Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “SNV”

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 73 records · Page 4Linked to original sources
PubMed1990

The efficiency of RNA 3'-end formation is determined by the distance between the cap site and the poly(A) site in spleen necrosis virus.

The efficiency of RNA 3'-end formation of spleen necrosis virus (SNV) is determined by the distance between the cap site and the poly(A) site. When the distance between the cap site and the poly(A) site was shorter than 500 bases, only 3-9% of the RNA was polyadenylated at the SNV poly(A) site. However, when the distance between the cap site and the poly(A) site was 1400 bases or more, 70% of the total RNA was polyadenylated at the SNV poly(A) site. In contrast, the poly(A) signal sequences of the thymidine kinase (tk) and SV40 late genes functioned at high efficiency, even with a distance between the cap site and the poly(A) site that was short enough to inactivate the SNV poly(A) signal. Therefore, this distance-dependent inactivation of RNA 3'-end formation is specific for SNV sequences and perhaps for related retroviruses. This finding explains the difference between the 5' and 3' poly(A) sites in many retrovirus RNAs.

Animals↗
PubMed1977

Formation of reticuloendotheliosis virus pseudotypes of Rous sarcoma virus.

Superinfection of chicken embryo fibroblasts transformed by the defective Bryan strain of Rous sarcoma virus (BH-RSV) with two different reticuloendotheliosis viruses (REVs), REV strain T (REV-T) or spleen necrosis virus (SNV), resulted in the production of infectious sarcoma virus pseudotypes. These pseudotypes were neutralized by antiserum prepared against SNV and were unable to infect chicken cells preinfected with either REV-T or SNV. These results suggest that defective BH-RSV is able to use the glycoprotein from REV to form infectious pseudotypes. On the other hand, neither REV-T nor SNV was able to supply a functional reverse transcriptase to the polymerase-negative mutant BH-RSValpha, nor was REV-T or SNV able to complement the defect in the internal protein gene of the temperature-sensitive avian sarcoma virus mutant NY45.

Animals↗
PubMed1995

Mapping of receptor binding domains in the envelope protein of spleen necrosis virus.

Spleen necrosis virus (SNV) is an amphotropic retrovirus originally isolated from a duck. Although of avian origin, it also replicates on some mammalian cells. SNV-derived retroviral vectors work with high efficiency and have a high potential for various gene transfer applications. However, little is known about the envelope-receptor interactions of this virus. We constructed a series of recombinant envelope proteins to characterize the SU peptide of SNV. We found that, in contrast to the envelope proteins of other retroviruses, truncated envelope proteins of SNV are transported to the cell surface. Surprisingly, particles displaying truncated envelope proteins can still infect cells, although at reduced efficiencies. Furthermore, these proteins can confer partial superinfection interference. Our data suggest that peptides throughout SU are involved in envelope-receptor interactions. To more precisely determine the localization of the main receptor binding domain, point mutations were introduced at certain regions of the SNV SU which are highly conserved among retroviruses belonging to the same receptor interference group. We identified one point mutation in the middle of SU (position 192) which drastically reduced infectivity and strongly reduced the ability to confer superinfection interference. The level of expression was not abolished, and translocation to the cell membrane of the mutant envelope occurred efficiently. This indicates that amino acid 192 may be directly involved in receptor binding.

Amino Acid Sequence↗
PubMed1996

Mutational analysis of the envelope protein of spleen necrosis virus.

Spleen necrosis virus (SNV) is an amphotropic type C retrovirus originally isolated from a duck. The envelope protein is related to that of type D retroviruses, and SNV appears to use the same receptor as do simian retroviruses. However, little is known about envelope-receptor interactions of SNV. We constructed a series of envelope mutants to characterize the SU peptide of SNV. Point mutations were introduced throughout SU in regions that are conserved among all retroviruses belonging to the same receptor interference group. The biological and biochemical properties of these mutants were analyzed. All mutants were transported efficiently to the cell surface. Almost all mutations in the amino-terminal one-third caused a conformational change of the envelope and a significant drop in infectivity and abolished the ability to confer superinfection interference. Similar observations were made with only two of seven mutants with mutations in the middle of SU. Four mutations in this region had little or no effect on biological activity. One mutant envelope protein (Asp to Arg at position 192) was processed normally but showed little infectivity and had no ability to confer superinfection interference. A detailed mutational analysis suggested that this amino acid forms a hydrogen bond to its cellular receptor. Mutations within the carboxy-terminal part of SU had very little or no effect on biological function. Aberrantly processed envelope proteins were proteolytically cleaved at a new point upstream of and differing in sequence from the conserved retroviral SU/TM cleavage site. Surprisingly, these mutants still retained some infectivity (0.01 to 1% of that of the wild type). Our data indicate that the envelope of SNV behaves in a manner very different from that of the envelopes of other studied retroviruses.

