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PubMed1977

Biochemical and immunological properties of gag genecoded structural proteins of endogenous tyep C RNA tumor viruses of diverse mammalian species.

The major nonglycosylated structure proteins of mammalian type C RNA tumor viruses are synthesized in the form of a high molecular weight precursor coded for by a viral gene disignated "gag". Previous genetic analysis of a prototype virus isolated of mouse origin has led to a determination of the internal arragnement of the regions within the gag gene coding for individual structural proteins. In the present study, the biochemical properties of structural proteins of type C virus isolates of additional mammalian species were analyzed. The results obtained indicate that the biochemical properties of immunologically cross-reactive proteins have been highly conserved throughout the evolution of this group of viruses. Moreover, these findings provide a means of mapping the gag genes of a broad range of mammalian type C viruses. In view of the results obtained, a new nomenclature system for type C viral gag gene-coded translational products is proposed.

Animals↗

PubMed2003

Incidence of hyponatraemia and hyponatraemic seizures in severe respiratory syncytial virus bronchiolitis.

AIM: To document the incidence and early evolution of hyponatraemia (serum sodium < 136 mmol l(-1)) associated with respiratory syncytial virus (RSV) bronchiolitis in infants requiring intensive care. METHODS: In a retrospective review over two winter seasons, 130 infants were admitted with confirmed RSV infection, of whom 39 were excluded because of either pre-existing risk factors for hyponatraemia: diuretic therapy (n = 14), cardiac disease (n = 10), renal disease (n = 2) or lack of admission sodium data (n = 13). RESULTS: The incidence of admission hyponatraemia in the remaining infants (median age 6 wk) was 33% (30/91), with 11% (10/91) exhibiting a serum sodium less than 130 mmol l(-1) . Hyponatraemic and normonatraemic infants were of a similar age (median 6 vs 7 wk, p = 0.82). With fluid restriction and diuretic therapy, the incidence of hyponatraemia at 48 h had decreased to 3.3%, odds ratio 0.07 (95% confidence interval 0.02-0.24, p < 0.001). Four infants (4%) suffered hyponatraemic seizures at admission (sodium 114-123 mmol l(-1)); three had received hypotonic intravenous fluids at 100-150 ml kg(-1) d(-1) before referral to intensive care. All four were managed successfully with hypertonic (3%) saline, followed by fluid restriction, resulting in immediate termination of seizure activity and normalization of serum sodium values over 48 h. CONCLUSION: Hyponatraemia is common among infants with RSV bronchiolitis presenting to intensive care. Neurological complications may occur and fluid therapy in vulnerable infants should be tailored to reduce this risk.

Apnea↗

PubMedDate not supplied

[The time scale in poxvirus evolution].

Unlike vertebrates and RNA-containing viruses, the objective estimate of molecular clock for DNA-containing viruses was so far absent. An extended central conservative genomic region of orthopoxviruses (about 102 kbp) and the sequence of DNA polymerase gene (about 3 kbp) of the viruses belonging to various genera from the family Poxviridae were analyzed. During this analysis, the known dating of variola virus (VARV) transfer from West Africa to South America (XVI century) and our own data on close phylogenetic relations between the modem West African and South American VARV isolates were used. As a result of this work, it was calculated for the first time that the rate of mutation accumulation in these DNA-containing viruses amounted to 0.9-1.2 x 10(-6) substitutions per site per year. The poxviruses started separating from the ancestor virus to form the modem genera approximately 500 thousand years ago; the ancestor of the genus Orthopoxvirus separated about 300 thousand years ago; and its division into the modem studied species took place approximately 14 thousand years ago.

DNA, Viral↗

PubMed2003

Evolution of wild type and mutants of the YMDD motif of hepatitis B virus polymerase during lamivudine therapy.

