Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “viral evolution”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 721 records · Page 40Linked to original sources
PubMedDate not supplied

Epidemiological, viral and serological studies concerning the evolution of some acute respiratory diseases between November 1992 and March 1993 in nine districts of the south-east area of Romania.

Viral and serological studies led to the conclusion that parainfluenza type 3 and influenza type A(H3N2) viruses were the most implicated in the etiology of acute respiratory diseases (ARD), viral pneumonia and clinical influenza in nine districts of the south-east area of Romania during the November 1992--March 1993 period. Epidemiological survey pointed on the 0-1 year group of age as the most affected by the above mentioned respiratory diseases.

Acute Disease↗
PubMedDate not supplied

Epidemiological, viral and serological studies concerning the evolution of some acute respiratory diseases between November 1992 and March 1993 in nine districts of the south-east area of Romania.

Viral and serological studies led to the conclusion that parainfluenza type 3 and influenza type A(H3N2) viruses were the most implicated in the etiology of acute respiratory diseases (ARD), viral pneumonia and clinical influenza in nine districts of the south-east area of Romania during the November 1992-March 1993 period. Epidemiological survey pointed on the 0-1 year group of age as the most affected by the above mentioned respiratory diseases.

Acute Disease↗
PubMed2001

Quantification of intrinsic residual viral replication in treated HIV-infected patients.

The intrinsic rate of viral replication in HIV-infected patients treated with antiretroviral combination therapy is estimated by using a mathematical model of viral dynamics. This intrinsic replication is found to be episodic, varying considerably in quantity between patients (even among those achieving long-term undetectable levels of viremia) and is always reduced by increasing the potency of the antiviral drug regimen. The analysis reveals that even in conditions of perfect patient adherence and drug penetration a substantial level of residual viral replication is expected. The rate of evolution in the viral quasispecies, and thus also the probability of new drug-resistant viral strains being created, is proportional to the total amount of residual viral replication. Under most circumstances, the viral population continues to turn over rapidly during therapy, albeit at a much reduced level.

Anti-HIV Agents↗
PubMed2006

Minority memory genomes can influence the evolution of HIV-1 quasispecies in vivo.

One of the consequences of viral quasispecies dynamics is the presence, in the mutant spectrum, of minority memory genomes that reflect those variants that were dominant at an earlier phase of the same evolutionary lineage. Replicative and cellular (or anatomical) contributions to quasispecies memory were previously defined during intrahost evolution of human immunodeficiency virus type 1 (HIV-1) [Briones, C., Domingo, E., Molina-París, C., 2003. Memory in retroviral quasispecies: experimental evidence and theoretical model for human immunodeficiency virus. J. Mol. Biol. 331, 213-229.]. However, the effects of replicative memory regarding virus evolution in vivo have not been investigated. Here we document that a multidrug-resistant (MDR) HIV-1, present at memory level, determined the ensuing evolution of the virus in an infected patient. Nucleotide sequencing and detailed phylogenetic analyses of sequential viral populations and individual molecular clones evidenced that the progeny of a minority MDR genome during a treatment interruption contributed the dominant genomes when an antiretroviral treatment was restored. An extension of a mathematical model of establishment and maintenance of memory, based on quasispecies theory, supports the experimental data. Therefore a replicative memory subpopulation, not detectable in a consensus nucleotide sequence, affected decisively subsequent states of viral evolution in vivo.

Anti-HIV Agents↗
PubMedDate not supplied

Hepatic artery hemodynamics in acute viral hepatitis.

