DANIEL J. J. CARR, Ph.D.
Currently, the lab is investigating the host response to ocular herpes simplex virus type 1 (HSV-1) and genital herpes simplex virus type 2 (HSV-2) using mouse models. The primary focus involves the role of chemokines in the initiation of the host response following infection concentrating on a family of chemokines that operate exclusively through the chemokine receptor CXCR3. In addition, we are also investigating the anti-viral action of type I and type II interferons (IFNs) and the potential use of these endogenous cytokines in controlling HSV-1 reactivation. Delivery vehicles for the IFN transgenes include viral vectors as well as nanoparticles. Moreover, we are also incorporating a discovery proteomic approach to identify novel proteins that are specifically up- or down-regulated by the type I or type II IFNs associated with the anti-viral effect. These projects involve the development and use of transgenic and targeted gene disruption mice as well as chimeras. In a related project, we have also initiated a study to determine changes in innervation patterns within the cornea as they relate to infection. Ultimately, we would like to identify novel pathways or molecules that we can then target to dampen or block virus replication, reactivation, and induction of inflammatory events that lead to collateral and unwarranted tissue damage.
Full CV can be accessed here.
|B.S.||1983||Southern Methodist University, Dallas, Biology|
|Ph.D.||1987||University of Texas Medical Branch, Galveston, Microbiology|
|Post-Doctoral||1989||University of Alabama-Birmingham, Physiology & Biophysics|
|Assistant Professor||1991||LSU Medical Center, New Orleans, Microbiology, Immunology & Parasitology|
|Associate Professor||1997||LSU Medical Center, New Orleans, Microbiology, Immunology & Parasitology|
|Associate Professor||1999||University of Oklahoma Health Sciences Center, Ophthalmology and Microbiology & Immunology|
R01 AI053108 The Neuroimmunology of Viral Infections. 04/01/03 – 03/31/10.
R01 AI067309 The Role of CXCL9 in Genital HSV-2 Infection 07/01/0 –06/30/10
Al-Khatib, K., B.R.G. Williams, R.H. Silverman, W. Halford, and D.J.J. Carr. 2005. Dichotomy between survival and lytic gene expression in RNase L- and PKR-deficient mice transduced with an adenoviral vector expressing murine IFN-b following ocular HSV-1 infection. Experimental Eye Res. 80:167-173.
Wickham, S., B. Lu, J. Ash, and D.J.J. Carr. 2005. Chemokine receptor deficiency is associated with increased chemokine expression in the peripheral and central nervous systems and increased resistance to herpetic encephalitis. J. Neuroimmunol. 162:51-59.
Carr, D.J.J., R.H. Silverman, I.L. Campbell, and B.R.G. Williams. 2005. PKR is required for IFN-a1 transgene-induced resistance to genital herpes simplex virus type 2. J. Virol. 79:9341-9345.
Austin, B.A., C. James, R.H. Silverman, and D.J.J. Carr. 2005. Critical Role for the OAS/RNase L Pathway in Response to IFN-β During Acute Ocular HSV-1 Infection. J. Immunol. 175:1100-1106.
Carr, D.J.J., J. Ash, T. Lane, and W. Kuziel. 2006. Abnormal immune response of CCR5-deficient mice to ocular infection with herpes simplex virus type 1. J. Gen. Virol. 87:489-499.
Carr, D.J.J., T. Wuest, L. Tomanek, R.H. Silverman, and B.R.G. Williams. 2006. The lack of PKR enhances susceptibility of mice to genital HSV-2 infection. Immunol., 118:520-526.
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.
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. 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. Oligoadenylate synthetase/protein kinase R pathways and ab TCR+ T cells are required for adenovirus vector: IFN-g inhibition of herpes simplex virus-1 in cornea. J. Immunol. 178:5166-5172.