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Pierre E. Rollin - One of the best experts on this subject based on the ideXlab platform.
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Hantavirus Pulmonary Syndrome clinical findings evaluating a surveillance case definition
Vector-borne and Zoonotic Diseases, 2012Co-Authors: Barbara Knust, Adam Macneil, Pierre E. RollinAbstract:Abstract Clinical cases of Hantavirus Pulmonary Syndrome (HPS) can be challenging to differentiate from other acute respiratory diseases, which can lead to delays in diagnosis, treatment, and disease reporting. Rapid onset of severe disease occurs, at times before diagnostic test results are available. This study's objective was to examine the clinical characteristics of patients that would indicate HPS to aid in detection and reporting. Test results of blood samples from U.S. patients suspected of having HPS submitted to the Centers for Disease Control and Prevention from 1998–2010 were reviewed. Patient information collected by case report forms was compared between HPS-confirmed and test-negative patients. Diagnostic sensitivity, specificity, predictive values, and likelihood ratios were calculated for individual clinical findings and combinations of variables. Of 567 patients included, 36% were HPS-confirmed. Thrombocytopenia, chest x-rays with suggestive signs, and receiving supplemental oxygenation ...
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Hantavirus Pulmonary Syndrome united states 1993 2009
Emerging Infectious Diseases, 2011Co-Authors: Adam Macneil, Thomas G. Ksiazek, Pierre E. RollinAbstract:Hantavirus Pulmonary Syndrome (HPS) is a severe respiratory illness identified in 1993. Since its identification, the Centers for Disease Control and Prevention has obtained standardized information about and maintained a registry of all laboratory-confirmed HPS cases in the United States. During 1993-2009, a total of 510 HPS cases were identified. Case counts have varied from 11 to 48 per year (case-fatality rate 35%). However, there were no trends suggesting increasing or decreasing case counts or fatality rates. Although cases were reported in 30 states, most cases occurred in the western half of the country; annual case counts varied most in the southwestern United States. Increased hematocrits, leukocyte counts, and creatinine levels were more common in HPS case-patients who died. HPS is a severe disease with a high case-fatality rate, and cases continue to occur. The greatest potential for high annual HPS incidence exists in the southwestern United States.
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two cases of Hantavirus Pulmonary Syndrome in randolph county west virginia a coincidence of time and place
American Journal of Tropical Medicine and Hygiene, 2007Co-Authors: Julie R Sinclair, Thomas G. Ksiazek, James N. Mills, Pierre E. Rollin, Joel M Montgomery, Darin S Carroll, Boris I Pavlin, Katherine Mccombs, James A Comer, Stuart T NicholAbstract:Hantavirus Pulmonary Syndrome (HPS) is caused by an infection with viruses of the genus Hantavirus in the western hemisphere. Rodent hosts of Hantaviruses are present throughout the United States. In July 2004, two HPS case-patients were identified in Randolph County, WV: a wildlife science graduate student working locally and a Randolph County resident. We interviewed family members and colleagues, reviewed medical records, and conducted environmental studies at likely exposure sites. Small mammals were trapped, and blood, urine, and tissue samples were submitted to the Centers for Disease Control and Prevention for laboratory analyses. These analyses confirmed that both patients were infected with Monongahela virus, a Sin Nombre Hantavirus variant hosted by the Cloudland deer mouse, Peromyscus maniculatus nubiterrae. Other than one retrospectively diagnosed case in 1981, these are the first HPS cases reported in West Virginia. These cases emphasize the need to educate the public throughout the United States regarding risks and prevention measures for Hantavirus infection.
