding-site anti-gp120 antibody that is potently and broadly neutralizing. Evolution of affinity of this antibody demonstrates in this case that affinity can be increased while reactivity to variants of human immunodeficiency virus type 1 is broadened. The neutralizing ability of this antibody is improved, as assayed with laboratory and primary clinical isolates of human immunodeficiency virus type 1. The ability to produce human antibodies of exceptional affinity and broad neutralizing ability has implications for the therapeutic and prophylactic application of antibodies for human immunodeficiency virus type 1 infection.

Amino Acid Sequence↗
PubMed2002

Nelfinavir-resistant, amprenavir-hypersusceptible strains of human immunodeficiency virus type 1 carrying an N88S mutation in protease have reduced infectivity, reduced replication capacity, and reduced fitness and process the Gag polyprotein precursor aberrantly.

The evolution of human immunodeficiency virus type 1 (HIV-1) strains with reduced susceptibility to protease inhibitors (PIs) is a major cause of PI treatment failure. A subset of subjects failing a therapy regimen containing the PI nelfinavir developed mutations at position 88 in the protease region. The N88S mutation occurring in some of these subjects induces amprenavir hypersusceptibility and a reduction of fitness and replication capacity. Here we demonstrate that substitutions L63P and V77I in protease, in combination, partially compensate for the loss of fitness, loss of replication capacity, loss of specific infectivity, and aberrant Gag processing induced by the N88S mutation. In addition, these mutations partially ablate amprenavir hypersusceptibility. Addition of mutation M46L to a strain harboring mutations L63P, V77I, and N88S resulted in a reduction of fitness and infectivity without changing Gag-processing efficiency, while amprenavir hypersusceptibility was further diminished. The ratio of reverse transcriptase activity to p24 protein was reduced in this strain compared to that in the other variants, suggesting that the M46L effect on fitness occurred through a mechanism different from a Gag-processing defect. We utilized these mutant strains to undertake a systematic comparison of indirect, single, cycle-based measures of fitness with direct, replication-based fitness assays and demonstrated that both yield consistent results. However, we observed that the magnitude of the fitness loss for one of the mutants varied depending on the assay used.

Carbamates↗
PubMed1986

Hepatitis B virus infection in multitransfused haemophiliacs.

A longitudinal study of 44 haemophilic children, all in a treatment programme with factor concentrates, was undertaken to evaluate the occurrence, characteristics, and evolution of hepatitis B virus (HBV) infection. Twenty four children (55%) (group I) showed signs of HBV infection, while 20 (45%) (group II) did not. Age at onset of treatment, number of infusions, and total amount of concentrate received did not show significant differences between the two groups. In group I only four children (16%) had symptomatic acute hepatitis. Chronic liver disease was present in nine patients (38% of infected children). The early age of infection would seem to be an important factor for predicting chronic evolution. Evidence of delta infection in three children with severe liver disease seemed to confirm the high pathogenicity of this agent. Because of the risks associated with chronic HBV infection a careful follow up of patients positive for hepatitis B surface antigen is mandatory.

Age Factors↗
PubMed1999

Evolution and horizontal transfer of dUTPase-encoding genes in viruses and their hosts.

dUTPase is a ubiquitous and essential enzyme responsible for regulating cellular levels of dUTP. The dut gene exists as single, tandemly duplicated, and tandemly triplicated copies. Crystallized single-copy dUTPases have been shown to assemble as homotrimers. dUTPase is encoded as an auxiliary gene in a number of virus genomes. The origin of viral dut genes has remained unresolved since their initial discovery. A comprehensive analysis of dUTPase amino acid sequence relationships was performed to explore the evolutionary dynamics of dut in viruses and their hosts. Our data set, comprised of 24 host and 51 viral sequences, includes representative sequences from available eukaryotes, archaea, eubacteria cells, and viruses, including herpesviruses. These amino acid sequences were aligned by using a hidden Markov model approach developed to align divergent data. Known secondary structures from single-copy crystals were mapped onto the aligned duplicate and triplicate sequences. We show how duplicated dUTPases might fold into a monomer, and we hypothesize that triplicated dUTPases also assemble as monomers. Phylogenetic analysis revealed at least five viral dUTPase sequence lineages in well-supported monophyletic clusters with eukaryotic, eubacterial, and archaeal hosts. We have identified all five as strong examples of horizontal transfer as well as additional potential transfer of dut genes among eubacteria, between eubacteria and viruses, and between retroviruses. The evidence for horizontal transfers is particularly interesting since eukaryotic dut genes have introns, while DNA virus dut genes do not. This implies that an intermediary retroid agent facilitated the horizontal transfer process between host mRNA and DNA viruses.

