T cells and pathogenesis of hantavirus cardiopulmonary syndrome and hemorrhagic fever with renal syndrome
UMass Chan Affiliations
Division of Infectious Diseases and Immunology, Department of MedicineCenter for Infectious Disease and Vaccine Research
Document Type
Journal ArticlePublication Date
2011-07-01Keywords
CD8+ T cellendothelial cell
hantavirus
hantavirus cardiopulmonary syndrome
hemorrhagic fever with renal syndrome
immunopathogenesis
regulatory T cell
Immunity
Immunology and Infectious Disease
Immunology of Infectious Disease
Infectious Disease
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We previously hypothesized that increased capillary permeability observed in both hantavirus cardiopulmonary syndrome (HCPS) and hemorrhagic fever with renal syndrome (HFRS) may be caused by hantavirus-specific cytotoxic T cells attacking endothelial cells presenting viral antigens on their surface based on clinical observations and in vitro experiments. In HCPS, hantavirus-specific T cell responses positively correlated with disease severity. In HFRS, in one report, contrary to HCPS, T cell responses negatively correlated with disease severity, but in another report the number of regulatory T cells, which are thought to suppress T cell responses, negatively correlated with disease severity. In rat experiments, in which hantavirus causes persistent infection, depletion of regulatory T cells helped infected rats clear virus without inducing immunopathology. These seemingly contradictory findings may suggest delicate balance in T cell responses between protection and immunopathogenesis. Both too strong and too weak T cell responses may lead to severe disease. It is important to clarify the role of T cells in these diseases for better treatment (whether to suppress T cell functions) and protection (vaccine design) which may need to take into account viral factors and the influence of HLA on T cell responses.Source
Viruses. 2011 Jul;3(7):1059-73. doi: 10.3390/v3071059. Epub 2011 Jul 6. Link to article on publisher's siteDOI
10.3390/v3071059Permanent Link to this Item
http://hdl.handle.net/20.500.14038/35020PubMed ID
21994770Related Resources
Link to Article in PubMedRights
© 2011 by the authors; licensee MDPI, Basel, Switzerland.Distribution License
http://creativecommons.org/licenses/by/3.0/ae974a485f413a2113503eed53cd6c53
10.3390/v3071059
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Except where otherwise noted, this item's license is described as © 2011 by the authors; licensee MDPI, Basel, Switzerland.