Accession Number : ADA181718
Title : Human Immune Responses to Dengue Viruses.
Descriptive Note : Final rept. 1 Sep 82-30 Jun 86,
Corporate Author : MASSACHUSETTS UNIV MEDICAL CENTER WORCESTER MA
Personal Author(s) : Ennis,Francis A
PDF Url : ADA181718
Report Date : 01 Aug 1986
Pagination or Media Count : 70
Abstract : The purpose of this contract was to analyze the immune responses to dengue infections. During the past few years we have focused on three immune responses; lysis of dengue virus-infected cells by peripheral blood mononuclear cells (PBMC) of non-immune donors; antibody-dependent complement-mediated lysis of dengue virus-infected cells; and interferon induction from PBMC by dengue virus. Results indicate that both PBMC-mediated cytotoxicity and antibody-dependent cell-mediated cytotoxicity (ADCC) can cause significant lysis of dengue-infected Raji cells; The PBL (Peripheral Blood Lymphocytes) that are active in lysing dengue virus-infected cells are heterogeneous and are contained in Leu11+ and T3+ susets. Results also indicated that PBL produced IFN in response on dengue virus-infected cells and that the production of IFN by PBL is due to stimulation of PBL by dengue virus-infected cells. The ability of dengue in infected cells. Treatment of monocytes with IFN decreased the yield of infectious virus more than 99% and the percentage of dengue-antigen positive cells by 98%. These results suggest that IFNs produced by PBL in response to dengue virus-infected cells may have an important role in controlling dengue infection and in the pathogenesis of dengue hemorrhagic fever and shock syndrome.
Descriptors : *DENGUE, *IMMUNITY, *INTERFERON, BLOOD, BLOOD CELLS, CELLS(BIOLOGY), DONORS(MEDICINE), FEVERS, GROUP B ARBOVIRUSES, HEMORRHAGIC FEVERS, HUMANS, IMMUNOLOGY, INDUCTION SYSTEMS, INFECTIOUS DISEASES, LYMPHOCYTES, LYSIS, MONOCYTES, NUCLEI, PATHOGENESIS, PRODUCTION, RESPONSE(BIOLOGY), SHOCK(PATHOLOGY), SIGNS AND SYMPTOMS, VIRUSES, YIELD, STIMULATION(PHYSIOLOGY)
Subject Categories : Medicine and Medical Research
Distribution Statement : APPROVED FOR PUBLIC RELEASE