Hantavirus Immunology

Khaiboullina, Svetlana; Jeor, Stephen C. St.

doi:10.1089/088282402320914548

Cited by 67 publications

(55 citation statements)

References 137 publications

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“…Virus infection of humans results in hemorrhagic fever with renal syndrome (HFRS) or hantavirus cardiopulmonary syndrome (HCPS), both of which are caused by enhanced vascular permeability (34,45). The absence of cytopathic effects in infected human endothelial cell cultures has led to the hypothesis that hantavirus pathogenesis in humans is due to immune-mediated mechanisms targeting the infected cells (58,67,71).…”

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confidence: 99%

Seoul Virus-Infected Rat Lung Endothelial Cells and Alveolar Macrophages Differ in Their Ability To Support Virus Replication and Induce Regulatory T Cell Phenotypes

Klein

2012

J Virol

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confidence: 99%

Seoul Virus-Infected Rat Lung Endothelial Cells and Alveolar Macrophages Differ in Their Ability To Support Virus Replication and Induce Regulatory T Cell Phenotypes

Klein

2012

J Virol

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“…Of the 205 screen IgM ϩ IgG Ϫ sera, only 7 (3%) were positive for SNV-specific IgM at our facility. Two of the seven SNV IgM ϩ sera were from Brazilian patients; the sera were presumed to represent Andes or Andes-like hantavirus infection (2,14) and were excluded from further analysis. The five remaining SNV IgM ϩ sera were sent to PHL/CDC for confirmatory testing, where only one was confirmed to be SNV IgM ϩ .…”

Section: Resultsmentioning

confidence: 99%

“…Sin Nombre virus (SNV), which is transmitted to humans via inhalation of aerosols of excreta from infected rodents, particularly deer mice (Peromyscus maniculatus) (2)(3)(4)(5). HPS is characterized by fever, thrombocytopenia, bilateral pulmonary infiltrates, and hemoconcentration (3,4,6).…”

Section: T He Major Hantavirus-associated Illness In North America Ismentioning

confidence: 99%

Impact of the Yosemite Hantavirus Outbreak on Hantavirus Antibody Testing at a National Reference Laboratory

Prince

Lieberman

2013

Clin Vaccine Immunol

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In conjunction with the 2012 Yosemite hantavirus outbreak, the number of sera our facility tested for hantavirus antibodies increased. We tracked test results and used the data set to determine if a more efficient testing algorithm was possible. Sera were screened using laboratory-developed pan-hantavirus IgG and IgM enzyme immunoassays (EIAs), with an index of >1.10 defined as positive. Sera that were IgM positive by screening (screen IgM ؉ ) were tested for Sin Nombre virus (SNV)-specific IgM using a laboratory-developed EIA; screen IgM ؉ IgG ؉ sera were also tested for SNV IgG using a laboratory-developed immunoblot assay. SNV antibody-positive samples were sent to state public health laboratories (PHL) or the CDC for confirmation. Of 3,946 sera tested from July through December 2012, 205 were screen IgM ؉ IgG negative (IgG ؊ ); 7/205 were SNV IgM ؉ , but only 1/5 sent to PHL/CDC was confirmed as SNV IgM ؉ . Of 61 screen IgM ؉ IgG ؉ sera, 16 were SNV antibody positive; 13/16 sera (from 11 patients) went to PHL/CDC, where SNV infection was confirmed for all patients. Of 12 confirmed patients, 7 had been exposed at Yosemite. A modified algorithm defining screen indices of >2.00 as positive identified 11/12 confirmed cases while reducing the number of sera requiring SNV-specific antibody testing by 65%; the patient missed was not tested until 3 months after the onset of symptoms. Hantavirus antibody testing at our facility identified 12 SNV-infected patients, including 7 exposed at Yosemite. Some screen IgM ؉ IgG ؊ SNV IgM ؉ results were false positives, emphasizing the value of PHL/CDC confirmatory testing. We identified a modified algorithm requiring analysis of fewer specimens for SNV-specific antibodies without loss of sensitivity. T he major hantavirus-associated illness in North America is hantavirus pulmonary syndrome (HPS) (1). HPS is caused bySin Nombre virus (SNV), which is transmitted to humans via inhalation of aerosols of excreta from infected rodents, particularly deer mice (Peromyscus maniculatus) (2-5). HPS is characterized by fever, thrombocytopenia, bilateral pulmonary infiltrates, and hemoconcentration (3, 4, 6). Treatment is supportive, and approximately 35% of HPS patients do not survive (4).On 16 August 2012, a California Department of Public Health press release announced the diagnosis of HPS in two California residents who had recently visited Yosemite National Park and advised visitors to take precautions to prevent exposure to SNV (7). Another press release issued 30 August 2012 announced four more cases of HPS among recent Yosemite visitors (8). The next day, the National Park Service recommended that individuals who had visited Yosemite National Park between 10 June and 24 August 2012 seek medical attention at the first sign of symptoms consistent with SNV infection (9).Detection of SNV-specific IgM is the main laboratory tool for identifying acute SNV infection (10, 11). Our facility is one of only two reference laboratories in the United States to offer such testing, and here we doc...

