Daniel J.J. Carr, Ph.D. Associate Professor of Ophthalmology, Microbiology and Immunology Ph.D.: University of Texas Medical Branch, Galveston, TX. Pre OUHSC: LSU Health Sciences Center at New Orleans; University of Alabama at Birmingham Research: Neuroimmunology; ocular immunology; the use of gene therapy in infectious diseases; the immune response to viral infection focusing on herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2); the effects of stress and hormones on immune function.
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Research Interests: |
The main interest of my laboratory is focused on the host response to infectious pathogens using the neurotropic HSV-1 and HSV-2 herpesviruses as the prototypic pathogens. HSV-1 and HSV-2 are highly successful viruses that evade the immune response to establish a life-long latent infection in neurons and satellite cells of the peripheral and central nervous systems. One goal is to identify those immune mediators that antagonize virus replication and trafficking to the nervous system during the acute infection and reactivation of latent virus. To this end, my laboratory is focusing on two key elements of innate immunity: type I interferon (IFN) and chemokines. Specifically, using a gene therapy approach in the ectopic expression of type I IFNs, we are characterizing the anti-viral efficacy of the IFN transgenes against HSV-1 infection in primary cell cultures and in vivo. Along these lines, we are also in the process of developing alternative delivery systems to target transgene expression in specific tissues. Likewise, we are investigating the role of chemokines and their receptors in the inflammatory process of ocular and genital infection with HSV-1 and HSV-2 respectively focusing on two key chemokines, CXCL9 and CXCL10 as well as the chemokine receptor, CXCR3. Employing transgenic and knockout mice as well as chimeric animals, we plan to define the importance of each of these chemokines in innate immunity as well as the adaptive immune response to virus infection.
H.H. Garza Jr. (1991-1995), currently in private business (Hebronville, TX)
William P. Halford (1992-1996), currently a Assistant Professor of Veterinary Molecular Biology, Montana State University, Bozeman, MT)
Sansanee Noisakran (1995-2000); currently a senior postdoctoral fellow (National Center for Genetic Engineering and Biotechnology, Bangkok, Thailand)
Khaldun Al-khatib (2001-2004); currently a resident in Internal Medicine (Baylor College of Medicine, Houston, TX)
Recent publications (taken from 90 peer-reviewed articles):
Wuest, T., Austin, B.A., S. Uematsu, M. Thapa, S. Akira, and D.J.J. Carr. 2006. Intact TLR 9 and type I interferon signaling pathways are required to augment HSV-1 induced corneal CXCL9 and CXCL10. J. Neuroimmunol. 179:46-52.
Carr, D.J.J. and I.L. Campbell. 2006. Herpes simplex virus type 1 induction of chemokine production is unrelated to virus load in the cornea but not nervous system. Viral Immunol. 19:741-746.
Wuest, T., J. Farber, A. Luster, and D.J.J. Carr. 2006. CD4+ T cell migration into the cornea is reduced in CXCL9 deficient but not CXCL10 deficient mice following herpes simplex virus type 1 infection. Cell. Immunol. 243:83-89.
Thapa, M., W.A. Kuziel, and D.J.J. Carr. 2007. Susceptibility of CCR5 deficient mice to genital herpes simplex virus type 2 is linked to NK cell mobilization. J. Virol. 81:3704-3713.
Austin, B.A., W.P. Halford, B.R.G. Williams, and D.J.J. Carr. 2007. OAS/PKR pathways and a/b TCR+ T cells are required for Ad:IFN-g inhibition of HSV-1 in cornea. J. Immunol. 178:5166-5172.
Last edited 8/22/08
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