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 109 records · Page 6Linked to original sources
PubMed1992

Multiple sequence elements are involved in RNA 3' end formation in spleen necrosis virus.

The function of the poly(A) signal in spleen necrosis virus (SNV) is dependent upon the distance between the cap site and the poly(A) site, while the function of the SV40 late poly(A) signal is independent of the distance. Deletions in the SNV poly(A) sequence do not alter the distance-dependent function. SNV/SV40 chimeric poly(A) signals show intermediate behavior between the SNV and SV40 poly(A) signals. These results indicate that multiple sequence elements are involved in the functions of either the SNV or SV40 poly(A) signals. This intermediate behavior is also observed with poly(A) signals from the mouse alpha-globin and herpes simplex virus thymidine kinase genes.

Base Sequence↗
PubMed1985

Surgical aspects of systemic necrotizing vasculitis.

Thirty patients with systemic necrotizing vasculitis (SNV) of the polyarteritis nodosa type were reviewed. Eleven patients (36%) had only gastrointestinal manifestations of the disease. Four patients (13%) had only pulmonary involvement. Seven patients (23%) had both gastrointestinal and pulmonary manifestations of SNV. With use of an approved protocol from the National Institute of Allergy and Infectious Diseases of cyclophosphamide and prednisone, remission was attained in 29 of 30 patients (96%). However, 18 patients (60%) underwent major surgical procedures for either diagnosis or complications of the disease. Six patients underwent eight thoracotomies; six operations were required for diagnosis and two for drainage of right-sided empyemas. Ten patients underwent 14 exploratory laparotomies. Six abdominal explorations were performed for diagnostic purposes, and eight were required for treatment of complications. Two patients required digital amputations because of ischemic necrosis. Two patients (11%) developed five postoperative complications, one of whom subsequently died. Arteriographic studies were performed in 16 patients (53%). Vascular abnormalities consistent with those described for SNV were demonstrated in six cases (38%). There was no correlation of clinical manifestations, subsequent therapy, and arteriographic findings with regard to the development of intra-abdominal complications. Pulmonary complications occurred only in patients who had pulmonary infiltrates secondary to SNV.

Abdomen↗
PubMed1997

Protection against developmental retardation in apolipoprotein E-deficient mice by a fatty neuropeptide: implications for early treatment of Alzheimer's disease.

Stearyl-Nle17-VIP (SNV) is a novel agonist of vasoactive intestinal peptide (VIP) exhibiting a 100-fold greater potency than the parent molecule and specificity for a receptor associated with neuronal survival. Here, mice deficient in apolipoprotein E (ApoE), a molecule associated with the etiology of Alzheimer's disease, served as a model to investigate the developmental and protective effects of SNV. In comparison to control animals, the deficient mice exhibited (a) reduced amounts of VIP messenger RNA; (b) decreased cholinergic activity (c) significant retardation in the acquisition of developmental milestones: forelimb placing behavior and cliff avoidance behavior; and (d) learning and memory impairments. Daily injections of SNV to ApoE-deficient newborn pups resulted in increased cholinergic activity and marked improvements in the time of acquisition of behavioral milestones, with peptide-treated animals developing as fast as control animals and exhibiting improved cognitive functions after cessation of peptide treatment. Specificity was demonstrated in that treatment with a related peptide (PACAP), pituitary adenylate cyclase-activating peptide, produced only limited amelioration. As certain genotypes of ApoE increase the probability of Alzheimer's disease, early counseling and preventive treatments may now offer an important route for therapeutics design.

Alzheimer Disease↗
PubMed1999

Validity of a vasculitis activity index for systemic necrotizing vasculitis.