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discriminators between Hantavirus infected and uninfected persons enrolled in a trial of intravenous ribavirin for presumptive Hantavirus Pulmonary Syndrome
Clinical Infectious Diseases, 2002Co-Authors: Louisa E Chapman, Thomas G. Ksiazek, Barbara A. Ellis, Pierre E. Rollin, Gregory J Mertz, Frederick Koster, Mark J Sotir, K F Baum, Andrew T PaviaAbstract:To provide a potentially therapeutic intervention and to collect clinical and laboratory data during an outbreak of Hantavirus Pulmonary Syndrome (HPS), 140 patients from the United States with suspected HPS were enrolled for investigational intravenous ribavirin treatment. HPS was subsequently laboratory confirmed in 30 persons and not confirmed in 105 persons with adequate specimens. Patients with HPS were significantly more likely than were Hantavirus-negative patients to report myalgias from onset of symptoms through hospitalization, nausea at outpatient presentation, and diarrhea and nausea at the time of hospitalization; they were significantly less likely to report respiratory symptoms early in the illness. The groups did not differ with regard to time from the onset of illness to the point at which they sought care; time from onset, hospitalization, or enrollment to death was significantly shorter for patients with HPS. At the time of hospitalization, patients with HPS more commonly had myelocytes, metamyelocytes, or promyelocytes on a peripheral blood smear, and significantly more of them had thrombocytopenia, hemoconcentration, and hypocapnia. Patterns of clinical symptoms, the pace of clinical evolution, and specific clinical laboratory parameters discriminated between these 2 groups.
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intravenous ribavirin for Hantavirus Pulmonary Syndrome safety and tolerance during 1 year of open label experience
Antiviral Therapy, 1999Co-Authors: Louisa E Chapman, Ali S. Khan, Thomas G. Ksiazek, Pierre E. Rollin, Gregory J Mertz, Frederick Koster, C J Peters, Heidi M Jolson, Kenneth F Baum, Andrew T PaviaAbstract:Intravenous ribavirin was provided non-selectively for investigational open-label use among persons with suspected Hantavirus Pulmonary Syndrome (HPS) in the United States between 4 June 1993 and 1 September 1994. Therapy was initiated prior to laboratory confirmation of Hantavirus infection because most deaths from HPS occur within 48 h of hospitalization. Thirty patients with confirmed HPS, 105 patients without HPS and 5 patients without adequate diagnostic testing for HPS were enrolled. This observational study arguably provides the most complete information available on ribavirin-associated adverse effects. Although ribavirin was generally well tolerated, 71% of recipients became anaemic and 19% underwent transfusion. An apparent excess of hyperamylasaemia/pancreatitis was either therapy-associated or due to enrollment bias. The 30 enrolled HPS patients had a case-fatality rate of 47% (14/30). It is not possible to assess efficacy with this study design. However, comparison of survival curves for the 30 enrolled HPS patients and 34 patients who developed HPS during the same time period but were not enrolled did not suggest an appreciable drug effect. A randomized, placebo-controlled trial that enrolls patients during the prodrome phase would be necessary to assess the efficacy and further define the safety of intravenous ribavirin for HPS.
Thomas G. Ksiazek - One of the best experts on this subject based on the ideXlab platform.
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Hantavirus Pulmonary Syndrome united states 1993 2009
Emerging Infectious Diseases, 2011Co-Authors: Adam Macneil, Thomas G. Ksiazek, Pierre E. RollinAbstract:Hantavirus Pulmonary Syndrome (HPS) is a severe respiratory illness identified in 1993. Since its identification, the Centers for Disease Control and Prevention has obtained standardized information about and maintained a registry of all laboratory-confirmed HPS cases in the United States. During 1993-2009, a total of 510 HPS cases were identified. Case counts have varied from 11 to 48 per year (case-fatality rate 35%). However, there were no trends suggesting increasing or decreasing case counts or fatality rates. Although cases were reported in 30 states, most cases occurred in the western half of the country; annual case counts varied most in the southwestern United States. Increased hematocrits, leukocyte counts, and creatinine levels were more common in HPS case-patients who died. HPS is a severe disease with a high case-fatality rate, and cases continue to occur. The greatest potential for high annual HPS incidence exists in the southwestern United States.