BACKGROUND AND AIM: Long-term lamivudine treatment for chronic hepatitis B virus (HBV) infection induces the emergence of lamivudine resistant HBV YMDD mutant strains. The aim of the present study was to observe the clone evolution of YMDD wild type and mutant strains in pretreatment and post-treatment samples during lamivudine therapy and analyze their clinical significance. METHODS: Ten serum samples (five before and five after 48 weeks of therapy) obtained from five patients chronically infected with HBV and treated with lamivudine were studied. Part of the HBV polymerase gene flanking the YMDD motif was sequenced after polymerase chain reaction (PCR) amplification. Meanwhile, 20-24 clones were selected at random from each sample and YMDD wild type and mutant strains were detected by real-time fluorimetry PCR established in our laboratory. RESULTS: The YMDD mutants were not detectable in all five patients before treatment and were found in four patients after 48 weeks of therapy by sequencing directly on PCR products. Analysis of individual clones showed that the ratios of mutant strains in each of the five patients were 0, 9.5, 0, 4.5 and 5.6%, respectively, before therapy and 100, 100, 65, 100 and 0%, respectively, after 48 weeks of therapy. M552I was detected before therapy in one patient but M552V became the domain strain after therapy. Until 52 weeks of therapy, serum HBV DNA and alanine aminotransferase (ALT) breakthrough were found in two of the four patients with YMDD mutations. The fifth patient experienced breakthrough of ALT but HBV DNA remained undetectable. CONCLUSIONS: The mutant strains of YMDD motif of HBV polymerase could be found in patients before lamivudine treatment, indicating that antiviral therapy allows the rapid selection of resistant strains. The replication ability of the M552V mutant strain might be stronger than that of the M552I mutant strain.

Alanine Transaminase↗

PubMed1991

[Immunodeficiency viruses].

In the first part of this article some structural and biological aspects of the HIV viruses are presented, in our opinion among the most interesting ones, connected with the AIDS viruses. Viral infection and its evolution, particularly related with infection by HIV-2, will be presented later, in the light of our experience, obtained over several years work with African people infected by the virus. The AIDS viruses are complex retroviruses, with their own identity, but also with marked structural and biological resemblances to other retroviruses, equally pathogenical for animals. The lentivirinae subfamily to which the AIDS viruses belong includes other agents, usually classified according to the host they infect. In this way, the lentiviruses of the primates contain in the same group, besides those of HIV-1 and HIV-2, viruses that infect monkeys such as SIVMAC, SIVAGM, SIVSMM, etc. The comparative study of molecular genetics and biology of human and animal retroviruses in recent years has permitted significant progress in the understanding of the possible mechanisms that lead to the Immunodepressive Acquired Syndrome that characterizes AIDS. The presence of a gene that deactivates the activated lymphocytes only present in the lentiviruses of the primates, as well as the known tropism of those viruses to CD4 lymphocytes, and not found in the other groups, are biological aspects that are pointed out. We also refer to other characteristics of HIVs such as the cytolytic and sincicial capacity of these viruses in lymphocyte culture. Finally we present an analysis of what we were able to observe in individuals infected by HIV-2 in their own and African habitat.

Acquired Immunodeficiency Syndrome↗

PubMed2006

An aged host promotes the evolution of avirulent coxsackievirus into a virulent strain.

The emergence of new, more pathogenic viruses necessitates elucidation of factors that promote viral evolution. Aging, a potential factor, is associated with increased susceptibility to viral infections. We used the enterovirus coxsackievirus B3 (CVB3) to investigate the effects of host age on pathogenicity and viral gene sequence. Old mice infected with a normally amyocarditic strain of CVB3, CVB3/0, had significantly higher mean heart viral titers compared with CVB3/0-infected adult mice. To determine whether a change in the CVB3/0 viral population could contribute to the higher titers observed in the old infected mice, CVB3/0 was passed once through an old or adult host and the changes in pathogenicity and viral genome were examined after subsequent infection of old or adult mice. Adult mice infected with CVB3/0 that was passed through an old host (CVB3/0(Old)) exhibited significantly higher heart viral titers, pathology, and weight loss than adult mice infected with either stock CVB3/0 or CVB3/0 passed through an adult host (CVB3/0(Adult)). Sequence analysis of virus isolated from CVB3/0(Old)-infected mice revealed 13 specific and reproducible nucleotide changes. These changes result in a sequence that matches the virulent CVB3/20 strain and are associated with promoting cardiovirulence. In contrast, we observed only one nucleotide change, low heart viral titers, and no heart and liver pathology in adult mice infected with CVB3/0(Adult). These results demonstrate that the aged host promotes rapid selection of a pathogenic variant of CVB3 from an avirulent strain and introduces a host-virus paradigm for studies of viral infection in the aged.