Amino Acid Sequence↗
PubMed2000

Suppression of inflammation in primary systemic vasculitis restores vascular endothelial function: lessons for atherosclerotic disease?

BACKGROUND: Chronic inflammatory rheumatic disorders are associated with excess cardiovascular mortality. This may result from arteriosclerosis following inflammatory damage to the vessel wall by vasculitis. Our hypothesis that vasculitis results in arteriosclerosis by causing vascular endothelial dysfunction was tested in patients with primary systemic necrotizing vasculitis (SNV). METHODS AND RESULTS: Endothelial function was assessed in cross-sectional and longitudinal studies of patients with primary SNV by measuring flow-mediated, endothelium-dependent brachial artery vasodilatation. These patients exhibited marked endothelial dysfunction compared with controls. Remission induction in patients with active primary SNV restored endothelial function. CONCLUSIONS: Endothelial function is significantly impaired in adults with primary SNV, supporting the hypothesis that premature arteriosclerosis in chronic inflammatory rheumatic disorders results from endothelial dysfunction secondary to vasculitis. Normalization of endothelial function after the treatment of primary SNV suggests that early suppression of disease activity in chronic inflammatory rheumatic disorders may reduce long-term vascular damage. The role of inflammation in atheroma formation is increasingly appreciated; this work raises questions regarding the potential for anti-inflammatory therapy in atherosclerosis itself.

Brachial Artery↗
PubMedDate not supplied

Natural history of Sin Nombre virus in western Colorado.

A mark-recapture longitudinal study of immunoglobulin G (IgG) antibody to Sin Nombre virus (SNV) in rodent populations in western Colorado (1994-results summarized to October 1997) indicates the presence of SNV or a closely related hantavirus at two sites. Most rodents (principally deer mice, Peromyscus maniculatus, and pinyon mice, P. truei) did not persist on the trapping webs much beyond 1 month after first capture. Some persisted more than 1 year, which suggests that even a few infected deer mice could serve as transseasonal reservoirs and mechanisms for over-winter virus maintenance. A positive association between wounds and SNV antibody in adult animals at both sites suggests that when infected rodents in certain populations fight with uninfected rodents, virus amplification occurs. At both sites, male rodents comprised a larger percentage of seropositive mice than recaptured mice, which suggests that male mice contribute more to the SNV epizootic cycle than female mice. In deer mice, IgG antibody prevalence fluctuations were positively associated with population fluctuations. The rates of seroconversion, which in deer mice at both sites occurred mostly during late summer and midwinter, were higher than the seroprevalence, which suggests that the longer deer mice live, the greater the probability they will become infected with SNV.

Animals↗
PubMedDate not supplied

Antibody to sin nombre virus in rodents associated with peridomestic habitats in west central Montana.

Most human cases of hantavirus pulmonary syndrome are acquired in the peridomestic environment, yet studies of the ecology and infection dynamics in the reservoir host, the deer mouse (Peromyscus maniculatus), have focused on sylvan populations. We describe a 2.5-year study of hantavirus infection in rodents associated with peridomestic habitats in west central Montana. Antibodies reactive with Sin Nombre virus (SNV) were found in five species. Overall SNV antibody prevalence was highest among deer mice (25% of individuals tested). As has been demonstrated for sylvan populations, the antibody-positive component of the deer mouse population consisted of a higher proportion of adults and males. However, the prevalence of antibodies to SNV was higher in this study than has been reported in most sylvan studies. The average monthly proportion of deer mouse blood samples with antibodies to SNV ranged from approximately 20% to 25% and was highest in the late spring/early summer. The higher SNV antibody prevalence in peridomestic compared with sylvan settings may be related to behavioral differences and/or potentially longer survival of the virus deposited inside buildings. Peridomestic settings presented higher concentrations of virus and may present a higher risk of human infection than do sylvan settings.

Animals↗
PubMed2005

Epizootiology of Sin Nombre and El Moro Canyon hantaviruses, southeastern Colorado, 1995-2000.

