David Camerini
Molecular Biology & Biochemistry
School of Biological Sciences
Phone: (949) 824-3381
Email: dcamerin@uci.edu
http://www.faculty.uci.edu/scripts/UCIFacultyProfiles/detailMBB.cfm?ID=4930
http://www.faculty.uci.edu/profile.cfm?faculty_id=4930
David Camerini
Dr. Camerini’s group has studied virus host interactions of the important human pathogen, HIV-1, for many years. Host immunosuppression by HIV-1 leads to a variety of malignancies including Kaposi’s sarcoma and central nervous system lymphoma. The current focus includes the determinants and mechanisms of pathogenesis in CCR5 tropic patient isolates of HIV-1, the role of novel epithelial beta-defensins in innate anti-HIV-1 immunity and the mechanism of viral cDNA synthesis. They are studying the mechanisms of cell killing by HIV-1 and the contributions of the envelope, nef and vpr genes to viral replication and cytopathic effects in normal human T cells and lymphoid tissues. The role of epithelial cell derived beta-defensins in combating HIV-1, is being studied by producing predicted mature forms of these anti-microbial peptides and testing their efficacy and mechanisms of action in normal human T cells and lymphoid tissues. Dr. Camerini’s group is also testing the hypothesis that HIV-1 cDNA synthesis proceeds via a genomic RNA lariat formed by the host spliceosome and resolved by the host RNA debranching enzyme. Their data support this hypothesis, indicating that many previously unknown intracellular interactions of the HIV-1 reverse transcription complex with human RNA splicing complexes and associated factors will be characterized. These data will provide new opportunities to disrupt HIV-1 replication and the development of AIDS. Moreover, a lariat intermediate may be relevant to the replication of other retroviruses that cause cancer including the human T cell leukemia virus (HTLV).
Selected Publications:
Zimmerman, E. S., Chen, J., Andersen, J. L., Ardon, O., Dehart, J. L., Blackett, J., Choudhary, S. K., Camerini, D., Nghiem, P., and Planelles, V. (2004). Human immunodeficiency virus type 1 Vpr-mediated G2 arrest requires Rad17 and Hus1 and induces nuclear BRCA1 and gamma-H2AX focus formation. Mol Cell Biol 24(21), 9286-94.
Ye, Y., De Leon, J., Yokoyama, N., Naidu, Y., and Camerini, D. (2005). DBR1 siRNA inhibition of HIV-1 replication. Retrovirology 2, 63.
Choudhary, S. K., Choudhary, N. R., Kimbrell, K. C., Colasanti, J., Ziogas, A., Kwa, D., Schuitemaker, H., and Camerini, D. (2005). R5 human immunodeficiency virus type 1 infection of fetal thymic organ culture induces cytokine and CCR5 expression. J Virol 79(1), 458-71.
Parsons, C. H., Adang, L. A., Overdevest, J., O'Connor, C. M., Taylor, J. R., Jr., Camerini, D., and Kedes, D. H. (2006). KSHV targets multiple leukocyte lineages during long-term productive infection in NOD/SCID mice. J Clin Invest 116(7), 1963-73.
Choudhary, S. K., Vrisekoop, N., Jansen, C. A., Otto, S. A., Schuitemaker, H., Miedema, F., and Camerini, D. (2007). Low immune activation despite high levels of pathogenic human immunodeficiency virus type 1 results in long-term asymptomatic disease. J Virol 81(16), 8838-42.
Olivieri, K., Scoggins, R. M., Bor, Y. C., Matthews, A., Mark, D., Taylor, J. R., Jr., Chernauskas, D., Hammarskjold, M. L., Rekosh, D., and Camerini, D. (2007). The envelope gene is a cytopathic determinant of CCR5 tropic HIV-1. Virology 358(1), 23-38. |