Aging↗

PubMed1997

Asian genotypes of JC virus in Native Americans and in a Pacific Island population: markers of viral evolution and human migration.

The human polyomavirus JC (JCV) causes the central nervous system demyelinating disease progressive multifocal leukoencephalopathy. Previously, we showed that 40% of Caucasians in the United States excrete JCV in the urine as detected by PCR. We have now studied 68 Navaho from New Mexico, 25 Flathead from Montana, and 29 Chamorro from Guam. By using PCR amplification of a fragment of the VP1 gene, JCV DNA was detected in the urine of 45 (66%) Navaho, 14 (56%) Flathead, and 20 (69%) Chamorro. Genotyping of viral DNAs in these cohorts by cycle sequencing showed predominantly type 2 (Asian), rather than type 1 (European). Type 1 is the major type in the United States and Hungary. Type 2 can be further subdivided into 2A, 2B, and 2C. Type 2A is found in China and Japan. Type 2B is a subtype related to the East Asian type, and is now found in Europe and the United States. The large majority (56-89%) of strains excreted by Native Americans and Pacific Islanders were the type 2A subtype, consistent with the origin of these strains in Asia. These findings indicate that JCV infection of Native Americans predates contact with Europeans, and likely predates migration of Amerind ancestors across the Bering land bridge around 12,000-30,000 years ago. If JCV had already differentiated into stable modern genotypes and subtypes prior to first settlement, the origin of JCV in humans may date from 50,000 to 100,000 years ago or more. We conclude that JCV may have coevolved with the human species, and that it provides a convenient marker for human migrations in both prehistoric and modern times.

Biomarkers↗

PubMed1999

Genomic evolution, patterns of global dissemination, and interspecies transmission of human and simian T-cell leukemia/lymphotropic viruses.

Using both env and long terminal repeat (LTR) sequences, with maximal representation of genetic diversity within primate strains, we revise and expand the unique evolutionary history of human and simian T-cell leukemia/lymphotropic viruses (HTLV/STLV). Based on the robust application of three different phylogenetic algorithms of minimum evolution-neighbor joining, maximum parsimony, and maximum likelihood, we address overall levels of genetic diversity, specific rates of mutation within and between different regions of the viral genome, relatedness among viral strains from geographically diverse regions, and estimation of the pattern of divergence of the virus into extant lineages. Despite broad genomic similarities, type I and type II viruses do not share concordant evolutionary histories. HTLV-I/STLV-I are united through distinct phylogeographic patterns, infection of 20 primate species, multiple episodes of interspecies transmission, and exhibition of a range in levels of genetic divergence. In contrast, type II viruses are isolated from only two species (Homo sapiens and Pan paniscus) and are paradoxically endemic to both Amerindian tribes of the New World and human Pygmy villagers in Africa. Furthermore, HTLV-II is spreading rapidly through new host populations of intravenous drug users. Despite such clearly disparate host populations, the resultant HTLV-II/STLV-II phylogeny exhibits little phylogeographic concordance and indicates low levels of transcontinental genetic differentiation. Together, these patterns generate a model of HTLV/STLV emergence marked by an ancient ancestry, differential rates of divergence, and continued global expansion.

Animals↗

PubMed1992

Natural selection and dynamical coexistence of defective and complementing virus segments.

Defective interfering (DI) particles are known to coexist with wildtype viruses under high multiplicity of infection. The complementing segments of coviruses (multiparticle, segmented viruses) coexist under similar conditions. In all cases, within-cell reproductive advantage to one of the segments is rather common. This fact, and the observation that DI particles are parasites, whereas covirus segments are mutualists, call for a non-trivial model of stable dynamical coexistence. The methodical novelty is the application of the structured deme model to virus dynamics. It assumes that biochemical ("ecological") interactions occur among segments within a coinfection group, established through random infection of the cells, and there is complete mixing of the various types emerging from all the coinfection groups (cells) in the virus pool between two infections. Through the application of the model, analytic results on the coexistence of virus segments are obtained for the following cases: virus-DI particle, virus-DI particle-resistant virus, covirus pair, virus-covirus.