Sin Nombre virus (SNV) is an etiologic agent of hantavirus pulmonary syndrome. To better understand the natural history of this virus we studied population dynamics and temporal pattern of infection of its rodent hosts in southeastern Colorado (USA) from 1995 to 2000. We present evidence for the presence of two hantaviruses, SNV in deer mice (Peromyscus maniculatus) and El Moro Canyon virus in western harvest mice (Reithrodontomys megalotis), at our study sites. Sin Nombre virus appeared only sporadically in deer mouse populations; overall prevalence of antibody to SNV was 2.6%. El Moro Canyon virus was enzootic: seroconversions occurred throughout the year; antibody prevalence (11.9% overall) showed a delayed-density-dependent pattern, peaking as relative abundance of mice was declining. Males of both host species were more frequently infected than were females. An apparently lower mean survivorship (persistence at the trapping site) for SNV antibody-positive deer mice could indicate a detrimental effect of SNV on its host, but might also be explained by the fact that antibody-positive mice were older when first captured.

Age Factors↗
PubMed2005

Long-term dynamics of Sin Nombre viral RNA and antibody in deer mice in Montana.

Infections with hantaviruses in the natural host rodent may result in persistent, asymptomatic infections involving shedding of virus into the environment. Laboratory studies have partially characterized the acute and persistent infection by Sin Nombre virus (SNV) in its natural host, the deer mouse (Peromyscus maniculatus). However, these studies have posed questions that may best be addressed using longitudinal studies involving sequential sampling of individual wild-caught, naturally infected mice. Using enzyme immunoassay and polymerase chain reaction (PCR) analysis of monthly blood samples, we followed the infection status of deer mice in a mark-recapture study in Montana for 2 yr. Only six of 907 samples without IgG antibody to SNV contained detectable SNV RNA, suggesting that there is a very brief period of viremia before the host develops detectable antibody. The simultaneous presence of both antibody and viral RNA in blood was detected in consecutive monthly samples for as long as 3 mo. However, chronic infection was typified by alternating characteristics of PCR positivity and PCR negativity. Two possible interpretations of these results are that 1) viral RNA may be consistently present in the blood of chronically infected deer mouse, but that viral RNA is near the limits of PCR detectability or 2) SNV RNA sporadically appears in blood as a consequence of unknown physiological events. The occurrence of seasonal patterns in the proportion of samples that contains antibody and that also contained SNV RNA demonstrated a temporal association between recent infection (antibody acquisition) and presence of viral RNA in blood.

Animals↗
PubMed1993

The matrix region is responsible for the differential ability of two retroviruses to function as helpers for vector propagation.

We have investigated the ability of two related reticuloendotheliosis viruses to propagate a spleen necrosis virus (SNV) based retroviral vector in canine osticosarcoma (D17) cells. Reticuloendotheliosis virus strain A (REV-A) consistently propagated the vector more efficiently than SNV in cell culture. To identify the area of the viral genome responsible for the superior helper function of REV-A, we constructed chimeric viruses between SNV and REV-A. Analysis of helper function indicated that a virus comprised of the SNV genome, but containing the matrix region of REV-A, could propagate the vector as well as REV-A. Although REV-A is also a superior virus for vector propagation in chicken embryo fibroblast cells, the region of the viral genome that confers superior helper function does not map to the gag region of REV-A in this cell type.

Amino Acid Sequence↗
PubMed2005

Sciatic nerve varices.

OBJECTIVE(S): To describe patients presenting with sciatic nerve varices (SNV), presenting pitfalls in diagnosis and management. DESIGN: Case series. METHODS: Patients were investigated using duplex ultrasonography pre-operatively in three cases. Treatment was undertaken both by surgery and by foam sclerotherapy. RESULTS: Clinically, SNV appeared just below the popliteal skin crease, lateral to the small saphenous vein (SSV). In two cases SNV occurred alone, in two further cases SNV occurred in conjunction with varices from other sources. Symptoms of 'sciatic' pain were present in all. Foam sclerotherapy (1% Polidocanol) was undertaken in one case with a varix. Complete obliteration of the vein and resolution of all symptoms was achieved at the 1-month follow-up examination. Surgical management was used in the other cases. CONCLUSION: The sciatic nerve vein follows the fibular saphenous nerve (lying superficial to the fascia in the leg). This nerve arises from the common peroneal nerve (in the popliteal fossa), and is a major branch of the sciatic nerve. Varices of the associated vein appear to be the result of a dysplasia. This condition may be more common than is currently recognised.