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Hantavirus Pulmonary Syndrome the sound of a mouse roaring
The Journal of Infectious Diseases, 2007Co-Authors: Joel M Montgomery, Thomas G. Ksiazek, Ali S. KhanAbstract:In the spring of 1993, a mouse roared. It was an unusual sound that took months to be registered by astute clinicians and the public health system [1]. Today, Hantavirus Pulmonary Syndrome (HPS) is widely recognized as a distinctive clinical entity; it is associated with a precipitous cardiorespiratory decomposition, thrombocytopenia, and atypical lymphocytes on a peripheral blood smear and is transmitted by rodents throughout the Americas [2]. The deer mouse (Peromyscus maniculatus) and Sin Nombre virus were quickly identified as the primary reservoir and etiological agent of disease, respectively, in the originally recognized outbreak in the southwestern United States
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two cases of Hantavirus Pulmonary Syndrome in randolph county west virginia a coincidence of time and place
American Journal of Tropical Medicine and Hygiene, 2007Co-Authors: Julie R Sinclair, Thomas G. Ksiazek, James N. Mills, Pierre E. Rollin, Joel M Montgomery, Darin S Carroll, Boris I Pavlin, Katherine Mccombs, James A Comer, Stuart T NicholAbstract:Hantavirus Pulmonary Syndrome (HPS) is caused by an infection with viruses of the genus Hantavirus in the western hemisphere. Rodent hosts of Hantaviruses are present throughout the United States. In July 2004, two HPS case-patients were identified in Randolph County, WV: a wildlife science graduate student working locally and a Randolph County resident. We interviewed family members and colleagues, reviewed medical records, and conducted environmental studies at likely exposure sites. Small mammals were trapped, and blood, urine, and tissue samples were submitted to the Centers for Disease Control and Prevention for laboratory analyses. These analyses confirmed that both patients were infected with Monongahela virus, a Sin Nombre Hantavirus variant hosted by the Cloudland deer mouse, Peromyscus maniculatus nubiterrae. Other than one retrospectively diagnosed case in 1981, these are the first HPS cases reported in West Virginia. These cases emphasize the need to educate the public throughout the United States regarding risks and prevention measures for Hantavirus infection.
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newly recognized Hantaviruses associated with Hantavirus Pulmonary Syndrome in northern brazil partial genetic characterization of viruses and serologic implication of likely reservoirs
Vector-borne and Zoonotic Diseases, 2005Co-Authors: Elizabeth Salbe Travassos Da Rosa, Thomas G. Ksiazek, Valeria P. Martínez, Paula Padula, James N. Mills, Mauro R. Elkhoury, Elizabeth D. Santos, Wellington Da Silva Mendes, G C B Araujo, Jorge F S T RosaAbstract:Following the occurrence of the first laboratory-confirmed cases of Hantavirus Pulmonary Syndrome (HPS) in Maranhao State, Brazil, rodents were trapped and rodent materials screened by ELISA for antibodies to Sin Nombre and Andes Hantaviruses. Antibody-positive samples were tested by RT-PCR, amplified products were sequenced, and phylogenetic trees were constructed for comparison with known Hantaviruses. From 104 rodent blood samples collected (40 Bolomys lasiurus, 52 Holochilus sciureus, 12 Oligoryzomys fornesi, and one Proechimys guyannensis), 21 (20.2%) were antibody-positive (one B. lasiurus, five O. fornesi, and 15 H. sciureus). Hantavirus RNA was amplified by PCR from two O. fornesi and four H. sciureus. Viral sequencing identified two Hantavirus genotypes. The genotype recovered from O. fornesi, is designated herein as Anajatuba (ANAJ) and the genotype recovered from H. sciureus is designated Rio Mearim (RIME). Phylogenetic analysis of a 643-nucleotide region of the N segment showed both viruses to...
