Boyd Professor and Head

Contact Information:
Email: docall@lsuhsc.edu
Office Phone: 318-675-5750
Laboratory Phone: 318-675-5759
Office Fax: 318-675-5764

Education/Training:
Postdoctoral Study, University of Alberta Medical Center
Ph.D., 1968, University of Mississippi Medical Center
B.S., 1962, Biology and Chemistry, Loyola University - New Orleans

Major Research Interests:  
Herpesvirus Gene Regulation, Persistent Infection, and Pathogenesis

Herpesvirus infection usually results in cell death and production of virus, but may result in persistent infection.  Using equine herpesvirus as a model, we seek to identify which of the 78 herpesviral genes and proteins play a role in gene regulation and in mediating persistent infection and the molecular mechanisms involved.  Using technologies such as recombinant DNA, gene cloning, molecular hybridization, in vitro translation, DNA microarrays, DNA sequencing, site-specific mutagenesis, PCR, transactivation assays and expression vector technology, we are determining the functions of the regulatory genes of both the viral genome and the genome of defective interfering particles (DIP) that mediate and maintain persistent infection.  Since the DIP genome lacks most viral genes and contains hybrid forms of regulatory genes, elucidation of the alterations in viral gene regulation may reveal the molecular events required for persistent infection.

Representative Publications:

Albrecht, R. A., S. K. Kim, Y. Zhang, Y. Zhao, and D. J. O'Callaghan. 2004. The equine herpesvirus 1 EICP27 protein enhances gene expression via an interaction with TATA box-binding protein . Virology 324:311-326.

Kim, S. K. R. A. Albrecht, and D. J. O'Callaghan. 2004. A negative regulatory element (bp -204 to -177) of the EICP0 promoter of equine herpesvirus 1 abrogates the EICP0 protein's trans-activation of its own promoter. J. Virol. 78:11696-11706.

Frampton, A. R., W. F. Goins, J. B. Cohen, N. Osterrieder, D. J. O'Callaghan, and J. C. Glorioso. 2005. Equine herpesvirus type 1 (EHV-1) utilizes a novel herpesvirus entry receptor. J. Virol. 79: 3169-3173.

Smith, P. M., S. M. Kahan, C. B. Rorex, J. von Einem, N. Osterrieder, and D. J. O'Callaghan. 2005. Expression of the full length form of gp2 of equine herpesvirus 1 (EHV-1) completely restores respiratory virulence to the attenuated EHV-1 strain KyA in CBA mice J. Virol . in press.

Albrecht, R. A., S. K. Kim, and D. J. O'Callaghan. 2005. The EICP27 protein of equine herpesvirus 1 is recruited to viral promoters by its interaction with the immediate-early protein. Virology 333: 74-87.

Buczynski, K., S. K. Kim, and D. J. O'Callaghan. 2005. Initial characterization of 17 viruses harboring mutant forms of the immediate-early gene of equine herpesvirus 1 Virus Genes 31: 229-239.

Ebner, P. D. and D. J. O'Callaghan. 2006. Genetic complexity of EHV-1 DI particles and identification of novel EICP22/EICP27 hybrid proteins produced during persistent infection. Virus Genes 32:313-320.

von Einem, J., D. Schumacher, D. J. O'Callaghan, and N. Osterrieder. 2006. The a-TIF (VP16) homologue (ETIF) of equine herpesvirus 1 (EHV-1) is essential for secondary envelopment and virus egress . J. Virol . 80: 2609-2620.

Kim, S. K., C. B. Ahn, R. A. Albrecht, and D. J. O'Callaghan. 2006. The unique IR2 protein of equine herpesvirus 1 (EHV-1) negatively regulates EHV-1 gene expression. J. Virol. 80: 5041-5049.

von Einem, J., P.M. Smith, G.R. Van de Walle, D.J. O'Callaghan, and N. Osterrieder.  2007.  In vitro and In vivo characterization of equine herpesvirus 1 (EHV-1) mutants devoid of the viral chemokine-binding glycoprotein G (gG).  Virology 362: 151-162.

Ahn, B.C., J. E. Breitenbach, S. K. Kim, and D. J. O’Callaghan.  2007. The equine herpesvirus-1 IR3 gene that lies antisense to the sole immediate-early (IE) gene is trans-activated by the IE protein, and is poorly expressed to a protein.  Virology 363: 15 – 25.

O'Callaghan, D. J . and N. Osterrieder. 2007. Equine Herpesviruses . Encyclopedia of Virology. 3rd. B. Mahy and M. Van Regenmortel (ed.) Elsevier Publishing Co., Oxford, UK. in press.