Hantavirus pulmonary syndrome: at the crossroads

Khan, Ali S.; Young, Joni C.

doi:10.1097/00001432-200104000-00016

Cited by 22 publications

(12 citation statements)

References 24 publications

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“…The more recently described hantavirus pulmonary syndrome (HPS) or hantavirus cardiopulmonary syndrome (HCPS) (here referred to as HPS) has a lower incidence of infection when compared to HFRS, however mortality rates range from 40–50% [3]. Cases of HPS have been diagnosed throughout the America's and are most commonly associated with infection of either Sin Nombre or Andes viruses (SNV and ANDV, respectively) [3], [4].…”

Section: Introductionmentioning

confidence: 99%

Pathogenesis and Host Response in Syrian Hamsters following Intranasal Infection with Andes Virus

et al. 2011

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Hantavirus pulmonary syndrome (HPS), also referred to as hantavirus cardiopulmonary syndrome (HCPS), is a rare but frequently fatal disease caused by New World hantaviruses. In humans HPS is associated with severe pulmonary edema and cardiogenic shock; however, the pathogenesis of this disease remains unclear largely due to a lack of suitable animal models for the study of disease progression. In this study we monitored clinical, virological, pathophysiological parameters and host immunological responses to decipher pathological factors and events in the lethal Syrian hamster model of HPS following intranasal inoculation of Andes virus. Transcriptional profiling of the host gene responses demonstrated a suppression of innate immune responses in most organs analyzed during the early stage of infection, except for in the lung which had low level activation of several pro-inflammatory genes. During this phase Andes virus established a systemic infection in hamsters, with viral antigen readily detectable in the endothelium of the majority of tissues analyzed by 7–8 days post-inoculation. Despite wide-spread infection, histological analysis confirmed pathological abnormalities were almost exclusively found in the lungs. Immediately preceding clinical signs of disease, intense activation of pro-inflammatory and Th1/Th2 responses were observed in the lungs as well as the heart, but not in peripheral organs, suggesting that localized immune-modulations by infection is paramount to pathogenesis. Throughout the course of infection a strong suppression of regulatory T-cell responses was noted and is hypothesized to be the basis of the aberrant immune activations. The unique and comprehensive monitoring of host immune responses to hantavirus infection increases our understanding of the immuno-pathogenesis of HPS and will facilitate the development of treatment strategies targeting deleterious host immunological responses.

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Section: Introductionmentioning

confidence: 99%

Pathogenesis and Host Response in Syrian Hamsters following Intranasal Infection with Andes Virus

et al. 2011

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“…S in Nombre virus (SNV) and Andes virus (ANDV), both members of the genus Hantavirus within the family Bunyaviridae, are the predominant etiological agents of hantavirus pulmonary syndrome (HPS) in North and South America, respectively (1)(2)(3). Hantaviruses are negative-strand, single-stranded RNA viruses with three segments, denoted small (S), medium (M), and large (L).…”

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confidence: 99%

A Lethal Disease Model for Hantavirus Pulmonary Syndrome in Immunosuppressed Syrian Hamsters Infected with Sin Nombre Virus

Brocato

Hammerbeck

Bell

et al. 2014

J Virol

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Sin Nombre virus (SNV) is a rodent-borne hantavirus that causes hantavirus pulmonary syndrome (HPS) predominantly in North America. SNV infection of immunocompetent hamsters results in an asymptomatic infection; the only lethal disease model for a pathogenic hantavirus is Andes virus (ANDV) infection of Syrian hamsters. Efforts to create a lethal SNV disease model in hamsters by repeatedly passaging virus through the hamster have demonstrated increased dissemination of the virus but no signs of disease. In this study, we demonstrate that immunosuppression of hamsters through the administration of a combination of dexamethasone and cyclophosphamide, followed by infection with SNV, results in a vascular leak syndrome that accurately mimics both HPS disease in humans and ANDV infection of hamsters. Immunosuppressed hamsters infected with SNV have a mean number of days to death of 13 and display clinical signs associated with HPS, including pulmonary edema. Viral antigen was widely detectable throughout the pulmonary endothelium. Histologic analysis of lung sections showed marked inflammation and edema within the alveolar septa of SNV-infected hamsters, results which are similar to what is exhibited by hamsters infected with ANDV. Importantly, SNV-specific neutralizing polyclonal antibody administered 5 days after SNV infection conferred significant protection against disease. This experiment not only demonstrated that the disease was caused by SNV, it also demonstrated the utility of this animal model for testing candidate medical countermeasures. This is the first report of lethal disease caused by SNV in an adult small-animal model.

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“…Pathogenic New World hantaviruses cause a hantavirus cardiopulmonary syndrome (HCPS) in the Americas, whereas pathogenic Old World hantaviruses cause a hemorrhagic fever with renal syndrome (HFRS) in Europe and Asia (4,17,29,41,58). Andes virus (ANDV) and Sin Nombre virus (SNV) cause HCPS and are the most pathogenic hantavirus species found in South and North America, respectively, with a case fatality rate between 20 to 40% (32).…”

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confidence: 99%