Humans↗
PubMed2004

Development of reassortant viruses between pathogenic hantavirus strains.

Segment reassortment of negative strand viruses is an important mechanism for the development of new virus strains with altered pathogenicity. This study reports on in vitro generation of reassortants between Andes (ANDV) and Sin Nombre (SNV) viruses. Although they both cause hantavirus pulmonary syndrome (HPS), ANDV is the only hantavirus that has been transmitted from person to person (). Following dual infection of cells with ANDV and SNV, 8.9% of 337 progeny plaques contained reassortants, of which 66% were diploid, and 34% were monoploid. The monoploid reassortants contained the S and L segments of SNV and ANDV M segment. Analysis of replication of the monoploid reassortant indicated its efficiency was similar to ANDV rather than SNV. Results described in this study illustrate the ability to rapidly generate new hantavirus genotypes between genetically unrelated viruses by gene reassortment and provide a tool to dissect the pathogenesis of these important viruses.

Animals↗
PubMed2005

Spleen necrosis virus-based vector delivery of anti-HIV-1 genes potently protects human hematopoietic cells from HIV-1 infection.

In this study, we report on the efficacy of using a spleen necrosis virus (SNV)-based vector delivery system to block human immunodeficiency virus type I (HIV-1) replication in human hematopoietic cells. These efforts were directed towards the development of human immune system cell resistance to HIV-1 infection, based on the strategy of "intracellular immunization" via generation of a series of anti-HIV-1 therapeutic constructs carrying scFvs, single-chain variable fragments, against HIV-1 integrase and reverse transcriptase in combination with the trans-dominant mutant of HIV-1 Rev, RevM10. The efficiency of the anti-HIV-1 constructs were tested in viral challenge assays with different doses of HIV-1 NL4-3, Bal, 89.6 and R7-GFP strains. These experiments demonstrated the reduction of HIV-1 replication by these retroviral vector constructs in a range of 4- to 10-fold in CD4+ T-lymphocytes, human peripheral blood mononuclear cells (PBMCs), and primary human macrophages. We observed selective efficiency of SNV-based therapeutics in H9, C8166 and Jurkat T-lymphocytic cell lines, demonstrating the most efficient inhibition of HIV-1 replication in Jurkat T-cells. Thus, these data are the first demonstration of the ability of SNV-based retroviral vectors with select transgenes, which may have certain molecular advantages over other retroviral vector systems, to combat HIV-1 replication in human hematopoietic cells and support the potential for using SNV-expressed constructs in anti-HIV-1 molecular therapeutics.

Gene Transfer Techniques↗
PubMed1998

Articulated thoughts of maritally violent and nonviolent men during anger arousal.

The cognitive correlates of anger arousal were investigated in community-based samples of maritally violent (MV), maritally distressed-nonviolent (DNV), and maritally satisfied-nonviolent (SNV) husbands. Participants performed the Articulated Thoughts in Simulated Situations (ATSS) paradigm while listening to anger-arousing audiotapes. Trained raters coded for irrational beliefs, cognitive biases, hostile attributional biases, and anger control statements. Results indicated that MV men articulated significantly more irrational thoughts and cognitive biases than DNV and SNV men. MV men articulated more hostile attributional biases than DNV and SNV men across all ATSS scenarios. SNV men, however, articulated more anger control statements during ATSS anger arousal than MV or DNV participants. Discriminant function analyses indicated that specific thoughts discriminated between the groups and differentiated mildly from severely violent participants. ATSS cognitive distortions (a) were not correlated with questionnaire measures of cognitive distortion, and (b) were superior to questionnaire measures in discriminating between the groups. The findings are interpreted in light of recent advances in understanding the relationship between information processing, anger, and marital aggression.

Adult↗
PubMed2002

A new technique for establishing dry weight in hemodialysis patients via whole body bioimpedance.

