Sin Nombre Viral RNA Load in Patients with Hantavirus Cardiopulmonary Syndrome

Xiao, Ruobing; Yang, Shuhu; Koster, Fred; Ye, Chunyan; Stidley, Chris A.; Hjelle, Brian

doi:10.1086/508494

Cited by 69 publications

(62 citation statements)

References 18 publications

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“…As a whole, the clinical and epidemiological data of this patient correspond to descriptions of moderate or less severe cases of HPS [1,13], mainly because the treatment of pulmonary edema did not require endotracheal intubation and mechanical ventilation [14]. He was a previously healthy young male whose professional activities involved recent contact with an environment contaminated by rodent reservoirs of viral agents of the syndrome.…”

Section: Discussionsupporting

confidence: 53%

“…This phenomenon has been frequently observed in HPS and may have no correlation with the amount or composition of the administered fluids, or with renal function [18]. In fact, hyponatremia can be associated with hypoalbuminemia due to acute phase response and capillary leak syndrome [14,20]. Elevated hematocrit (52.9%) and low platelets (55,000/mm 3 ) in the second day of admission raised the hypothesis of dengue; in addition, hydrothorax can be due to severe dengue with capillary leakage [21].…”

Section: Discussionmentioning

confidence: 99%

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Hantavirus pulmonary syndrome in Brasilia periphery: a diagnostic challenge

Santos

Sá

Turra

et al. 2009

J Infect Dev Ctries

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Background: Hantavirus pulmonary syndrome (HPS) is an emerging rodent-borne disease in the American continent, characterized by acute respiratory distress and a high case-fatality ratio. The present work describes a case of HPS, with favorable outcome, whose initial features were mistaken for leptospirosis or other less severe acute infections. Methodology: The case of a 32-year-old male with an uneventful course of HPS is reported. He was inadvertently infected at work by exposure to a rodent-contaminated environment in Brasília, Federal District vicinity, during May 2008. Results and Conclusions: Fever, headache and myalgia after exposure to a rodent-contaminated environment raised clinical suspicion. Noncardiac pulmonary edema, hydrothorax, neutrophilia with band forms 26%, high hematocrit, thrombocytopenia, and elevated liver enzymes were observed. Leptospirosis and dengue were the main differential diagnoses because both pathogens are endemic in the area. Hantavirus IgM antibody-capture ELISA was positive, while tests for dengue, leptospirosis and yellow fever were negative. The prognosis for HPS is ominous and misdiagnoses may increase mortality. Better chances of survival depend on prompt intensive care support. Reports of moderate or less typical cases can raise the suspicion index among primary care and hospital-based physicians about this uncommon but severe condition that often affects previously healthy young individuals from developing countries, and subjects who interact with rodent-infested environments in North America. High awareness of HPS allowed successful management of the patient, even before establishing the diagnosis, by serological tests at the reference laboratory of the Ministry of Health. Clinical suspicion favored warning local health authorities about a new case of HPS.

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Section: Discussionsupporting

confidence: 53%

Section: Discussionmentioning

confidence: 99%

Hantavirus pulmonary syndrome in Brasilia periphery: a diagnostic challenge

Santos

Sá

Turra

et al. 2009

J Infect Dev Ctries

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“…Preliminary studies of ANDV infections suggest that plasma and serum viral loads are too often below the limit of detection of the assay to be useful in the prediction of disease severity (53). However, we speculated that if ApoH interacts with ANDV as efficiently as has been reported for HBV (47), and if serum components did not interfere with ApoH-virus binding, ApoHcoated magnetic beads would be capable of capturing ANDV even when present in a complex biological mixture.…”

Section: Resultsmentioning

confidence: 93%

Andes Virus Antigens Are Shed in Urine of Patients with Acute Hantavirus Cardiopulmonary Syndrome

Godoy

Marsac

Stefas³

et al. 2009

J Virol

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Hantavirus cardiopulmonary syndrome (HCPS) is a highly pathogenic emerging disease (40% case fatality rate) caused by New World hantaviruses. Hantavirus infections are transmitted to humans mainly by inhalation of virus-contaminated aerosol particles of rodent excreta and secretions. At present, there are no antiviral drugs or immunotherapeutic agents available for the treatment of hantaviral infection, and the survival rates for infected patients hinge largely on early virus recognition and hospital admission and aggressive pulmonary and hemodynamic support. In this study, we show that Andes virus (ANDV) interacts with human apolipoprotein H (ApoH) and that ApoH-coated magnetic beads or ApoH-coated enzyme-linked immunosorbent assay plates can be used to capture and concentrate the virus from complex biological mixtures, such as serum and urine, allowing it to be detected by both immunological and molecular approaches. In addition, we report that ANDV-antigens and infectious virus are shed in urine of HCPS patients.

