MECHANISM OF THE H-2 EFFECT OF VIRAL LEUKEMOGENESIS
Project Number5R01CA019931-15
Contact PI/Project LeaderLILLY, FRANK
Awardee OrganizationALBERT EINSTEIN COLLEGE OF MEDICINE
Description
Abstract Text
Resistance to pathogenic agents such as retroviruses may be genetic
or acquired. We propose studies of the erythroleukemic disease of mice
induced by the complex Friend strain (FV) of mouse leukemia virus (MuLV)
in which both types of resistance can be observed and appear to depend in
part on similar underlying immunologic mechanisms involving the major
histocompatibility complex of the mouse, H-2. Our findings may serve as
models for the study of analogous aspects of HIV disease.
Mice of certain genotypes that differ in the D region of H-2
show markedly different levels of genetic susceptibility or resistance to
FV, but the mechanism of this presumably immunologic effect has never
been definitively demonstrated. In particular, we will study the
mechanisms whereby H-2 haplotypes that confer resistance to FV in
homozygous mice no longer do so in congenic heterozygotes. We propose
studies of this effect that will precisely identify the D region genes
involved by the use of genetic mapping with recombinant and mutant H-2
haplotypes, by the analysis of relevant strains of transfected cells and
of transgenic mice and by studies based on the known properties of genes
mapping in this region. We will also study aspects of the cellular
immune response to FV that appear critical in the development of acquired
resistance to the virus. We will identify specific amino acid sequences
in the viral gag/pol and env genes that, together with H-2D region gene
products, constitute the structures seen by FV-specific cytotoxic T
lymphocytes (CTL). We will develop virus-related RNA constructs that are
defective for replication and nonpathogenic but enriched for the
determinants of the epitopes recognized by CTL that we will have
identified. We will package these epitope-enriched constructs in FV
particles which should then be able to generate a strong immune response
in host mice both by stimulation of the class II H-22 gene-restricted
pathway for antigen presentation and by stimulation of the class I H-22
gene-restricted endogenous pathway. The efficacy of these agents as
candidate vaccines will be determined.
Public Health Relevance Statement
Data not available.
NIH Spending Category
No NIH Spending Category available.
Project Terms
Friend virusMHC class I antigenantigen presentationbone marrow transplantationcellular immunitycytotoxic T lymphocyteerythroleukemiagenetic mappinggenetically modified animalslaboratory mousemajor histocompatibility complexmicroorganism immunologytissue /cell culturetissue mosaicismtransfectionviral leukemogenesisvirus RNAvirus antigen
No Sub Projects information available for 5R01CA019931-15
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