Abstract

The human Herpes viruses lead a life of peaceful co-existence with their host, until these viruses are reactivate from their latent state. Even though most individuals are immune to these viruses, production of new virus can nonetheless occur. Generally, this ability of the virus to do so is attributed to specific gene functions that allow the virus infected cell to become temporarily invisible to the immune system. We intend to investigate, using biochemical, cell-biological and molecular biological methods, the mechanisms by which three human Herpes viruses may do so: Varicella Zoster Virus, Human Herpesvirus-6 and human Herpesvirus-7. In addition, using the technique of gene targeting, we shall construct in animal model for HSV-1 and -2.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Research Program Projects (P01)
Project #
7P01AI042257-02
Application #
6100187
Study Section
Project Start
1998-09-01
Project End
1999-08-31
Budget Start
1997-10-01
Budget End
1998-09-30
Support Year
2
Fiscal Year
1998
Total Cost
Indirect Cost

  Institution

Name
Immune Disease Institute, Inc.
Department
Type
DUNS #
115524410
City
Boston
State
MA
Country
United States
Zip Code
02115

  Publications

Sen, Jayita; Liu, Xueqiao; Roller, Richard et al. (2013) Herpes simplex virus US3 tegument protein inhibits Toll-like receptor 2 signaling at or before TRAF6 ubiquitination. Virology 439:65-73
Brockman, Mark A; Verschoor, Admar; Zhu, Jia et al. (2006) Optimal long-term humoral responses to replication-defective herpes simplex virus require CD21/CD35 complement receptor expression on stromal cells. J Virol 80:7111-7
Zhao, Xinyan; Deak, Eszter; Soderberg, Kelly et al. (2003) Vaginal submucosal dendritic cells, but not Langerhans cells, induce protective Th1 responses to herpes simplex virus-2. J Exp Med 197:153-62
Verschoor, Admar; Brockman, Mark A; Gadjeva, Mihaela et al. (2003) Myeloid C3 determines induction of humoral responses to peripheral herpes simplex virus infection. J Immunol 171:5363-71
Tirabassi, Rebecca S; Ploegh, Hidde L (2002) The human cytomegalovirus US8 glycoprotein binds to major histocompatibility complex class I products. J Virol 76:6832-5
Furman, Margo H; Dey, Neelendu; Tortorella, Domenico et al. (2002) The human cytomegalovirus US10 gene product delays trafficking of major histocompatibility complex class I molecules. J Virol 76:11753-6
Lorenzo, Mayra E; Jung, Jae U; Ploegh, Hidde L (2002) Kaposi's sarcoma-associated herpesvirus K3 utilizes the ubiquitin-proteasome system in routing class major histocompatibility complexes to late endocytic compartments. J Virol 76:5522-31
Furman, Margo H; Ploegh, Hidde L; Tortorella, Domenico (2002) Membrane-specific, host-derived factors are required for US2- and US11-mediated degradation of major histocompatibility complex class I molecules. J Biol Chem 277:3258-67
Furman, Margo H; Ploegh, Hidde L (2002) Lessons from viral manipulation of protein disposal pathways. J Clin Invest 110:875-9
Karpova, Alla Y; Trost, Maren; Murray, John M et al. (2002) Interferon regulatory factor-3 is an in vivo target of DNA-PK. Proc Natl Acad Sci U S A 99:2818-23

Showing the most recent 10 out of 19 publications