OBJECTIVE: To establish the validity of an index designed to measure activity in systemic necrotizing vasculitis (SNV). METHODS: The Vasculitis Activity Index (VAI) was designed to incorporate appropriately weighted clinical measurements that reflect disease activity in SNV. We performed a pilot study to guide the modification and subsequent testing of the initial design. The data necessary to calculate the VAI are direct ratings by a clinical observer of the degree of activity in 9 organ systems and 3 indirect measures of vasculitis activity. These data are recorded on 0-4 visual analog scales. Physician's global assessment (PGA) is used as the "gold standard" measurement of disease activity. The VAI was validated using 2 independent data sets: the questionnaire data set, derived from test case histories ("paper cases") sent to 100 practicing rheumatologists, and the clinic data set, obtained from use of the VAI in 204 regular care visits of 74 patients with SNV. RESULTS: The VAI correlated highly with the PGA: Pearson's correlation coefficient R = 0.84 (95% confidence interval [95% CI] 0.80-0.88) for the questionnaire data set, and R = 0.92 (95% CI 0.90-0.94) for the clinic data set. The mean of the interobserver coefficients of variation for the test case histories was lower for the VAI than for the PGA (mean difference 0.45; P = 0.002), indicating that the VAI has less interobserver variation than does the PGA. The change in VAI between clinic visits for individual patients correlated highly with the change in PGA (R = 0.88, 95% CI = 0.83-0.91). The VAI data collection form requires about 1 minute to complete, including computation of the score. CONCLUSION: The VAI is a valid measure of vasculitis activity that correlates highly with the PGA. In addition, the VAI has less interobserver variation than the PGA and has a high level of sensitivity to change over time. Additional testing of the VAI appears warranted.

Health Surveys↗
PubMed2001

Small-vessel vasculitis surrounding a spared temporal artery: clinical and pathological findings in a series of twenty-eight patients.

OBJECTIVE: Occasionally, a temporal artery biopsy reveals small-vessel vasculitis (SVV) surrounding a spared temporal artery, the significance of which is unclear. We analyzed the final diagnosis in a series of patients with this condition and tried to identify histopathologic features with potential usefulness in predicting the ultimate diagnosis. METHODS: We performed a clinical and histopathologic review of 28 patients in whom SVV surrounding a spared temporal artery was the first histologic finding that led to the diagnosis of vasculitis. For comparison purposes, we analyzed the pattern of small vessel involvement in 30 patients with biopsy-proven giant cell arteritis (GCA). RESULTS: GCA was considered the most likely diagnosis in 12 patients, based on the absence of clinical evidence of additional organ involvement and normal findings on muscle biopsy and electrophysiologic study. Three patients had systemic necrotizing vasculitis (SNV), based on the demonstration of typical lesions on subsequent muscle, nerve, or kidney biopsy. After extensive evaluation, 4 patients remained unclassifiable. Nine patients were incompletely studied. Fibrinoid necrosis was significantly more frequent in patients with SNV (P = 0.0022), whereas involvement of vasa vasorum was more frequent in patients classified as having GCA (P = 0.022). No differences in the pattern of small vessel involvement were found in patients with SVV surrounding a spared temporal artery who were classified as having GCA compared with patients with biopsy-proven GCA. Granulocytes were observed at similar frequency in all conditions. CONCLUSION: SVV may be the only abnormal feature in a temporal artery biopsy and the only histologic evidence of vasculitis. The diagnosis of GCA can be reasonably established in most of these patients when there is no apparent evidence of additional organ involvement. However, when fibrinoid necrosis is observed or the temporal artery vasa vasorum are not involved, SNV must be extensively excluded.

Adult↗
PubMed1997

Hantavirus pulmonary syndrome: CD8+ and CD4+ cytotoxic T lymphocytes to epitopes on Sin Nombre virus nucleocapsid protein isolated during acute illness.

In 1993 a number of cases of unexplained adult respiratory syndrome occurred in the southwestern United States. The illness was characterized by a prodrome of fever, myalgia, and other symptoms followed by the rapid onset of a capillary leak syndrome with hemoconcentration, thrombocytopenia, and pulmonary edema. Viral RNA sequences in the lungs identified a new member of the hantavirus genus, Sin Nombre virus (SNV), unique to North America. Pulmonary endothelial cells were heavily infected but were not necrotic. We speculated that this capillary leak syndrome was initiated by immune responses to the SNV-infected pulmonary endothelial cells. We isolated a CD8+ cytotoxic T lymphocyte (CTL) clone directly from the blood of a patient with the acute hantavirus pulmonary syndrome (HPS) which recognizes a SNV specific epitope on the virus nucleocapsid protein (aa 234-242) that is restricted by HLA C7 and produces IFN gamma but not IL-4. We identified a second CD8+ CTL epitope located within another site aa 131-139 on the nucleocapsid protein, which is HLA B35 restricted, and a CD4+ CTL epitope located on a third site on nucleocapsid protein aa 372-380 using lymphocytes obtained during HPS from another patient that were stimulated in vitro. Hantavirus specific CD8+ and CD4+ CTL may contribute to the immunopathology and capillary leak syndrome observed in the HPS.