In order to evaluate the effect of the acute viral hepatitis on arterial blood flow we performed duplex Doppler US on 30 patients with acute viral hepatitis (AVH) and compared the results with those obtained on 20 normal volunteers. Hepatic artery flow (HAF) was significantly increased with the patients suffering from acute viral hepatitis. The data obtained show that the increase of arterial blood flow is not always associated with the increase of arterial velocities. We could put in evidence the presence of the hepatic artery response to altered portal blood flow (arterial buffer) during a AVH. If the increase of HAF is absolutely necessary for recovery from hepatitis, excessive increase of HAF seems to increase the time of recovery. In our study, the evolution of acute viral hepatitis was good when the HAF values did not exceed 65% of liver supply. The increase of arterial blood flow over 65% seems to limit the portal supply of the liver and in this way the amounts of regenerating substances which bathe the liver cells. The HAF value plays an important role in acute viral hepatitis evolution, so that the exploration of HAF and hepatic artery velocities may be a reliable examination in order to monitor the evolution of this disease.

Acute Disease↗
PubMed2000

The evolution of antiviral therapy for external ocular viral infections over twenty-five years.

PURPOSE: To review the past 25 years of the evolution of antiviral therapy for the treatment of common external ocular viral infections (herpes simplex virus type 1, varicella-zoster virus, and adenovirus). METHODS: A broad-based literature review in the fields of virology, antiviral research, and ophthalmology will be carried out. The pathogenesis of the major external ocular viral infections and history of antiviral development will be cited. Important conceptual breakthroughs as well as historical landmarks will be emphasized. RESULTS: The successful development of effective antivirals to treat the most common external ocular viral infections have dramatically reduced morbidity and sight loss. The immune pathogenesis of herpetic stromal keratitis is better understood. CONCLUSIONS: Remarkable progress in the development of antiviral therapy has occurred over the past quarter century. Future needs include improved antivirals and immunomodulators and vaccines to prevent and treat herpetic ocular infections and adenovirus keratoconjunctivitis.

Antiviral Agents↗
PubMed2002

Viral immune evasion: a masterpiece of evolution.

Coexistence of viruses and their hosts imposes an evolutionary pressure on both the virus and the host immune system. On the one hand, the host has developed an immune system able to attack viruses and virally infected cells, whereas on the other hand, viruses have developed an array of immune evasion mechanisms to escape killing by the host's immune system. Generally, the larger the viral genome, the more diverse mechanisms are utilized to extend the time-window for viral replication and spreading of virus particles. In addition, herpesviruses have the capacity to hide from the immune system by their ability to establish latency. The strategies of immune evasion are directed towards three divisions of the immune system, i.e., the humoral immune response, the cellular immune response and immune effector functions. Members of the herpesvirus family are capable of interfering with the host's immune system at almost every level of immune clearance. Antibody recognition of viral epitopes, presentation of viral peptides by major histocompatibility complex (MHC) class I and class II molecules, the recruitment of immune effector cells, complement activation, and apoptosis can all be impaired by herpesviruses. This review aims at summarizing the current knowledge of viral evasion mechanisms.

Animals↗
PubMed1998

Longitudinal HIV-1 RNA levels in a cohort of homosexual men.

HIV-1 RNA levels measured during early chronic infection strongly predict subsequent clinical events. In the short term, HIV-1 is in a steady state, but the stability of viral levels over time is incompletely understood. We used reverse transcriptase polymerase chain reaction (RT-PCR) to examine changes in serum HIV-1 RNA levels in 111 HIV-1-infected homosexual men during the period from 1982 to 1992 and their relation to clinical outcomes. HIV-1 RNA levels increased by a median of 0.08 log10 copies/ml/year (p=.0001). HIV-1 RNA levels rose either gradually or abruptly for the majority of subjects; 41% had no increase. Among subjects surviving at least 8 years, HIV-1 RNA was stable during the first 4 years after seroconversion (median. 0.00 log10 copies/ml/year), but rose in years five through eight (median, 0.06 log10 copies/ml/year; p=.04). The annual HIV-I RNA level was more predictive of AIDS (relative hazard [RH], 1.75 per 0.5 log difference; 95% confidence interval [CI], 1.38-2.21; likelihood ratio [LR], 26.2) than the initial level alone (RH, 1.39; 95% CI. 1.10-1.76; LR, 8.5). We conclude that most HIV-1-infected persons lack a long-term viral setpoint and that failure to account for evolution of the viral level can lead to underestimation of the risk of progression.

