Hantavirus cardiopulmonary syndrome: immune response and pathogenesis

Borges, Alessandra Abel; Campos, Geraldo Maia; Moreli, Marcos Lázaro; Souza, Rodrigo Wagner Alves de; Aquino, Víctor Hugo; Saggioro, Fabiano Pinto; Figueiredo, Luíz Tadeu Moraes

doi:10.1016/j.micinf.2006.04.019

Cited by 58 publications

(48 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Hantaviruses primarily infect endothelial cells, but replication in these cells is not directly cytopathic (32,33,57,83,86,88). Multiple mechanisms have been proposed to account for the vascular leakage caused by hantaviruses, including, predominantly, T cell-mediated immunopathology (4,17,39,76,79). Consistent with this, SNV-specific T cells induce permeability of human endothelial cells expressing SNV antigens in vitro (29).…”

mentioning

confidence: 77%

T Cells Are Not Required for Pathogenesis in the Syrian Hamster Model of Hantavirus Pulmonary Syndrome

Hammerbeck

Hooper

2011

J Virol

View full text Add to dashboard Cite

Andes virus (ANDV) is associated with a lethal vascular leak syndrome in humans termed hantavirus pulmonary syndrome (HPS). In hamsters, ANDV causes a respiratory distress syndrome closely resembling human HPS. The mechanism for the massive vascular leakage associated with HPS is poorly understood; however, T cell immunopathology has been implicated on the basis of circumstantial and corollary evidence. Here, we show that following ANDV challenge, hamster T cell activation corresponds with the onset of disease. However, treatment with cyclophosphamide or specific T cell depletion does not impact the course of disease or alter the number of surviving animals, despite significant reductions in T cell number. These data demonstrate, for the first time, that T cells are not required for hantavirus pathogenesis in the hamster model of human HPS. Depletion of T cells from Syrian hamsters did not significantly influence early events in disease progression. Moreover, these data argue for a mechanism of hantavirus-induced vascular permeability that does not involve T cell immunopathology.

show abstract

mentioning

confidence: 77%

T Cells Are Not Required for Pathogenesis in the Syrian Hamster Model of Hantavirus Pulmonary Syndrome

Hammerbeck

Hooper

2011

J Virol

View full text Add to dashboard Cite

show abstract

“…Specific positive IgM in the first sample examined, or quadrupling of IgG titers in paired samples are confirmatory. The levels of IgG are detectable throughout the life of the individual, allowing studies about the prevalence of HPS [36]. Diagnosis can also be done by PCR techniques, already performed in research centers in Brazil, but routine use of this technique is limited due to its costs [37,38].…”

Section: Diagnosismentioning

confidence: 99%

Twenty years of hantavirus pulmonary syndrome in Brazil: a review of epidemiological and clinical aspects

Pinto

Hamidad

Filho

et al. 2014

J Infect Dev Ctries

View full text Add to dashboard Cite

Hantavirus infection is transmitted to humans by wild rodents and the most common clinical form in Brazil is the Hantavirus Pulmonary Syndrome (HPS). The first serological evidence of the disease was identified in 1990, in Recife, Pernambuco State, and later in 1993 in Juquitiba, State of São Paulo. Since then there has been a progressive increase in case notification in all regions of the country. The clinical aspects of the disease in Brazil are characterized by a prodromal phase, with nonspecific signs and symptoms of an acute febrile illness. After about three days, respiratory distress develops, accompanied by dry cough that turns progressively productive, evolving to dyspnea and respiratory failure with cardiogenic shock. Although the majority of patients receive hospital care in intensive care therapy units, case-fatality rate in Brazil ranges from 33% to 100% depending on the region. Besides it has to be added the problem of differential diagnosis with other prevalent diseases in the country, like dengue and leptospirosis. Questions about the impact of uncontrolled urbanization and other environmental changes caused by human action have been raised. Due to increasing incidence and high case-fatality, there is an urge to respond to such questions to recommend preventative measures. This article aims to review the main acquisitions in clinical and epidemiological knowledge about HPS in Brazil in the last twenty years.

show abstract

“…Therefore, in the natural host hantaviruses are thought to induce appropriate immune responses and persist without obvious pathogenic symptoms. Spillover of the virus to humans by aspiration of aerosolized excreta from infected animals has to be considered a dead-end pathway, leading to hemorrhagic fever with renal syndrome or hantavirus cardiopulmonary syndrome, with case fatality rates up to 50% depending on the hantavirus species involved (1)(2)(3)(4).…”

mentioning

confidence: 99%

Hantaan Virus Triggers TLR3-Dependent Innate Immune Responses

Handke

Oelschlegel

Franke

et al. 2009

The Journal of Immunology

View full text Add to dashboard Cite

Immediately after viral infection, innate responses including expression of IFN-α/β and IFN-stimulated genes (ISGs) are elicited ubiquitously by recruitment of specific pathogen recognition receptors. The velocity to induce IFN-α/β and ISGs in response to an infection is often decisive for virulence. Interestingly, in primary endothelial cells ISGs are induced later by hantaviruses pathogenic to humans than those considered to be nonpathogenic or of low virulence. Here we demonstrate that pathogenic Hantaan (HTNV) and putatively nonpathogenic Prospect Hill hantavirus (PHV) differentially activate innate responses in the established cell lines A549 and HuH7. STAT1α phosphorylation was detectable 3 h after PHV inoculation but not within the first 2 days after HTNV inoculation. The velocity to induce the ISGs MxA and ISG15 correlated inversely with amounts of virus produced. Moreover, expression of the inflammatory chemokine CCL5 was also induced differentially. Both hantaviruses induced innate responses via TRAF3 (TNF receptor-associated factor 3), and TLR3 was required for HTNV-induced expression of MxA, but not for the MxA induction triggered by PHV. Infection of RIG-I-deficient HuH7.5 cells revealed that RIG-I (retinoic acid receptor I) was not necessary for induction of innate responses by PHV. Taken together, these data suggest that HTNV and PHV elicit different signaling cascades that converge via TRAF3. Early induction of antiviral responses might contribute to efficient elimination of PHV. Subsequent to clearance of the infection, innate responses most likely cease; vice versa, retarded induction of antiviral responses could lead to increased HTNV replication and dissemination, which might cause a prolonged inflammatory response and might contribute to the in vivo virulence.

show abstract

Hantavirus cardiopulmonary syndrome: immune response and pathogenesis

Cited by 58 publications

References 33 publications

T Cells Are Not Required for Pathogenesis in the Syrian Hamster Model of Hantavirus Pulmonary Syndrome

T Cells Are Not Required for Pathogenesis in the Syrian Hamster Model of Hantavirus Pulmonary Syndrome

Twenty years of hantavirus pulmonary syndrome in Brazil: a review of epidemiological and clinical aspects

Hantaan Virus Triggers TLR3-Dependent Innate Immune Responses

Contact Info

Product

Resources

About