Biological Evolution↗

PubMed2006

Complete genome analysis of 33 ecologically and biologically diverse Rift Valley fever virus strains reveals widespread virus movement and low genetic diversity due to recent common ancestry.

Rift Valley fever (RVF) virus is a mosquito-borne RNA virus responsible for large explosive outbreaks of acute febrile disease in humans and livestock in Africa with significant mortality and economic impact. The successful high-throughput generation of the complete genome sequence was achieved for 33 diverse RVF virus strains collected from throughout Africa and Saudi Arabia from 1944 to 2000, including strains differing in pathogenicity in disease models. While several distinct virus genetic lineages were determined, which approximately correlate with geographic origin, multiple exceptions indicative of long-distance virus movement have been found. Virus strains isolated within an epidemic (e.g., Mauritania, 1987, or Egypt, 1977 to 1978) exhibit little diversity, while those in enzootic settings (e.g., 1970s Zimbabwe) can be highly diverse. In addition, the large Saudi Arabian RVF outbreak in 2000 appears to have involved virus introduction from East Africa, based on the close ancestral relationship of a 1998 East African virus. Virus genetic diversity was low (approximately 5%) and primarily involved accumulation of mutations at an average of 2.9 x 10(-4) substitutions/site/year, although some evidence of RNA segment reassortment was found. Bayesian analysis of current RVF virus genetic diversity places the most recent common ancestor of these viruses in the late 1800s, the colonial period in Africa, a time of dramatic changes in agricultural practices and introduction of nonindigenous livestock breeds. In addition to insights into the evolution and ecology of RVF virus, these genomic data also provide a foundation for the design of molecular detection assays and prototype vaccines useful in combating this important disease.

Animals↗

PubMedDate not supplied

Biological characteristics of rhabdoviruses in different host cells.

Rhabdoviruses are a group of viruses capable of infecting vertebrates, invertebrates and plants and showing a wide range of host-parasite relationships. Biological characteristics of viruses can vary according to the type of cells in which they grow. The Authors analyze differences in viral structure and multiplication related to the host. Some final considerations on the evolution of this group of viruses are also reported.

Cells, Cultured↗

PubMed2002

Genetic diversity in the VP1 gene of foot-and-mouth disease virus serotype Asia 1.

Complete nucleotide sequence of the 1D (VP1-encoding) gene of 61 foot-and-mouth disease (FMD) serotype Asia I virus isolates recovered from different outbreaks in India between 1985 and 1999 including two vaccine strains currently used were determined. The sequences were compared with each other and those from other Asian countries. On the basis of phylogenetic analysis the viruses could be grouped into four genotypes (genotypes I-IV). All the 61 isolates from India belong to a single genotype (genotype-II) which is further subdivided into three lineages (B1, B2 and B3) under the same genotype. The viruses of the lineage B1 and B3 were found to be more prevalent before 1996 while the viruses of lineage B2 appeared to be new variants responsible for most of the recent outbreaks. Most of the isolates of lineage B1 lack one amino acid in the VP1 protein (position 44) whereas most of the isolates of lineage B2 and B3 contain it which indicates the possibility of these lineages having evolved independently. The rate of evolution of FMDV Asia 1 virus was also estimated and found to be 2.7 x 10(-2) synonymous substitutions per nucleotide per year.

Amino Acid Sequence↗

PubMed2004

Apoptosis in unicellular organisms: mechanisms and evolution.

Data about the programmed death (apoptosis) in unicellular organisms, from bacteria to ciliates, are discussed. Firstly apoptosis appeared in lower eukaryotes, but its mechanisms in these organisms are different from the classical apoptosis. During evolution, the apoptotic process has been improving gradually, with reactive oxygen species and Ca2+ playing an essential role in triggering apoptosis. All eukaryotic organisms have apoptosis inhibitors, which might be introduced by viruses. In the course of evolution, caspases and apoptosis-inducing factor appeared before other apoptotic proteins, with so-called death receptors being the last among them. The functional analogs of eukaryotic apoptotic proteins take parts in the programmed death of bacteria.

Animals↗

PubMedDate not supplied

Polymorphism in HIV-1 non-subtype B protease and reverse transcriptase and its potential impact on drug susceptibility and drug resistance evolution.