Adult↗
PubMed2004

Nitric oxide as an endogenous mutagen for Sendai virus without antiviral activity.

Nitric oxide (NO) may affect the genomes of various pathogens, and this mutagenesis is of particular interest for viral pathogenesis and evolution. Here, we investigated the effect of NO on viral replication and mutation. Exogenous or endogenous NO had no apparent antiviral effect on influenza A virus and Sendai virus. The mutagenic potential of NO was analyzed with Sendai virus fused to a green fluorescent protein (GFP) gene (GFP-SeV). GFP-SeV was cultured in SW480 cells transfected with a vector expressing inducible NO synthase (iNOS). The mutation frequency of GFP-SeV was examined by measuring loss of GFP fluorescence of the viral plaques. GFP-SeV mutation frequency in iNOS-SW480 cells was much higher than that in parent SW480 cells and was reduced to the level of mutation frequency in the parent cells by treatment with an NO synthase (NOS) inhibitor. Immunocytochemistry showed generation of more 8-nitroguanosine in iNOS-SW480 cells than in SW480 cells without iNOS transfection. Authentic 8-nitroguanosine added exogenously to GFP-SeV-infected CV-1 cells increased the viral mutation frequency. Profiles of the GFP gene mutations induced by 8-nitroguanosine appeared to resemble those of mutations occurring in mouse lungs in vivo. A base substitution that was characteristic of both mutants (those induced by 8-nitroguanosine and those occurring in vivo) was a C-to-U transition. NO-dependent oxidative stress in iNOS-SW480 cells was also evident. Together, the results indicate unambiguously that NO has mutagenic potential for RNA viruses such as Sendai virus without affecting viral replication, possibly via 8-nitroguanosine formation and cellular oxidative stress.

Animals↗
PubMed2002

Evolution of phenotypic drug susceptibility and viral replication capacity during long-term virologic failure of protease inhibitor therapy in human immunodeficiency virus-infected adults.

Continued use of antiretroviral therapy despite the emergence of drug-resistant human immunodeficiency virus (HIV) has been associated with the durable maintenance of plasma HIV RNA levels below pretherapy levels. The factors that may account for this partial control of viral replication were assessed in a longitudinal observational study of 20 HIV-infected adults who remained on a stable protease inhibitor-based regimen despite ongoing viral replication (plasma HIV RNA levels consistently >500 copies/ml). Longitudinal plasma samples (n = 248) were assayed for drug susceptibility and viral replication capacity (measured by using a single-cycle recombinant-virus assay). The initial treatment-mediated decrease in plasma viremia was directly proportional to the reduction in replicative capacity (P = 0.01). Early virologic rebound was associated the emergence of a virus population exhibiting increased protease inhibitor phenotypic resistance, while replicative capacity remained low. During long-term virologic failure, plasma HIV RNA levels often remained stable or increased slowly, while phenotypic resistance continued to increase and replicative capacity decreased slowly. The emergence of primary genotypic mutations within protease (particularly V82A, I84V, and L90M) was temporally associated with increasing phenotypic resistance and decreasing replicative capacity, while the emergence of secondary mutations within protease was associated with more-gradual changes in both phenotypic resistance and replicative capacity. We conclude that HIV may be constrained in its ability to become both highly resistant and highly fit and that this may contribute to the continued partial suppression of plasma HIV RNA levels that is observed in some patients with drug-resistant viremia.

Adult↗
PubMed1995

Viral resistance and the selection of antiretroviral combinations.