BACKGROUND: Quantitative techniques are necessary to achieve dry weight (DW) in patients with kidney failure. Bioimpedance spectroscopy (BIS) is a non-invasive method that determines the volume of body fluid compartments. The current work evaluates the use of BIS data in hemodialysis patients for the prediction of DW. METHODS: A new technique has been devised for the estimation of DW that involves the intersection of two slopes, slope normovolemia (SNV) and slope hypervolemia (SHV). These slopes characterize the variation in extracellular water (ECW) with body weight (BW) in the states of normovolemia and hypervolemia, respectively. SNV was established via measurements of ECW and BW in 30 healthy subjects. In a longitudinal study in new hemodialysis patients, successive reduction of post-dialysis weight (PDW) was attempted until clinical signs of normovolemia were presented. Measurements of ECW and BW that were acquired at the beginning of each treatment were used to determine SHV. RESULTS: SNV was found to be 0.239 L/kg and 0.214 L/kg for male and female healthy subjects, respectively. A significant DeltaPDW predicted by the new method (-4.98 kg) was highly correlated to the DeltaPDW achieved in the study (-5.85 kg, R = 0.839). Blood pressure was reduced (P < 0.001) and an 86% decrease in antihypertensive agents was achieved. CONCLUSION: The method of intersecting slopes (SHV with SNV) via BIS is a new method for the prediction DW. This approach will offer considerable improvement for the routine management of DW in the dialysis setting.

Adult↗
PubMed1998

beta3 Integrins mediate the cellular entry of hantaviruses that cause respiratory failure.

Newly emerged hantaviruses replicate primarily in the pulmonary endothelium, cause acute platelet loss, and result in hantavirus pulmonary syndrome (HPS). We now report that specific integrins expressed on platelets and endothelial cells permit the cellular entry of HPS-associated hantaviruses. Infection with HPS-associated hantaviruses, NY-1 and Sin Nombre virus (SNV), is inhibited by antibodies to beta3 integrins and by the beta3-integrin ligand, vitronectin. In contrast, infection with the nonpathogenic (no associated human disease) Prospect Hill virus was inhibited by fibronectin and beta1-specific antibodies but not by beta3-specific antibodies or vitronectin. Transfection with recombinant alphaIIb beta3 or alphav beta3 integrins rendered cells permissive to NY-1 and SNV but not Prospect Hill virus infection, indicating that alphaIIb beta3 and alphav beta3 integrins mediate the entry of NY-1 and SNV hantaviruses. Furthermore, entry is divalent cation independent, not blocked by arginine-glycine-aspartic acid peptides and still mediated by, ligand-binding defective, alphaIIb beta3-integrin mutants. Hence, NY-1 and SNV entry is independent of beta3 integrin binding to physiologic ligands. These findings implicate integrins as cellular receptors for hantaviruses and indicate that hantavirus pathogenicity correlates with integrin usage.

Animals↗
PubMed1995

Evaluation of the magnitude of the 1993 hantavirus outbreak in the southwestern United States.

In May 1993, an outbreak of hantavirus pulmonary syndrome (HPS) in the southwestern United States was caused by the previously unrecognized Sin Nombre virus (SNV). Most HPS patients had an influenza-like prodrome, followed by rapid onset of pulmonary edema (fatality rate, 52%). To define the magnitude of the outbreak, patients with milder illnesses who sought medical care in the outbreak area during the outbreak period were assessed for infection with SNV. Of 299 study subjects, 43 had illnesses similar to the HPS prodrome. One laboratory finding, thrombocytopenia, was highly discriminatory between non-HPS patients (1%) and confirmed HPS patients (71%; P < .001) during the prodrome phase. No study subject had serologic evidence (IgM antibodies) of recent SNV infection. Five had IgG titers consistent with a previous hantavirus infection: 3 of these 5 were among the 43 patients who had illnesses similar to the HPS prodrome (P < .05). These data provide evidence that mild illness is rarely caused by SNV.

Adolescent↗
PubMed2006

Envelope proteins of spleen necrosis virus form infectious human immunodeficiency virus type 1 pseudotype vector particles, but fail to incorporate upon substitution of the cytoplasmic domain with that of Gibbon ape leukemia virus.

The wild-type (wt) envelope (Env) proteins of spleen necrosis virus (SNV), together with the transmembrane (TM) protein fused to antibody domains (scFv), have been used for the generation of stable packaging cell lines releasing pseudotyped cell targeting vectors derived from SNV and Murine leukemia virus (MLV). As a first step towards assessing whether HIV-1(SNV/TM-scFv) packaging cells could be established for the production of lentiviral cell targeting vectors, it is reported here that infectious HIV-1-derived particles pseudotyped with wt SNV Env proteins could be generated. Using novel chimeric SNV-derived Env proteins encompassing wt and engineered cytoplasmic domains (C-tail) of the Gibbon ape leukemia virus (GaLV) TM protein, it was further shown that the wt C-tail not only excludes the GaLV TM protein from incorporation into HIV-1 particles, but confers this phenotype to other retroviral envelopes upon C-terminal fusion.

Animals↗