Amino Acid Sequence↗
PubMed2003

Progression of chronic hepatitis C to liver fibrosis and cirrhosis in patients coinfected with hepatitis C virus and human immunodeficiency virus.

To evaluate the factors associated with the evolution of chronic hepatitis C in human immunodeficiency virus (HIV)-infected patients, a cross-sectional analysis of 41 HIV-infected patients with chronic hepatitis C (known as "HIV-HCV [hepatitis C virus]-coinfected patients") and a control group of patients with chronic hepatitis C who did not have HIV infection (known as "non-HIV-infected patients") was performed. The association of histological variables with demographic parameters, HCV load and genotype, HIV load, CD4(+) T cell count, and response to highly active antiretroviral therapy (HAART) was evaluated. HIV-HCV-coinfected patients showed a significantly higher HCV load, more-advanced fibrosis, and a higher liver fibrosis progression rate (FPR) than did non-HIV-infected patients. A high HCV load and a low CD4(+) T cell count were associated with a higher FPR. The immune response induced by HAART did not influence this progression. In conclusion, HIV-HCV-infected patients, mainly such patients with a high HCV load and an immunodepressed state, have a higher FPR. An independent effect of the immune response to HAART was not evident.

Adult↗
PubMed2026

Transcriptome mining and comparative genomics reveal 36 putative novel marafivirus species and conserved evolution of the marafibox regulatory element.

BACKGROUND: Marafiviruses are plant-infecting RNA viruses associated with several economically important crops, but their genomic diversity remains incompletely characterized. OBJECTIVE: This study aimed to identify previously unrecognized marafivirus genomes and investigate their genomic features and evolutionary relationships. METHODS: Publicly available plant transcriptome datasets were systematically mined to detect marafivirus-like sequences. Recovered genomes were analyzed using comparative sequence analysis, phylogenetic reconstruction, and genome organization characterization. RESULTS: A total of 62 marafivirus-like genomes were recovered from 33 independent sources representing diverse plant hosts. Polyprotein-based comparative and phylogenetic analyses grouped these genomes into 36 lineages likely representing novel species. All newly identified viruses clustered within the Marafivirus clade. Genome organization analysis revealed conserved polyprotein architecture and widespread presence of the marafibox promoter element. Conservation of additional open reading frames among closely related isolates aided identification of potentially functional genes. CONCLUSION: These findings substantially expand the known diversity of marafiviruses and demonstrate the effectiveness of transcriptome mining for discovering previously unrecognized plant viruses.

Phylogeny↗
PubMed2002

Modifications of the immune responsiveness in patients with hepatitis C virus infection following treatment with IFN-alpha/ribavirin.

The balance between T helper (h)1 and Th2 responsiveness seems to represent a key event in the evolution of hepatitis C virus (HCV) infection. In particular, Th1 cytokines [interleukin (IL-2) and interferon (IFN-gamma)] have been demonstrated to mediate the antiviral immune response. Serum levels of Th1 cytokines (IL-2 and IFN-gamma) as well as of Th2 products (IL-4 and IL-10) were determined in a group of HCV-positive patients before and after treatment with IFN-alpha and Ribavirin (RIB). Results indicate that responder patients exhibited increased levels of IFN-gamma and IL-10, while this enhancement was not observed in non-responder patients. In this respect, the major effect exerted by the combined therapy with IFN-alpha/RIB could be represented by the attainment of a re-equilibrium between inflammatory (Th1) and antiinflammatory (Th2) mechanisms. In this framework, according to current literature, novel therapeutical approaches to treat HCV infection are represented by administration of recombinant IL-2 and IL-10.