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discriminators between Hantavirus infected and uninfected persons enrolled in a trial of intravenous ribavirin for presumptive Hantavirus Pulmonary Syndrome
Clinical Infectious Diseases, 2002Co-Authors: Louisa E Chapman, Thomas G. Ksiazek, Barbara A. Ellis, Pierre E. Rollin, Gregory J Mertz, Frederick Koster, Mark J Sotir, K F Baum, Andrew T PaviaAbstract:To provide a potentially therapeutic intervention and to collect clinical and laboratory data during an outbreak of Hantavirus Pulmonary Syndrome (HPS), 140 patients from the United States with suspected HPS were enrolled for investigational intravenous ribavirin treatment. HPS was subsequently laboratory confirmed in 30 persons and not confirmed in 105 persons with adequate specimens. Patients with HPS were significantly more likely than were Hantavirus-negative patients to report myalgias from onset of symptoms through hospitalization, nausea at outpatient presentation, and diarrhea and nausea at the time of hospitalization; they were significantly less likely to report respiratory symptoms early in the illness. The groups did not differ with regard to time from the onset of illness to the point at which they sought care; time from onset, hospitalization, or enrollment to death was significantly shorter for patients with HPS. At the time of hospitalization, patients with HPS more commonly had myelocytes, metamyelocytes, or promyelocytes on a peripheral blood smear, and significantly more of them had thrombocytopenia, hemoconcentration, and hypocapnia. Patterns of clinical symptoms, the pace of clinical evolution, and specific clinical laboratory parameters discriminated between these 2 groups.
C J Peters - One of the best experts on this subject based on the ideXlab platform.
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community ecology of small mammal populations in panama following an outbreak of Hantavirus Pulmonary Syndrome
Journal of Vector Ecology, 2004Co-Authors: Luis A Ruedas, David S Tinnin, Fernando Gracia, Lorenzo Caceres, Arsenio Garcia, Jorge Salazarbravo, Bias Armien, Mario Avila Diaz, Gerardo Suzan, C J PetersAbstract:In late 1999 and early 2000, an outbreak of Hantavirus Pulmonary Syndrome (HPS) occurred in and around Los Santos, on the Azuero Peninsula of southwestern Panama. This HPS episode, resulting in 22% case fatality, was linked to the Costa Rican pigmy rice rat, Oligoryzomys fulvescens costaricensis, which harbored a then undescribed Hantavirus, Choclo virus. In addition, Cherrie's cane rat, Zygodontomys brevicauda cherriei, was identified as carrying a distinct Hantavirus, Calabazo virus with no known pathogenicity to humans. Herein we present the ecological results of the outbreak investigations in the Azuero region. A total of 164 animals were captured, of which 126 were potential small, non-volant mammal hosts of a Hantavirus: rodents in the family Muridae. There were significant differences in small mammal community structure between case sites and a negative control site. Differences were manifest in ecological measures of species diversity and in species evenness and heterogeneity measures, as indicated by Pairwise Euclidian distances and Morisita indices of community similarity. Our analyses suggest that human activities (i.e., deforestation for cattle ranching) coupled with environmental factors (i.e., increased precipitation) may have synergistically coalesced for an increased risk of HPS to area residents.
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Hantavirus Pulmonary Syndrome the new american hemorrhagic fever
Clinical Infectious Diseases, 2002Co-Authors: C J Peters, Ali S. KhanAbstract:The recognition of Hantavirus Pulmonary Syndrome (HPS) after the investigation of a cluster of unexplained respiratory deaths in the southwestern United States during the spring of 1993 showcased our ability to recognize new and emerging diseases, given the correct juxtaposition of a new clinical entity with circumscribed epidemiologic features that are analyzed with novel diagnostic methods. In less than a decade, HPS has become established as a pan-American zoonosis due to numerous viruses maintained by sigmodontine rodents with rodent- and virus-specific epidemiologic profiles. The classical features of the Syndrome-acute febrile illness associated with prominent cardiorespiratory compromise after direct contact or inhalation of aerosolized rodent excreta-has been extended to include clinical variants, including disease with frank hemorrhage, that have confirmed that this Syndrome is a viral hemorrhagic fever. Efforts are under way to refine prevention strategies, to understand the pathogenesis of the shock, and to identify therapeutic modalities.