Mounting scientific evidence suggests that viral replication and evolution of diversification, with the resulting emergence of variants including drug-resistant strains, is responsible for the gradual destruction of the immune system and is the mechanism of disease progression in HIV-infected patients. Monotherapy does not give long-term suppression of viral replication and evolution, and combination therapy is viewed as a potentially more effective long-term approach based on increased and more durable suppression of HIV replication. Because of the large number of drugs that could be used in combination therapy regimens, it is important to investigate, in clinical studies, only those combinations likely to be most effective. In vitro studies are therefore critical in the selection of such combinations. Resistance mutations to many antiretroviral agents have been documented and their patterns of emergence elucidated. A number of studies have since demonstrated the phenomenon of cross-resistance, in which resistant virus emerging under the selective pressure of one therapy is also cross-resistant to a second antiviral agent. This information can be used to avoid combining agents to which cross-resistance can occur. Suppression or "phenotypic reversal" of zidovudine resistance by the lamivudine-resistance mutation at codon 184 has been demonstrated in in vitro studies. It is encouraging that this finding has led to the clinical evaluation of these two agents with promising results. Moreover, in vitro scientific data are critical in facilitating the identification of potentially effective combination therapies.

Antiviral Agents↗
PubMed1982

Persistence of circulating HBsAg/IgM complexes in acute viral hepatitis, type B: an early marker of chronic evolution.

Serial serum samples from 110 patients with acute viral hepatitis type B were tested for HBsAg/IgM complexes by a newly developed solid-phase radioimmunoassay. In 102 patients the infection resolved and they recovered from the disease. In these patients, HBsAg/IgM complexes were either absent from the outset of disappeared from serum within four weeks of admission, long before HBsAg had cleared or serum alanine aminotransferase had returned to normal, 8 patients progressed to chronic HBsAg carrier state and chronic liver disease. In these patients, HBsAg/IgM complexes were detectable in the serum on admission, and never disappeared. These results indicate that persistence of circulating complexes containing HBsAg and IgM after the early phase of acute viral hepatitis type B is a predictor of disease chronicity. As early as the fifth week of illness those in whom chronic liver disease developed could be distinguished from those who recovered.

Adolescent↗
PubMed2002

Equine infectious anemia virus envelope evolution in vivo during persistent infection progressively increases resistance to in vitro serum antibody neutralization as a dominant phenotype.

Equine infectious anemia virus (EIAV) infection of horses is characterized by well-defined waves of viremia associated with the sequential evolution of distinct viral populations displaying extensive envelope gp90 variation; however, a correlation of in vivo envelope evolution with in vitro serum neutralization phenotype remains undefined. Therefore, the goal of the present study was to utilize a previously defined panel of natural variant EIAV envelope isolates from sequential febrile episodes to characterize the effects of envelope variation during persistent infection on viral neutralization phenotypes and to define the determinants of EIAV envelope neutralization specificity. To assess the neutralization phenotypes of the sequential EIAV envelope variants, we determined the sensitivity of five variant envelopes to neutralization by a longitudinal panel of immune serum from the source infected pony. The results indicated that the evolution of the EIAV envelope sequences observed during sequential febrile episodes produced an increasingly neutralization-resistant phenotype. To further define the envelope determinants of EIAV neutralization specificity, we examined the neutralization properties of a panel of chimeric envelope constructs derived from reciprocal envelope domain exchanges between selected neutralization-sensitive and neutralization-resistant envelope variants. These results indicated that the EIAV gp90 V3 and V4 domains individually conferred serum neutralization resistance while other envelope segments in addition to V3 and V4 were evidently required for conferring total serum neutralization sensitivity. These data clearly demonstrate for the first time the influence of sequential gp90 variation during persistent infection in increasing envelope neutralization resistance, identify the gp90 V3 and V4 domains as the principal determinants of antibody neutralization resistance, and indicate distinct complex cooperative envelope domain interactions in defining sensitivity to serum antibody neutralization.

Amino Acid Sequence↗
PubMed1999

Lack of evolutionary stasis during alternating replication of an arbovirus in insect and mammalian cells.