Drug Therapy, Combination↗
PubMed2006

Evolution of the susceptibility to antiviral drugs of A/H3N2 influenza viruses isolated in France from 2002 to 2005.

In 2002, prior to the generalization of zanamivir and oseltamivir utilization in France, we had decided to test a large panel of influenza strains to establish the baseline sensitivity of these viruses to anti-neuraminidase drugs. Since 2002, routine monitoring of resistance relies mainly on the results of neuraminidase enzyme assay. The profile of sensitivity of A/H3N2 viruses has not changed during these three influenza seasons. Neuraminidase N2 was shown to be more sensitive to oseltamivir carboxylate than to zanamivir. Amongst 788 viruses tested, only 10 were found with outliers IC(50) values (seven in 2003, one in 2004, and two in 2005). After the sequencing of the neuraminidase segment of these viruses, seven mutations on the stalk or the head of the glycoprotein (A18S, L23F, C42R, R143V, E199K, S332K, R431N) were detected. Moreover during seasons 2003-2005, 12 additional viruses were characterized by a complete lack of neuraminidase activity. In these viruses, viral resistance to NA inhibitors can be related with the presence of a defective neuraminidase RNA segment as evaluated by a plaque reduction assay, these viruses having a reduced dependence on its neuraminidase activity.

Antiviral Agents↗
PubMed2005

Effect of alternating passage on adaptation of sindbis virus to vertebrate and invertebrate cells.

Mosquito-borne alphaviruses, which replicate alternately and obligately in mosquitoes and vertebrates, appear to experience lower rates of evolution than do many RNA viruses that replicate solely in vertebrates. This genetic stability is hypothesized to result from the alternating host cycle, which constrains evolution by imposing compromise fitness solutions in each host. To test this hypothesis, Sindbis virus was passaged serially, either in one cell type to eliminate host alteration or alternately between vertebrate (BHK) and mosquito (C6/36) cells. Following 20 to 50 serial passages, mutations were identified and changes in fitness were assessed using competition assays against genetically marked, surrogate parent viruses. Specialized viruses passaged in a single cell exhibited more mutations and amino acid changes per passage than those passaged alternately. Single host-adapted viruses exhibited fitness gains in the cells in which they specialized but fitness losses in the bypassed cell type. Most but not all viruses passaged alternately experienced lesser fitness gains than specialized viruses, with fewer mutations per passage. Clonal populations derived from alternately passaged viruses also exhibited adaptation to both cell lines, indicating that polymorphic populations are not required for simultaneous fitness gains in vertebrate and mosquito cells. Nearly all passaged viruses acquired Arg or Lys substitutions in the E2 envelope glycoprotein, but enhanced binding was only detected for BHK cells. These results support the hypothesis that arbovirus evolution may be constrained by alternating host transmission cycles, but they indicate a surprising ability for simultaneous adaptation to highly divergent cell types by combinations of mutations in single genomes.

Adaptation, Physiological↗
PubMed1998

Evolutionary characteristics of influenza B virus since its first isolation in 1940: dynamic circulation of deletion and insertion mechanism.

