This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The projected need for Indian rhesus macaques for AIDS-related research exceeds availability from current domestic breeding programs and there is an urgent need to expand breeding programs for Indian rhesus macaques for future AIDS vaccine and pathogenesis studies. Further, rhesus macaques with defined histocompatibility complex genotypes and known pedigree are becoming increasingly important for research to understand the biologic variation in the immune response. The long-term objective of this application is to expand the Oregon Regional Primate Center's specific pathogen-free Indian rhesus resource and sufficiently characterize their MHC haplotype to permit selected pedigree breeding for MHC class I alleles useful in AIDS research.
The specific aims for accomplishing these objectives include intensively managing a subpopulation of the Center's SPF Indian rhesus macaque breeding colony to maximize production of genetically diverse females to expand the breeding capacity of the colony. Selective breeding of MHC-typed animals will be used to enhance production of future breeder males that are homozygous for the MAMU-A 01 allele, an important allele for assessing virus-specific cell-mediated immune function in simian immunodeficiency virus vaccine models for preventing AIDS virus infection. Breeder males that are homozygous for the MAMU-A 01 allele can be used to efficiently produce large numbers of offspring carrying the desired allele without inbreeding. The breeding colony will be initially typed for eight MHC alleles and managed for the production of MHC-defined offspring of known parentage. New sheltered field cage housing is proposed to protect the animals from infectious agents in the environment.
|Jaworski, J Pablo; Kobie, James; Brower, Zachary et al. (2013) Neutralizing polyclonal IgG present during acute infection prevents rapid disease onset in simian-human immunodeficiency virus SHIVSF162P3-infected infant rhesus macaques. J Virol 87:10447-59|
|Hansen, Scott G; Powers, Colin J; Richards, Rebecca et al. (2010) Evasion of CD8+ T cells is critical for superinfection by cytomegalovirus. Science 328:102-6|
|Okoye, Afam; Park, Haesun; Rohankhedkar, Mukta et al. (2009) Profound CD4+/CCR5+ T cell expansion is induced by CD8+ lymphocyte depletion but does not account for accelerated SIV pathogenesis. J Exp Med 206:1575-88|
|Murray, Shannon M; Picker, Louis J; Axthelm, Michael K et al. (2008) Replication in a superficial epithelial cell niche explains the lack of pathogenicity of primate foamy virus infections. J Virol 82:5981-5|
|Price, David A; Bitmansour, Arlene D; Edgar, John B et al. (2008) Induction and evolution of cytomegalovirus-specific CD4+ T cell clonotypes in rhesus macaques. J Immunol 180:269-80|
|Okoye, Afam; Meier-Schellersheim, Martin; Brenchley, Jason M et al. (2007) Progressive CD4+ central memory T cell decline results in CD4+ effector memory insufficiency and overt disease in chronic SIV infection. J Exp Med 204:2171-85|
|Margolin, David H; Saunders, Erika H; Bronfin, Benjamin et al. (2006) Germinal center function in the spleen during simian HIV infection in rhesus monkeys. J Immunol 177:1108-19|
|Murray, S M; Picker, L J; Axthelm, M K et al. (2006) Expanded tissue targets for foamy virus replication with simian immunodeficiency virus-induced immunosuppression. J Virol 80:663-70|
|Picker, Louis J; Reed-Inderbitzin, Edward F; Hagen, Shoko I et al. (2006) IL-15 induces CD4 effector memory T cell production and tissue emigration in nonhuman primates. J Clin Invest 116:1514-24|
|Picker, Louis J; Hagen, Shoko I; Lum, Richard et al. (2004) Insufficient production and tissue delivery of CD4+ memory T cells in rapidly progressive simian immunodeficiency virus infection. J Exp Med 200:1299-314|
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