Accession Number : ADB104013

Title :   Togavirus-Specific Immune Effector Mechanisms.

Descriptive Note : Annual progress rept. 1 Jan-31 Dec 83,

Corporate Author : MARYLAND UNIV BALTIMORE SCHOOL OF MEDICINE

Personal Author(s) : Cole, Gerald A. ; Schmaljohn, Alan L.

Report Date : DEC 1983

Pagination or Media Count : 56

Abstract : Interactions between alphaviruses, antibodies, and cells were examined as part of an overall effort to characterize relevant antigens and immune effector mechanisms. Antibody-dependent complement(C')-dependent cytolysis was sed to demonstrate that alphaviruses induce serum antibodies capable of lysing cells infected with heterologous alphavirus species. Similar ross-reactive antibodies were sought, with partial success, in our existing battery of monoclonal (MC) antibodies prepared against the Sindbis virus (SIN) envelope glycoproteins, E1 and E2. Only two MC antibodies were found to react not only with SIN and western equine encephalitis virus (WEE) but with Venezuelan equine encephalitis virus (VEE) and Semliki Forest virus (SF); these El-specific MC antibodies mediated C'-dependent lysis of VEE-infected cells and one protected mice against lethal VEE challenge. Neither lysed SF-infected cells and the one tested in vivo did not protect against SF challenge. MC antibodies were used to determine topographical relationships among viral epitopes bound by protective MC antibodies. A sandwich (antigen-captue) enzyme-linked immunosorbent assay (ELISA) was used to detect nanogram quantities of SIN antigen and to distinguish between epitopes on virion surfaces and those that became inaccessible to antibodies during viral morphogenesis at the cell surface.

Descriptors :   *IMMUNOLOGY, *ARBOVIRUSES, *ANTIBODIES, *CELLS(BIOLOGY), INTERACTIONS, SINDBIS VIRUS, NEUTRALIZATION, TISSUE CULTURE CELLS, ANTIGENS, LYSIS, PATHOGENESIS, WESTERN EQUINE ENCEPHALOMYELITIS VIRUS, VENEZUELAN EQUINE ENCEPHALOMYELITIS VIRUS, SEMLIKI VIRUS.

Subject Categories : Medicine and Medical Research
      Microbiology

Distribution Statement : APPROVED FOR PUBLIC RELEASE