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“…Both diseases are manifestations of enhanced vascular permeability leading to hemorrhage or acute pulmonary edema in patients days to weeks after infection (34,49,65,93). Acute thrombocytopenia is common to both syndromes, and acute disease is associated with cardiopulmonary dysfunction, high viral load, and the severity of platelet loss (11,39,53,90). As a result, both endothelial barrier functions and platelet directed responses that restore vascular barrier functions are compromised following hantavirus infection (49,64,93).…”

mentioning

confidence: 99%

Hantaviruses Direct Endothelial Cell Permeability by Sensitizing Cells to the Vascular Permeability Factor VEGF, while Angiopoietin 1 and Sphingosine 1-Phosphate Inhibit Hantavirus-Directed Permeability

Gavrilovskaya

Gorbunova

Mackow³

et al. 2008

J Virol

148

319

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Hantaviruses infect human endothelial cells and cause two vascular permeability-based diseases: hemorrhagic fever with renal syndrome and hantavirus pulmonary syndrome. Hantavirus infection alone does not permeabilize endothelial cell monolayers. However, pathogenic hantaviruses inhibit the function of ␣v␤3 integrins on endothelial cells, and hemorrhagic disease and vascular permeability deficits are consequences of dysfunctional ␤3 integrins that normally regulate permeabilizing vascular endothelial growth factor (VEGF) responses. Here we show that pathogenic Hantaan, Andes, and New York-1 hantaviruses dramatically enhance the permeability of endothelial cells in response to VEGF, while the nonpathogenic hantaviruses Prospect Hill and Tula have no effect on endothelial cell permeability. Pathogenic hantaviruses directed endothelial cell permeability 2 to 3 days postinfection, coincident with pathogenic hantavirus inhibition of ␣v␤3 integrin functions, and hantavirus-directed permeability was inhibited by antibodies to VEGF receptor 2 (VEGFR2). These studies demonstrate that pathogenic hantaviruses, similar to ␣v␤3 integrin-deficient cells, specifically enhance VEGF-directed permeabilizing responses. Using the hantavirus permeability assay we further demonstrate that the endothelial-cell-specific growth factor angiopoietin 1 (Ang-1) and the platelet-derived lipid mediator sphingosine 1-phosphate (S1P) inhibit hantavirus directed endothelial cell permeability at physiologic concentrations. These results demonstrate the utility of a hantavirus permeability assay and rationalize the testing of Ang-1, S1P, and antibodies to VEGFR2 as potential hantavirus therapeutics. The central importance of ␤3 integrins and VEGF responses in vascular leak and hemorrhagic disease further suggest that altering ␤3 or VEGF responses may be a common feature of additional viral hemorrhagic diseases. As a result, our findings provide a potential mechanism for vascular leakage after infection by pathogenic hantaviruses and the means to inhibit hantavirus-directed endothelial cell permeability that may be applicable to additional vascular leak syndromes.

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Sin Nombre Viral RNA Load in Patients with Hantavirus Cardiopulmonary Syndrome

Cited by 69 publications

References 18 publications

Hantavirus pulmonary syndrome in Brasilia periphery: a diagnostic challenge

Hantavirus pulmonary syndrome in Brasilia periphery: a diagnostic challenge

Andes Virus Antigens Are Shed in Urine of Patients with Acute Hantavirus Cardiopulmonary Syndrome

Hantaviruses Direct Endothelial Cell Permeability by Sensitizing Cells to the Vascular Permeability Factor VEGF, while Angiopoietin 1 and Sphingosine 1-Phosphate Inhibit Hantavirus-Directed Permeability

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