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intravenous ribavirin for Hantavirus Pulmonary Syndrome safety and tolerance during 1 year of open label experience
Antiviral Therapy, 1999Co-Authors: Louisa E Chapman, Ali S. Khan, Thomas G. Ksiazek, Pierre E. Rollin, Gregory J Mertz, Frederick Koster, C J Peters, Heidi M Jolson, Kenneth F Baum, Andrew T PaviaAbstract:Intravenous ribavirin was provided non-selectively for investigational open-label use among persons with suspected Hantavirus Pulmonary Syndrome (HPS) in the United States between 4 June 1993 and 1 September 1994. Therapy was initiated prior to laboratory confirmation of Hantavirus infection because most deaths from HPS occur within 48 h of hospitalization. Thirty patients with confirmed HPS, 105 patients without HPS and 5 patients without adequate diagnostic testing for HPS were enrolled. This observational study arguably provides the most complete information available on ribavirin-associated adverse effects. Although ribavirin was generally well tolerated, 71% of recipients became anaemic and 19% underwent transfusion. An apparent excess of hyperamylasaemia/pancreatitis was either therapy-associated or due to enrollment bias. The 30 enrolled HPS patients had a case-fatality rate of 47% (14/30). It is not possible to assess efficacy with this study design. However, comparison of survival curves for the 30 enrolled HPS patients and 34 patients who developed HPS during the same time period but were not enrolled did not suggest an appreciable drug effect. A randomized, placebo-controlled trial that enrolls patients during the prodrome phase would be necessary to assess the efficacy and further define the safety of intravenous ribavirin for HPS.
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spectrum of Hantavirus infection hemorrhagic fever with renal Syndrome and Hantavirus Pulmonary Syndrome
Annual Review of Medicine, 1999Co-Authors: C J Peters, Gary L Simpson, H LevyAbstract:Hantaviruses chronically infect rodents without apparent disease, but when they are spread by aerosolized excreta to humans, two major clinical Syndromes result: hemorrhagic fever with renal Syndrome (HFRS) and Hantavirus Pulmonary Syndrome (HPS). Both diseases appear to be immunopathologic, and inflammatory mediators are important in causing the clinical manifestations. In HPS, T cells act on heavily infected Pulmonary endothelium, and it is suspected that gamma interferon and tumor necrosis factor are major agents of a reversible increase in vascular permeability that leads to severe, noncardiogenic Pulmonary edema. HFRS has prominent systemic manifestations. The retroperitoneum is a major site of vascular leak and the kidneys suffer tubular necrosis. Both Syndromes are accompanied by myocardial depression and hypotension or shock. HFRS is primarily a Eurasian disease, whereas HPS appears to be confined to the Americas; these geographic distinctions correlate with the phylogenies of the rodent hosts and the viruses that coevolved with them.
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genetic reassortment among viruses causing Hantavirus Pulmonary Syndrome
Virology, 1998Co-Authors: Luis L Rodriguez, C J Peters, Jessica H Owens, Stuart T NicholAbstract:In order to determine the frequency and characteristics of reassortment among viruses causing Hantavirus Pulmonary Syndrome (HPS), mixed infections were initiated in tissue culture by using two closely related strains of Sin Nombre virus, CC107 (from eastern California) and NMR11 (from New Mexico), which share the same species of rodent host in nature, the deer mouse (Peromyscus maniculatus). Potential reassortant virus plaques were screened by multiplex RT-PCR, using primers specific for individual genome segments of each strain. Reassortant viruses involving the M and S segments and, to a lesser extent, the L segment were detected in 8.5% of 294 progeny plaques tested. In addition, approximately 30% of the progeny virus plaques appeared to contain S or M segments originating from both parental virus strains, i.e., they were diploid. Most of these diploid virus genotypes were not stable, becoming either reassortant or parental virus strains upon plaque-to-plaque virus passage. In contrast to the results above, only one virus reassortant and four diploids were observed among 163 progeny virus plaques from mixed infections between Sin Nombre virus NMR11 and the genetically more distant Black Creek Canal virus, an HPS-causing virus from Florida, which has the cotton rat (Sigmodon hispidus) as its natural host.
Stuart T Nichol - One of the best experts on this subject based on the ideXlab platform.
