Results 21 to 30 of about 22,694 (182)
Human exposure to particulate matter potentially contaminated with sin nombre virus. [PDF]
Ecohealth, 2013 The most common mechanism for human exposure to hantaviruses throughout North America is inhalation of virally contaminated particulates. However, risk factors associated with exposure to particulates potentially contaminated with hantaviruses are generally not well understood. In North America, Sin Nombre virus (SNV) is the most common hantavirus that
Richardson KS +4 more
europepmc +6 more sources
Regulatory T cell-like responses in deer mice persistently infected with Sin Nombre virus [PDF]
Proceedings of the National Academy of Sciences, 2007 Hantavirus cardiopulmonary syndrome is a zoonotic illness associated with a systemic inflammatory immune response, capillary leak, noncardiogenic pulmonary edema, and shock in humans. Cytokines, including TNF, IFN-γ, and lymphotoxin, are thought to contribute to its pathogenesis. In contrast, infected rodent reservoirs of hantaviruses experience few or
T. Schountz +6 more
semanticscholar +5 more sources
Temporal and Spatial Analysis of Sin Nombre Virus Quasispecies in Naturally Infected Rodents [PDF]
Journal of Virology, 1999 ABSTRACT Sin Nombre virus (SNV) is thought to establish a persistent infection in its natural reservoir, the deer mouse ( Peromyscus maniculatus ), despite a strong host immune response. SNV-specific neutralizing antibodies were routinely detected in deer mice which maintained virus RNA in the blood and ...
R. Feuer +4 more
semanticscholar +4 more sources
Complete genetic characterization and analysis of isolation of Sin Nombre virus [PDF]
Journal of Virology, 1995 This study reports completion of the genetic characterization of the entire genome of Sin Nombre (SN) virus (NMH10) detected in autopsy tissues from a patient who died of hantavirus pulmonary syndrome (HPS). The large (L) genome segment was found to be 6,562 nucleotides in length and encoded a putative L polymerase that was 2,153 amino acids in length.
Vladimir E. Chizhikov +5 more
semanticscholar +4 more sources
Peptide Antagonists That Inhibit Sin Nombre Virus and Hantaan Virus Entry through the β3-Integrin Receptor [PDF]
Journal of Virology, 2005 ABSTRACT Specific therapy is not available for the treatment of hantavirus cardiopulmonary syndrome caused by Sin Nombre virus (SNV). The entry of pathogenic hantaviruses into susceptible human cells is dependent upon expression of the α v β 3 integrin, and transfection of human β
R. Larson +3 more
semanticscholar +4 more sources
The coiled-coil domain structure of the Sin Nombre virus nucleocapsid protein. [PDF]
J Mol Biol, 2007 Hantaviruses can cause hemorrhagic fever with a renal syndrome and hantavirus pulmonary syndrome when transmitted to humans. The nucleocapsid protein of hantaviruses encapsidates viral genomic RNA and associates with transcription and replication complexes.
Boudko SP, Kuhn RJ, Rossmann MG.
europepmc +5 more sources
Emerging Infectious Diseases, 2004 Patients who later have a mild course of hantavirus cardiopulmonary syndrome (HCPS) are more likely to exhibit a high titer of neutralizing antibodies against Sin Nombre virus (SNV), the etiologic agent of HCPS, at the time of hospital admission. Because
Chunyan Ye +4 more
doaj +4 more sources
Seroprevalence against Sin Nombre virus in resident and dispersing deer mice. [PDF]
Vector Borne Zoonotic Dis, 2008 Through dispersal, deer mice (Peromyscus maniculatus) enter peridomestic settings (e.g., outbuildings, barns, cabins) and expose humans and other deer mouse populations to Sin Nombre virus (SNV). In June 2004, research on deer mouse dispersal was initiated at 2 locations in Montana.
Lonner BN +3 more
europepmc +5 more sources
Kinetics of immune responses in deer mice experimentally infected with Sin Nombre virus. [PDF]
J Virol, 2012 ABSTRACTDeer mice are the principal reservoir hosts of Sin Nombre virus, the etiologic agent of most hantavirus cardiopulmonary syndrome cases in North America. Infection of deer mice results in persistence without conspicuous pathology, and most, if not all, infected mice remain infected for life, with periods of viral shedding.
Schountz T +9 more
europepmc +6 more sources
Effects of Tumor Necrosis Factor Alpha on Sin Nombre Virus Infection In Vitro [PDF]
Journal of Virology, 2000 ABSTRACTPrevious data indicate that immune mechanisms may be involved in developing capillary leakage during Sin Nombre virus (SNV) infection. Therefore, we investigated production of tumor necrosis factor alpha (TNF-α) by human alveolar macrophages and human umbilical vein endothelial cells (HUVEC) after infection with SNV.
S. Khaiboullina +3 more
semanticscholar +5 more sources