HIV-1 non-subtype B viruses are predominant worldwide. At least 9 different HIV-1 group M subtypes and 14 circulating recombinant forms differ from one another by 10-15% in their pol gene, which includes the coding regions for the viral protease and reverse transcriptase (RT), the current targets of antiretroviral drugs. Inter-subtype genotypic diversity includes polymorphism at amino acid residues known to be related to drug resistance in HIV-1 subtype B. Whether polymorphism alters protease and RT function, drug susceptibility, or clinical response to treatment, is unclear. Worldwide dissemination of non-subtype B viruses and increasing availability of antiretroviral drugs in the developing world will expand drug use and the likelihood of drug resistance in non-subtype B viruses. In this review we define and characterize inter-subtype RT and protease polymorphism, and examine the evidence for genotypic and phenotypic differences between HIV-1 subtypes as well as the potential for different clinical responses and evolution of drug resistance among non-B infected individuals.

Anti-HIV Agents↗

PubMed2004

Effect of antiviral treatment on evolution of liver steatosis in patients with chronic hepatitis C: indirect evidence of a role of hepatitis C virus genotype 3 in steatosis.

BACKGROUND AND AIM: Recent studies suggest that liver steatosis in chronic hepatitis C may be the expression of a direct cytopathic effect of hepatitis C virus (HCV), particularly in patients infected with genotype 3. To investigate this hypothesis, we studied the relationship between steatosis evolution and HCV clearance after antiviral treatment in patients with chronic hepatitis C and paired liver biopsies. METHODS: A total of 151 patients (37 with HCV genotype 3; 114 with HCV non-3 genotypes) were selected according to the following criteria: presence of steatosis at initial biopsy; no antiviral treatment prior to the first biopsy; antiviral treatment received between the two biopsies; body mass index (BMI) <28 kg/m(2); absence of excessive alcohol intake; no serum hepatitis B surface antigen or human immunodeficiency virus antibodies; and absence of diabetes mellitus. Evolution of steatosis was examined by comparing steatosis grades between the two biopsies. RESULTS: Twenty five patients (16.5%) were sustained virological responders (SVR) to antiviral treatment. Steatosis evolution after antiviral treatment was as follows: improvement in 36% of cases; stability in 51%; and worsening in 13%. Steatosis improvement was significantly more frequent in SVR than in non-responders (NR) (64% v 31%; p<0.004). This significant difference occurred in patients infected with genotype 3 (91% v 19%; p<0.0001) but not in those infected with non-3 genotypes (43% v 34%; NS). Among the 25 SVR, improvement in steatosis was significantly more frequent in patients infected with genotype 3 than in those infected with non-3 genotypes (91% v 43%; p<0.04) whereas in NR, improvement in steatosis did not differ between those infected with genotype 3 and non-3 genotypes (19% v 34%; NS). In multivariate analysis, four factors were independently associated with steatosis improvement: sustained virological response to antiviral therapy (odds ratio (OR) 6.06 (95% confidence interval (CI) 1.61-22.9); p = 0.01), severe steatosis (OR 5.50 (95% CI 1.54-19.6); p = 0.01), HCV genotype 3 (OR 2.90 (95% CI 0.85-10.0); p = 0.07), and BMI >25 kg/m(2) (OR 0.24 (95% CI 0.08-0.73); p = 0.02). CONCLUSIONS: Our results showed significant improvement in steatosis in patients infected with HCV genotype 3, who achieved sustained viral clearance. This provides further evidence for direct involvement of HCV genotype 3 in the pathogenesis of hepatic steatosis.

Adult↗

PubMed2002

Cloning and genomic characterization of Felis domesticus papillomavirus type 1.