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Hantavirus Pulmonary Syndrome
Virus Research, 2011Co-Authors: Adam Macneil, Stuart T Nichol, Christina F. SpiropoulouAbstract:Hantavirus Pulmonary Syndrome (HPS) is a severe disease characterized by a rapid onset of Pulmonary edema followed by respiratory failure and cardiogenic shock. The HPS associated viruses are members of the genus Hantavirus, family Bunyaviridae. Hantaviruses have a worldwide distribution and are broadly split into the New World Hantaviruses, which includes those causing HPS, and the Old World Hantaviruses [including the prototype Hantaan virus (HTNV)], which are associated with a different disease, hemorrhagic fever with renal Syndrome (HFRS). Sin Nombre virus (SNV) and Andes virus (ANDV) are the most common causes of HPS in North and South America, respectively. Case fatality of HPS is approximately 40%. Pathogenic New World Hantaviruses infect the lung microvascular endothelium without causing any virus induced cytopathic effect. However, virus infection results in microvascular leakage, which is the hallmark of HPS. This article briefly reviews the knowledge on HPS-associated Hantaviruses accumulated since their discovery, less than 20 years ago.
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two cases of Hantavirus Pulmonary Syndrome in randolph county west virginia a coincidence of time and place
American Journal of Tropical Medicine and Hygiene, 2007Co-Authors: Julie R Sinclair, Thomas G. Ksiazek, James N. Mills, Pierre E. Rollin, Joel M Montgomery, Darin S Carroll, Boris I Pavlin, Katherine Mccombs, James A Comer, Stuart T NicholAbstract:Hantavirus Pulmonary Syndrome (HPS) is caused by an infection with viruses of the genus Hantavirus in the western hemisphere. Rodent hosts of Hantaviruses are present throughout the United States. In July 2004, two HPS case-patients were identified in Randolph County, WV: a wildlife science graduate student working locally and a Randolph County resident. We interviewed family members and colleagues, reviewed medical records, and conducted environmental studies at likely exposure sites. Small mammals were trapped, and blood, urine, and tissue samples were submitted to the Centers for Disease Control and Prevention for laboratory analyses. These analyses confirmed that both patients were infected with Monongahela virus, a Sin Nombre Hantavirus variant hosted by the Cloudland deer mouse, Peromyscus maniculatus nubiterrae. Other than one retrospectively diagnosed case in 1981, these are the first HPS cases reported in West Virginia. These cases emphasize the need to educate the public throughout the United States regarding risks and prevention measures for Hantavirus infection.
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Hantavirus Pulmonary Syndrome in central bolivia relationships between reservoir hosts habitats and viral genotypes
American Journal of Tropical Medicine and Hygiene, 2005Co-Authors: Darin S Carroll, James N. Mills, Joel M Montgomery, Patrick J Blair, Alberto Gianella, Naomi Iihoshi, Vidal Felices, Daniel G Bausch, James P Burans, Stuart T NicholAbstract:In August 2002, two cases of Hantavirus Pulmonary Syndrome (HPS) were confirmed in Mineros and Concepcion, within the Santa Cruz Department of Bolivia. Extensive alteration of the native ecosystem, from dense forest to pasture or sugarcane, had occurred in both regions. An ecologic assessment of reservoir species associated with the human disease identified a single Hantavirus antibody-positive Oligoryzomys microtis from Mineros and three Hantavirus antibody-positive Calomys callosus from Concepcion. In Mineros, the virus from the O. microtis was 90% similar to sequences published for Rio Mamore virus. Viral nucleotide sequences from two C. callosus were 87�88% similar to the sequence of Laguna Negra virus. The viral sequence from the C. callosus was 99% identical to viral sequences obtained from the HPS patient in this area, implicating C. callosus as the host and Laguna Negra virus as the agent responsible for the HPS case near Concepcion.