Acute Disease↗
PubMed1998

Retroviral recombination is nonrandom and sequence dependent.

Sequence variation plays a significant role in the pathogenesis and persistence of retroviral infections and is a major obstacle in the development of vaccines as well as therapies against lethal diseases caused by retroviruses. Recombination is one means by which sequence variation is generated. However, the basic molecular mechanisms of recombination are not adequately understood. In the present study, a spleen necrosis virus (SNV) recombination system was used to ask whether a known hot spot for mutation was also a hot spot for retroviral recombination. The system consisted of a pair of SNV vectors expressing two drug-resistance genes, constructed so that recombinants could be selected by a double resistant phenotype. Restriction enzyme site differences engineered into the vectors were used to map the location of recombination sites within relatively small intervals (55 to 420 bp). The vectors were modified to create two pairs that differed only by the presence of runs of identical nucleotides. The runs of identical nucleotides had been shown previously to be hot spots for frameshift mutations during SNV reverse transcription. Each vector pair was introduced into DSDh helper cells by infection. Viruses were harvested from doubly infected DSDh helper cells and used to infect D-17 target cells. Proviral sequences from 228 cell clones were analyzed by polymerase chain reaction and restriction enzyme digestion. Significant differences in the patterns of recombination were found between the two pairs of vectors. In particular, the frequency of recombination was higher than expected in the interval immediately following the runs. For both pairs of vectors, the overall pattern of recombination was nonrandom and one region was refractory toward recombination.

Animals↗
PubMed1991

Effect of polyions on the early events of Sindbis virus infection of Vero cells.

To clarify the role of electrostatic interactions in the binding of Sindbis virus (SNV) to cell membrane receptors, we investigated the effect of different polyions on the initial steps of infection of Vero cells by the virus. Several polyanions (mucin, heparin, polygalacturonic acid) and polycations (polylysine, protamine, polybrene) were able to reduce the replication of SNV when present in the viral adsorption period, whereas others (chondroitin sulfate, polymyxin B sulfate, histone) were devoid of any activity. Therefore the electric charge alone is not sufficient to explain the action of compounds. The effects of polyions on receptor binding, on bound virus, and on internalized virus have been examined. All the drugs inhibited SNV infection by affecting its binding to the cellular receptor. The results indicated that heparin and mucin act directly on the virus particle while polycations bind to the cell membrane receptor for the virus, protamine being effective on both targets. Since among polyanions glycosaminoglycans showed a strong inhibiting activity, the involvement of these molecules in the virus surface receptor was assessed by enzyme digestion of cell membrane with heparinase and chondroitin ABC lyase.

Animals↗
PubMed1995

Ultrastructural characteristics of Sin Nombre virus, causative agent of hantavirus pulmonary syndrome.

A previously unrecognized disease, hantavirus pulmonary syndrome, was described following an outbreak of severe, often lethal, pulmonary illness in the southwestern United States in May-June, 1993. We have now studied the morphologic features of the causative agent, Sin Nomber virus (SNV), by thin section electron microscopy and immunoelectron microscopy of infected Vero E6 cells. SNV virions were roughly spherical and had a mean diameter of 112 nm. They had a rather dense envelope and closely apposed fine surface projections, 7 nm in length. Filamentous nucleocapsids were present within virions. Viral inclusion bodies were present in the cytoplasm of infected cells; these appeared granular or filamentous, depending on the plane of section. All of these characteristics were similar to published descriptions of other hantaviruses; however, unlike all other hantaviruses and virtually all other member viruses of the family Bunyaviridae which bud upon smooth intracytoplasmic membranes, SNV budding occurred almost entirely upon the plasma membrane of infected cells. Virus budding was associated with the formation of long 28 nm diameter tubular projections. Occasional elongated 47 nm diameter virus-like particles were seen to bud upon intracytoplasmic membranes. As shown by immunoelectron microscopy, viral antigens were localized over virions, inclusions, and tubular projections associated with virion morphogenesis.