New antigenic variants of B/Yamagata/16/88-like lineage which appeared in the season of 1997 as a minor strain tended to predominate in the following season. Also, we could observe for the first time, three peaks of activity caused by H3N2 virus and two variants of B influenza virus. Antigenic and phylogenetic analyses revealed that B/Victoria/2/87-like variants appeared again in Japan in 1997 after a nine-year absence. Influenza B viruses evolved into three major lineages, including the earliest strain (I), B/Yamagata/16/88-like variants (II), which comprised of three sublineages (II-(i), II-(ii), II-(iii)), and B/Victoria/2/87-like variants (III). Evolution of influenza B virus hemagglutinin was apparently distinguishable from that of influenza A virus, showing a systematic mechanism of nucleotide deletion and insertion. This phenomenon was observed to be closely related to evolutionary pathways of I, II-(i), II-(ii), II-(iii) and III lineages. It was noteworthy to reveal that the nucleotide deletion and insertion mechanism of influenza B virus completed one cycle over a fifty-year period, and that a three nucleotide deletion was again observed in 1997 strains belonging to lineage II-(iii). It was evident that amino acid substitutions accompanying nucleotide insertions were highly conserved.

Antigens, Viral↗
PubMed2005

Differential targeting and shifts in the immunodominance of Epstein-Barr virus--specific CD8 and CD4 T cell responses during acute and persistent infection.

The evolution of Epstein-Barr virus (EBV)-specific T cell responses that occurs during the acute and persistent stages of infection remains poorly characterized despite its importance for developing immune interventions for EBV-associated disorders. This study assessed T cell responses to 113 EBV-derived epitopes in 40 subjects with acute or persistent EBV infection. Although no significant differences were seen in the breadth of CD8 and CD4 T cell responses, their magnitude differed significantly over time; acutely infected subjects generated especially strong responses to lytic viral antigens. The cross-sectional shift in immunodominance was also confirmed in subjects followed longitudinally from acute to persistent infection. In addition, human leukocyte antigen-matched siblings with discordant histories of symptomatic EBV infection showed no significant differences in their response patterns, suggesting that symptomatic EBV infection does not lead to unique persistent-stage responses. These data provide an assessment of immunodominance patterns and guidance for developing immunotherapeutic interventions for EBV-associated disorders.

Amino Acid Sequence↗
PubMedDate not supplied

Molecular epidemiology of infectious bronchitis virus isolates from China and Southeast Asia.

In order to trace the origin and evolution of avian infectious bronchitis virus (IBV) isolates in China and Southeast Asia, genomic sequencing was used for molecular characterization of 24 IBV isolates and two reference strains in comparison with the published sequences. The 5' region of the S1 genes, containing hypervariable regions I and II, and 3' region of the nucleocapsid genes, containing cytotoxic T lymphocyte epitopes, were used to construct phylogenetic trees for analysis. The results showed that the 24 isolates could be divided into three distinct groups, that is, American, Asian, and European. Some isolates formed a distinct Asian phylogenetic group, suggesting that IBV has existed for some time in Asia. Our results also showed that in vivo recombination of IBV may have occurred at a rather high frequency, contributing to the diversity of these IBV isolates. Importantly, recombination events have probably occurred between vaccine strains and field strains in the natural condition.

Animals↗
PubMed2000

Residual low-level viral replication could explain discrepancies between viral load and CD4+ cell response in human immunodeficiency virus-infected patients receiving antiretroviral therapy.

We report the evolution of chronic infection with human immunodeficiency virus type 1 (HIV-1) in a patient treated with stavudine plus didanosine, whose CD4+ lymphocyte count progressively decreased, despite a sustained plasma viral load <20 copies/mL. After 12 months of therapy, treatment was switched to zidovudine plus lamivudine plus nelfinavir. CD4+ T cell count decreased from 559 x 10(6)/L at month 0 to 259 x 10(6)/L at month 12. Plasma viral load decreased from 21,665 HIV-1 RNA copies/mL at baseline (month 0) to <20 copies/mL after 1 month of therapy with stavudine plus didanosine, and remained below 20 copies/mL until month 12, but always >5 copies/mL. Viral load in tonsilar tissue at month 12 was 125,000 copies/mg of tissue. After the change to triple-drug therapy, the plasma viral load decreased to 5 copies/mL, the CD4+ T cell count increased to 705 x 10(6)/L, and the viral load in tonsilar tissue decreased to <40 copies/mg of tissue at month 24. A low level of HIV-1 replication could explain the lack of immunologic response in patients with apparent virological response.

Adenoids↗