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Hantavirus Pulmonary Syndrome associated with monongahela virus pennsylvania
Emerging Infectious Diseases, 2000Co-Authors: Luther V Rhodes, Jan G. Humphreys, Thomas G. Ksiazek, Sherif R. Zaki, Stuart T Nichol, Cinnia Huang, Angela J Sanchez, James J Freeman, Kenneth KnechtAbstract:The first two recognized cases of rapidly fatal Hantavirus Pulmonary Syndrome in Pennsylvania occurred within an 8-month period in 1997. Illness in the two patients was confirmed by immunohistochemical techniques on autopsy material. Reverse transcription-polymerase chain reaction analysis of tissue from one patient and environmentally associated Peromyscus leucopus (white-footed mouse) identified the Monongahela virus variant. Physicians should be vigilant for such Monongahela virus-associated cases in the eastern United States and Canada, particularly in the Appalachian region.
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genetic reassortment among viruses causing Hantavirus Pulmonary Syndrome
Virology, 1998Co-Authors: Luis L Rodriguez, C J Peters, Jessica H Owens, Stuart T NicholAbstract:In order to determine the frequency and characteristics of reassortment among viruses causing Hantavirus Pulmonary Syndrome (HPS), mixed infections were initiated in tissue culture by using two closely related strains of Sin Nombre virus, CC107 (from eastern California) and NMR11 (from New Mexico), which share the same species of rodent host in nature, the deer mouse (Peromyscus maniculatus). Potential reassortant virus plaques were screened by multiplex RT-PCR, using primers specific for individual genome segments of each strain. Reassortant viruses involving the M and S segments and, to a lesser extent, the L segment were detected in 8.5% of 294 progeny plaques tested. In addition, approximately 30% of the progeny virus plaques appeared to contain S or M segments originating from both parental virus strains, i.e., they were diploid. Most of these diploid virus genotypes were not stable, becoming either reassortant or parental virus strains upon plaque-to-plaque virus passage. In contrast to the results above, only one virus reassortant and four diploids were observed among 163 progeny virus plaques from mixed infections between Sin Nombre virus NMR11 and the genetically more distant Black Creek Canal virus, an HPS-causing virus from Florida, which has the cotton rat (Sigmodon hispidus) as its natural host.
Anne Lavergne - One of the best experts on this subject based on the ideXlab platform.
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Hantavirus Pulmonary Syndrome caused by maripa virus in french guiana 2008 2016
Emerging Infectious Diseases, 2017Co-Authors: Séverine Matheus, Didier Hommel, Vincent Lacoste, Hatem Kallel, Claire Mayence, Laetitia Bremand, Stéphanie Houcke, Dominique Rousset, Benoit De Thoisy, Anne LavergneAbstract:We report 5 human cases of Hantavirus Pulmonary Syndrome found during surveillance in French Guiana in 2008-2016; of the 5 patients, 4 died. This pathogen should continue to be monitored in humans and rodents in effort to reduce the occurrence of these lethal infections in humans stemming from ecosystem disturbances.
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Hantavirus Pulmonary Syndrome Caused by Maripa Virus in French Guiana, 2008–2016
Emerging Infectious Diseases, 2017Co-Authors: Séverine Matheus, Didier Hommel, Vincent Lacoste, Hatem Kallel, Claire Mayence, Laetitia Bremand, Stéphanie Houcke, Dominique Rousset, Benoit De Thoisy, Anne LavergneAbstract:We report 5 human cases of Hantavirus Pulmonary Syndrome found during surveillance in French Guiana in 2008-2016; of the 5 patients, 4 died. This pathogen should continue to be monitored in humans and rodents in effort to reduce the occurrence of these lethal infections in humans stemming from ecosystem disturbances.
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Hantavirus Pulmonary Syndrome, French Guiana.
Emerging infectious diseases, 2010Co-Authors: Séverine Matheus, Félix Djossou, David Moua, Anne Marie Bourbigot, Didier Hommel, Vincent Lacoste, Philippe Dussart, Anne LavergneAbstract:A systematic serological survey of patients suffering from symptoms suggestive of Hantavirus Pulmonary Syndrome allowed us to identify a native case in French Guiana. Partial molecular characterization of the implicated Hantavirus revealed its close relationship with the Bolivian Rio Mamore virus. We tentatively named it Maripa virus.