Animals↗
PubMed2004

Systemic necrotizing vasculitides in Turkey: a comparative analysis of 40 consecutive patients.

OBJECTIVE: The aim of this study was to analyze and compare the demographic and clinical features and prognosis of patients with different systemic necrotizing vasculitides (SNV) in Turkey. PATIENTS AND METHODS: Twenty-three patients with Wegener's granulomatosis (WG), 15 with polyarteritis nodosa (PAN), and two with Churg-Strauss syndrome were included in the study. The clinical and laboratory features of patients with WG and PAN were compared, and survival analysis was performed for the WG patients. RESULTS: Twenty-one patients with WG had systemic disease involving kidneys, and two had localized disease. Fifteen patients were placed in the PAN group, 12 of whom were classified as having classic PAN and three with microscopic polyangiitis. Median follow-up time was 37 months (range 1-81) for WG patients and 41 months (range 5-132) for the PAN group. Upper respiratory tract, pulmonary, and renal involvement were significantly more frequent in the WG group than in PAN. Peripheral nervous system involvement was more frequent in the PAN group. In WG, survival was calculated as 59% at 35 months. High initial vasculitis damage index scores were found to be predictive for mortality. CONCLUSION: This study revealed that the most frequent type of SNV was WG in a tertiary rheumatology setting in Turkey. There was initial organ damage in most of the patients, frequently caused by severe renal involvement. In contrast to other published series, overt cardiovascular and gastrointestinal involvement were not observed in our patients with SNV.

Anti-Inflammatory Agents↗
PubMed2004

Cyclophosphamide treatment in systemic necrotizing vasculitis and lupus nephritis. How long? How much?

The gold standard for inducing remission in systemic necrotizing vasculitis (SNV) and severe lupus nephritis is (and remains) the combination of cyclophosphamide and glucocorticoids. Long-term treatment with cyclophosphamide is limited because of toxicity. Recent prospective studies in antineutrophil cytoplasmic antibody (ANCA)-associated SNV revealed that after achievement of clinical remission (usually within 3-4 months after starting cyclophosphamide) cyclophosphamide can be replaced by azathioprine with no increase in relapse rates if treatment is continued for at least 1 year. Methotrexate is inferior to cyclophosphamide because of increased relapse rates-particularly in those with renal involvement-during follow-up. An ongoing study comparing mycophenolate mofetil (MMF) with azathioprine will clarify whether MMF is as successful as azathioprine or even better. The concomitant use of tumor necrosis factor (TNF)-alpha blockers increases the efficacy of immunosuppression. TNF-alpha blockers may be added if SNV is refractory to standard immunosuppressive therapy. However, with this addition to therapy, systemic infections are more frequent. In patients with severe lupus nephritis (WHO IV) the efficacy of combined i.v. therapy with cyclophosphamide and glucocorticoids was shown by NIH trials. This NIH regimen competes with the EURO-Lupus nephritis schedule with a lower dose of i.v. cyclophosphamide followed by maintenance therapy with azathioprine. Long-term follow-up is, however, still lacking in the EURO-Lupus trial. Ongoing prospective studies will reveal whether cyclophosphamide may be substituted by MMF from the very beginning or whether MMF is superior to azathioprine during maintenance therapy of lupus nephritis.

Antibodies, Antineutrophil Cytoplasmic↗
PubMed1987

The spleen necrosis virus int gene product expressed in Escherichia coli has DNA binding activity and mediates att and U5-specific DNA multimer formation in vitro.

To facilitate the in vitro study of the spleen necrosis virus (SNV) int gene product, we expressed the viral int locus in an Escherichia coli expression vector. Antiserum made against the protein produced in bacteria precipitated a 44-kDa polypeptide from virus-infected chicken embryo fibroblasts. This result is consistent with the expected size of the SNV int polypeptide. In a protein blotting assay, the expressed protein binds strongly to DNA and was able to complex nonspecifically with both single- and double-stranded DNAs containing or lacking viral sequences. However, under solution conditions favoring transient DNA unwinding, DNA binding was confined to supercoiled molecules containing either the SNV att sequence (the viral cis-acting region required for integration) or the U5 region of the long terminal repeat alone. Under these conditions of specific binding, multimeric DNA species were formed by apparent intermolecular interaction between protein-DNA complexes. These data indicate that retroviral integration may require local DNA unwinding at the att site for complex formation between the int gene product and DNA. This complex may be an intermediate in the viral DNA insertion process.

