title: T cells and pathogenesis of hantavirus cardiopulmonary syndrome and hemorrhagic fever with renal syndrome.
abstract: 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.
authors: Center for Infectious Disease and Vaccine Research, Division of Infectious Diseases and Immunology, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01655, USA. Masanori.Terajima@umassmed.edu
authors: Masanori
authors: M
authors: Terajima
authors: Francis A
authors: FA
authors: Ennis
mesh_terms: D000818:Animals; D020022:Genetic Predisposition to Disease; D006476:Orthohantavirus / Q000276:immunology*; D018804:Hantavirus Pulmonary Syndrome / Q000235:genetics / Q000276:immunology* / Q000821:virology; D006480:Hemorrhagic Fever with Renal Syndrome / Q000235:genetics / Q000276:immunology* / Q000821:virology; D006801:Humans; D013601:T-Lymphocytes / Q000276:immunology* / Q000821:virology