The evolution of vesicular stomatitis virus (VSV) in a constant environment, consisting of either mammalian or insect cells, has been compared to the evolution of the same viral population in changing environments consisting in alternating passages in mammalian and insect cells. Fitness increases were observed in all cases. An initial fitness loss of VSV passaged in insect cells was noted when fitness was measured in BHK-21 cells, but this effect could be attributed to a difference of temperature during VSV replication at 37 degrees C in BHK-21 cells. Sequencing of nucleotides 1-4717 at the 3' end of the VSV genome (N, P, M and G genes) showed that at passage 80 the number of mutations accumulated during alternated passages (seven mutations) is similar or larger than that observed in populations evolving in a constant environment (two to four mutations). Our results indicate that insect and mammalian cells can constitute similar environments for viral replication. Thus, the slow rates of evolution observed in natural populations of arboviruses are not necessarily due to the need for the virus to compromise between adaptation to both arthropod and vertebrate cell types.

Adaptation, Physiological↗
PubMed1999

Consistent viral evolutionary changes associated with the progression of human immunodeficiency virus type 1 infection.

To understand the high variability of the asymptomatic interval between primary human immunodeficiency virus type 1 (HIV-1) infection and the development of AIDS, we studied the evolution of the C2-V5 region of the HIV-1 env gene and of T-cell subsets in nine men with a moderate or slow rate of disease progression. They were monitored from the time of seroconversion for a period of 6 to 12 years until the development of advanced disease in seven men. Based on the analysis of viral divergence from the founder strain, viral population diversity within sequential time points, and the outgrowth of viruses capable of utilizing the CXCR4 receptor (X4 viruses), the existence of three distinct phases within the asymptomatic interval is suggested: an early phase of variable duration during which linear increases ( approximately 1% per year) in both divergence and diversity were observed; an intermediate phase lasting an average of 1.8 years, characterized by a continued increase in divergence but with stabilization or decline in diversity; and a late phase characterized by a slowdown or stabilization of divergence and continued stability or decline in diversity. X4 variants emerged around the time of the early- to intermediate-phase transition and then achieved peak representation and began a decline around the transition between the intermediate and late phases. The late-phase transition was also associated with failure of T-cell homeostasis (defined by a downward inflection in CD3(+) T cells) and decline of CD4(+) T cells to </=200 cells/microliter. The strength of these temporal associations between viral divergence and diversity, viral coreceptor specificity, and T-cell homeostasis and subset composition supports the concept that the phases described represent a consistent pattern of viral evolution during the course of HIV-1 infection in moderate progressors. Recognition of this pattern may help explain previous conflicting data on the relationship between viral evolution and disease progression and may provide a useful framework for evaluating immune damage and recovery in untreated and treated HIV-1 infections.

Base Sequence↗
PubMed2005

Reducing the impact of viral respiratory infections in children.

This article reviews the epidemiology and clinical aspects of the major viral causes of upper and lower respiratory tract disease in children. Particular emphasis is placed on prevention and control of viral disease through the use of vaccines and antiviral agents. Evolution of new viral pathogens, such as avian influenza virus and the SARS-CoV, are discussed.

Age Distribution↗
PubMed2003

Role of viruses in human evolution.

The study of viral molecular genetics has produced a considerable body of research into the sequences and phylogenetic relationships of human and animal viruses. A review of this literature suggests that humans have been afflicted by viruses throughout their evolutionary history, although the number and types have changed. Some viruses show evidence of long-standing intimate relationship and cospeciation with hominids, while others are more recently acquired from other species, including African monkeys and apes while our line was evolving in that continent, and domesticated animals and rodents since the Neolithic. Viral selection for specific resistance polymorphisms is unlikely, but in conjunction with other parasites, viruses have probably contributed to selection pressure maintaining major histocompatibility complex (MHC) diversity and a strong immune response. They may also have played a role in the loss in our lineage of N-glycolylneuraminic acid (Neu5Gc), a cell-surface receptor for many infectious agents. Shared viruses could have affected hominid species diversity both by promoting divergence and by weeding out less resistant host populations, while viruses carried by humans and other animals migrating out of Africa may have contributed to declines in other populations. Endogenous retroviral insertions since the divergence between humans and chimpanzees were capable of directly affecting hominid evolution through changes in gene expression and development.

Animals↗