Amino Acid Sequence↗
PubMed1989

Expression of avian reticuloendotheliosis virus envelope confers host resistance.

We constructed two reticuloendotheliosis virus (REV) envelope gene expression plasmids, one containing the REV-A envelope gene, the other the spleen necrosis virus (SNV) envelope gene. Cell lines were generated by transfecting each of the REV envelope plasmids into D17 cells, a canine cell line. The levels of REV envelope glycoprotein in the cell lines were assayed by immunoprecipitating the envelope glycoproteins from lysates of cells that were labeled with [35S]methionine. Virological challenge assays determined the degree of resistance of each of the cell lines to REV-A or SNV infection. The expression of either envelope gene protected the cells from infection by either REV-A or SNV virus. Several cell lines were significantly more resistant to REV infection than the parental D17 cells, and two lines were 25,000-fold more resistant, approaching the resistance of REV-infected D17 cells to reinfection. The resistant cell lines were not able to confer resistance to susceptible cells by cocultivation. The level of resistance was correlated with the uniformity of expression of the REV envelope glycoproteins by the individual cells in a cell line and not with the absolute level of expression by the population of cells.

Animals↗
PubMed1990

N-linked glycosylation and reticuloendotheliosis retrovirus envelope glycoprotein function.

Different properties of the spleen necrosis virus (SNV) envelope glycoprotein were analyzed following biosynthesis in the presence of glycosylation inhibitors. Tunicamycin, which inhibits all asparagine N-linked glycosylation, prevented intracellular processing and translocation to the cell surface of the envelope protein. In contrast, castanospermine or deoxymannojirimycin, which block glycosidase trimming of the early high-mannose chains and subsequent complex type N-glycosylation, did not inhibit proteolytic cleavage or cellular translocation. The ability of unglycosylated and partially glycosylated envelope protein to bind the viral receptor was assayed using an infection interference assay. Tunicamycin abrogated SNV envelope glycoprotein-induced receptor interference, whereas the trimming glycosidase inhibitors had no effect on interference. Similarly, tunicamycin but not the glycosidase inhibitors reduced the titers of released virus 100-fold. We conclude that carbohydrate trimming and complex N-glycosylation are not essential for envelope glycoprotein translocation, proteolytic cleavage, receptor binding, or infectivity, whereas cotranslational high-mannose N-glycosylation is essential for all of the SNV envelope glycoprotein properties tested. Syncytia formation can be induced following transfection into D17 cells of an envelope glycoprotein expression plasmid. Unlike virus particle infectivity, cell fusion is strongly inhibited by the glycosidase inhibitors.

Animals↗
PubMed1986

Secretion of enzymatically active human renin from mammalian cells using an avian retroviral vector.

Recombinant plasmid-based retroviral expression vectors were constructed using a modified spleen necrosis virus (SNV) containing the Herpes simplex virus thymidine kinase gene promoter controlling the expression of the Tn5 neomycin phosphotransferase II gene (NPTII gene). The human renin (HRn) gene (hrn) was inserted into the 5' end of the SNV sequences such that in concatemeric plasmid DNA its expression was controlled by the strong promoter in the SNV long terminal repeat (LTR). Dog cells transfected with the concatemeric plasmid DNA secreted a small amount of a HRn-like 43-kDa protein. After cotransfection of chicken cells with concatemeric plasmid DNA and proviral DNA of reticuloendotheliosis virus strain A, infectious stocks of viruses were recovered. Cells infected with the virus carrying the viral LTR-hrn gene oriented for expression secreted the 43-kDa HRn-like protein at about 100-fold higher levels than the cells transfected with the plasmid DNAs. Biological activity of secreted HRn was determined by measuring levels of angiotensin I generated by incubating culture media with either a porcine or human angiotensinogen substrate. Infected dog cells produce about 40 ng of enzymatically active HRn per 10(6) cells per 24 h. These data indicate that retroviral expression vectors provide a good system for obtaining the secretion of high levels of enzymatically active heterologous proteins from mammalian cells.

Animals↗
PubMed2025

TSC angiofibroma and ungual fibroma have different mutation signatures, with recurrent mutations in KMT2C.