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“…25 Some studies indicate that increased vascular permeability is also associated with elevated levels of vascular endothelial growth factor produced by infected endothelial cells and macrophages. 28 …”

Section: Pathologymentioning

confidence: 99%

Hantavirus Nephropathy

Ferluga

Vizjak

2008

Journal of the American Society of Nephrology

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A 30-yr-old man was admitted to hospital with a 5-d history of flu-like symptoms: Headache, shivers, nausea, vomiting, backache, arthralgias, myalgias, and blurred vision. In the previous month, he had been in close contact with rodents in the village of Dobrava, which is endemically infested with two hantavirus strains, Puumala and Dobrava. 1 On admission, he was hypotensive with a BP of 85/55 mmHg and a serum creatinine level of 382 mol/L (normal range 44 to 97 mol/ L). On day 6, he became oliguric, somnolent, tachypnic, and tachycardic. Physical examination revealed eyelid edema and conjunctival injections with hemorrhages. Laboratory examination disclosed a 21,600/mm 3 white blood cell count. A platelet count of 34,000/ mm 3 , increased partial thromboplastin time of 65.7 s, and fibrin degradation products of 24.0 mg/L (normal range Ͻ1 mg/L) suggested disseminated intravascular coagulation. Urinalysis showed 1.3 g/d proteinuria and erythrocytes too numerous to count. Severe oliguria persisted, serum creatinine rose on day 7 to 640 mol/L, and on day 9 the patient started hemodialysis for 6 consecutive days. His urine output gradually rose, and he became polyuric during the third week of illness. The patient recovered and was discharged after 4 wk of hospitalization with all laboratory findings normalized except for a slightly increased serum creatinine level of 115 mol/L and mild hematuria. Serologic tests performed on days 6 and 19 revealed a more than four-fold increase in IgG titers by immunofluorescence assay and in IgM titers by capture ELISA using antigens prepared from Vero E6 cells infected with Hantaan strain 76-118, Seoul strain SR-11, Puumala strain Hällnäs B, or Dobrava prototype strain 3970. 1 Acute Puumala infection was confirmed by focus reduction neutralization test, the most sensitive means available for differentiating hantaviruses. 2 Light microscopy of a needle renal biopsy on day 10, encompassing the outer medulla and cortex and containing 11 glomeruli, showed features of mild to moderate acute tubular injury in the cortex, approximately 40% interstitial edema, and scattered, predominantly mononuclear cell infiltrates ( Figure 1A). Electron microscopy disclosed discrete peritubular capillary injury with an effusion of plasma fluid and recent and late extravasation of erythrocytes into the interstitium ( Figure 1B). Glomerular capillaries revealed some swelling of endothelia with reduced fenestrations and scarce subendothelial edema, in line with traces of glomerular IgM found by immunofluorescence. In the biopsy cylinder of the outer medulla, histomorphologic changes were much more pronounced and characteristically dominated by extensive interstitial hemorrhage ( Figure 1A). Compressed floating tubuli and barely visible outlines of congested peritubular capillaries could be seen in a sea created mostly by massive extrusion of erythrocytes, with only a sparse mix of inflammatory cells ( Figure 1A, inset). Focal tubular dilation and discrete damage to tubuli and peritubular capillaries wer...

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Hantavirus Immunology

Cited by 67 publications

References 137 publications

Seoul Virus-Infected Rat Lung Endothelial Cells and Alveolar Macrophages Differ in Their Ability To Support Virus Replication and Induce Regulatory T Cell Phenotypes

Seoul Virus-Infected Rat Lung Endothelial Cells and Alveolar Macrophages Differ in Their Ability To Support Virus Replication and Induce Regulatory T Cell Phenotypes

Impact of the Yosemite Hantavirus Outbreak on Hantavirus Antibody Testing at a National Reference Laboratory

Hantavirus Nephropathy

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