A novel papillomavirus was cloned from hyperkeratotic cutaneous lesions of a Persian domestic cat. The Felis domesticus papillomavirus (FdPV-1) genome counts 8300 bp and has a typical genome structure with an early region (E1, E2, E4, E6, E7), a late region (L1, L2), and a noncoding upstream regulatory region (URR or NCR1) between the end of L1 and the beginning of E6. The FdPV-1 also shows an unusual second noncoding region (NCR2) of 1.3 kb, situated between the end of E2 and the beginning of L2. This NCR2 is uniquely related to a similar region in the canine oral papillomavirus (COPV). Phylogenetic analysis places FdPV-1 together with COPV, the cottontail rabbit papillomavirus, human papillomavirus type 1 (HPV-1), and HPV-63 in the group of the benign cutaneous papillomaviruses. The position of FdPV-1 in the phylogenetic tree allows us to hypothesize that already in an early phase of the papillomavirus molecular evolution, a split occurred into viruses with a dual tropism primarily for cutaneous epithelia but also secondarily for mucosal surfaces, and viruses with a specific monotropism for mucosal surfaces. The close relationship between FdPV-1 and COPV, and between their Canidae and Felidae hosts, supports the hypothesis that papillomaviruses have speciated and coevolved together with their hosts throughout vertebrate evolution. A papillomavirus mutation rate of 0.73 to 0.96 x 10(-8) nucleotide substitutions per base per year was calculated.

Animals↗

PubMed2006

Structure, function and evolution of the hemagglutinin-esterase proteins of corona- and toroviruses.

Virus attachment to host cells is mediated by dedicated virion proteins, which specifically recognize one or, at most, a limited number of cell surface molecules. Receptor binding often involves protein-protein interactions, but carbohydrates may serve as receptor determinants as well. In fact, many different viruses use members of the sialic acid family either as their main receptor or as an initial attachment factor. Sialic acids (Sias) are 9-carbon negatively-charged monosaccharides commonly occurring as terminal residues of glycoconjugates. They come in a large variety and are differentially expressed in cells and tissues. By targeting specific Sia subtypes, viruses achieve host cell selectivity, but only to a certain extent. The Sia of choice might still be abundantly present on non-cell associated molecules, on non-target cells (including cells already infected) and even on virus particles themselves. This poses a hazard, as high-affinity virion binding to any of such "false'' receptors would result in loss of infectivity. Some enveloped RNA viruses deal with this problem by encoding virion-associated receptor-destroying enzymes (RDEs). These enzymes make the attachment to Sia reversible, thus providing the virus with an escape ticket. RDEs occur in two types: neuraminidases and sialate-O-acetylesterases. The latter, originally discovered in influenza C virus, are also found in certain nidoviruses, namely in group 2 coronaviruses and in toroviruses, as well as in infectious salmon anemia virus, an orthomyxovirus of teleosts. Here, the structure, function and evolution of viral sialate-O-acetylesterases is reviewed with main focus on the hemagglutinin-esterases of nidoviruses.

Amino Acid Sequence↗

PubMed1977

Immune surveillance against virus-induced tumors and nonrejectability of spontaneous tumors: contrasting consequences of host versus tumor evolution.

Spontaneous tumours are defined as tumors that develop in the absence of all experimental interference. In contrast to the widely documented, strong rejection reactions against most virus-induced tumors, spontaneous tumors evoke little or no detectable rejection reaction in intact or preimmunized syngeneic hosts. The difference can be viewed in relation to the contrasting natural history of the two conditions. Spontaneous tumors evolve in several steps, as a fule. "Tumor progression" is a microevolutionary process at the level of the somatic tissue where successive clonal variants replace each other. Each new variant gains the upper hand due to its greater independence of some restricting host mechanism. Independence of immune restrictions must be part of this process. Host selection for immune resistance apparently plays no major role here, presumably because most of the naturally occurring tumors arise after the host has passed the peak of its reproductive period. Protection against the oncogenic effects of ubiquitous tumor viruses is, on the other hand, the result of host selection for immune mechanisms favoring prompt rejection of virus-transformed cells. This is neither synonymous with nor related to protection against the viral infection per se, which is frequently successful and usually quite harmless. A certain relationship can be perceived between the degree of viral ubiquity and the strength of immune protection against the corresponding tumor cells. Natural selection for host recognition of commonly occurring, virally induced changes in neoplastic cell membranes can be surmised to occur, at least in part, by the fixation of appropriate immune responsiveness (Ir) genes. The role of Ir genes for tumor recognition can be approached by the genetic analysis of the F1 hybrid resistance effect. Unresponsiveness to spontaneous tumors may be overcome by target-cell modification, e.g., by chemical coupling, somatic cell hybridization, or viral "xenogenization".

Animals↗