T cells and pathogenesis of hantavirus cardiopulmonary syndrome and hemorrhagic fever with renal syndrome
UMass Chan AffiliationsDivision of Infectious Diseases and Immunology, Department of Medicine
Center for Infectious Disease and Vaccine Research
Document TypeJournal Article
KeywordsCD8+ T cell
hantavirus cardiopulmonary syndrome
hemorrhagic fever with renal syndrome
regulatory T cell
Immunology and Infectious Disease
Immunology of Infectious Disease
MetadataShow full item record
AbstractWe 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.
SourceViruses. 2011 Jul;3(7):1059-73. doi: 10.3390/v3071059. Epub 2011 Jul 6. Link to article on publisher's site
Permanent Link to this Itemhttp://hdl.handle.net/20.500.14038/35020
Related ResourcesLink to Article in PubMed
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Except where otherwise noted, this item's license is described as © 2011 by the authors; licensee MDPI, Basel, Switzerland.