PURPOSE: Tuberous sclerosis complex (TSC) is an autosomal dominant tumor suppressor syndrome characterized by tumors affecting multiple tissues, including skin, due to inactivating TSC1/TSC2 variants. Genome-wide profiling of somatic mutations in a unique collection of angiofibroma (FAF) and ungual fibroma (UF) TSC skin tumors was performed. METHODS: Genome sequencing was performed on 9 samples, comprising 4 FAF and 5 UF, along with 6 matched normal samples from 6 individuals with TSC. RESULTS: TSC-FAF and TSC-UF skin tumors have different mutation signatures, with a predominance of UV-related single-nucleotide variant (SNV; SBS7a and SBS7b) and dinucleotide variant (DNV; DBS1) signatures in FAF, and aging-related SNV (SBS1 and SBS5) signatures in UF. We also identified a novel DNV signature for TSC-UF, with frequent TG>CA and TT>GG substitutions. Furthermore, 3 inactivating somatic mutations in KMT2C were observed in 2 of 4 TSC-FAF and 5 mutations in other cancer genes. CONCLUSION: The distinct SNV mutation signatures seen in TSC-FAF and UF indicate that they develop through distinct pathogenic mechanisms, UV-induced mutagenesis in FAF, and aging-related mutagenesis in UF. The mechanism of the novel DNV signature in UFs merits further investigation. Our observation on the occurrence of KMT2C mutations suggests that KMT2C inactivation contributes to the pathogenesis of TSC-FAF.

Humans↗
PubMed2006

Quantitative analysis of paracetamol polymorphs in powder mixtures by FT-Raman spectroscopy and PLS regression.

A fast and simple method for the quantitative analysis of monoclinic (form I) and orthorhombic (form II) paracetamol was developed, based on FT-Raman spectroscopy and PLS regression. Three different preprocessing algorithms, namely orthogonal signal correction (OSC), standard normal variate transformation (SNV) and multiplicative scatter correction (MSC), were applied in order to eliminate effects caused by sample preparation and sample inhomogeneities. Subsequently, PLS regression models were fitted and their predictive performance was evaluated on the basis of the root mean squared error of cross-validation (RMSECV) over the complete data set. Furthermore, the data were split into two equal-sized training and test subsets by the Kennard-Stone design and the errors of calibration (RMSEC) and prediction (RMSEP) were calculated. It was found that the OSC preprocessing contributes to a significant increase in the predictive performance of the PLS regression model (RMSECV=0.500%, RMSEC=0.842% and RMSEP=0.538%) in the overall concentration range of form I, compared to the SNV (RMSECV=2.398%, RMSEC=0.911% and RMSEP=7.177%) and MSC (RMSECV=2.7648%, RMSEC=1.572% and RMSEP=4.838%). In addition, the model developed on OSC preprocessed data is more parsimonious, requiring a single latent variable, compared to three latent variables required by the models fitted to the SNV and MSC preprocessed data. The proposed multivariate calibration presents a significant improvement over existing methods for the quantitation of paracetamol polymorphs.

Acetaminophen↗
PubMed2004

Andes virus M genome segment is not sufficient to confer the virulence associated with Andes virus in Syrian hamsters.

Sin Nombre virus (SNV) and Andes virus (ANDV), members of the genus Hantavirus, in the family Bunyaviridae, are causative agents of hantavirus pulmonary syndrome (HPS) in North and South America, respectively. Although ANDV causes a lethal HPS-like disease in hamsters, SNV, and all other HPS-associated hantaviruses that have been tested, cause asymptomatic infections of laboratory animals, including hamsters. In an effort to understand the pathogenicity of ANDV in the hamster model, we generated ANDV/SNV reassortant viruses. Plaque isolation of viruses from cell cultures infected with both parental viruses yielded only one type of stable reassortant virus: large (L) and small (S) segments of SNV and M segment of ANDV. This virus, designated SAS reassortant virus, had in vitro growth and plaque morphology characteristics similar to those of ANDV. When injected into hamsters, the SAS reassortant virus was highly infectious and elicited high-titer, ANDV-specific neutralizing antibodies; however, the virus did not cause HPS and was not lethal. These data indicate that the ANDV M genome segment is not sufficient to confer the lethal HPS phenotype associated with ANDV.

Animals↗