Virology
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Clyde S. Crumpacker, Ph.D.

Professor of Medicine

Beth Israel Deaconess Med Ctr
Div. of Infectious Disease
330 Brookline Avenue, Da-617
Boston, MA 02215
Tel: 617-667-5863
Fax: 617-667-5541
email:ccrumpac@caregroup.harvard.edu
6 postdoctoral fellows, 3 graduate students

 

  

Our laboratory efforts are committed to the development of effective antiviral therapies for herpes viruses and human immunodeficiency virus (HIV-1). In particular, we are focusing on the mechanisms of new antiviral therapies, the structure and function of viral targets, and the mechanisms of resistance. During the past two years we have cloned and expressed the HSV DNA polymerase enzyme and employed this system to show that another HSV protein, the 65 kilodalton DNA binding protein can interact to stimulate the polymerase by 7-10-fold. This interaction provides a new potential site for antiviral activity, and we are actively exploring the precise mechanism of interactions between these two proteins.

Resistance of HIV-1 to antiviral drugs is becoming a major block to effective antiviral therapy for AIDS. We have shown that treatment with AZT can be associated with resistance to AZT and ddl. The reverse transcriptase gene of HIV-1 clinical isolates is being cloned and sequenced to define the mutations responsible for resistance in HIV. We have developed new molecular approaches to study resistance in HIV and CMV involving nucleic acid hybridization and these are being employed to study clinical viral isolates. The pathogenesis of herpes viruses and HIV are also being explored through studies on diseases caused by resistant viruses and the mechanisms of how HIV inhibits bone marrow proliferation.

 

References:

  1. Crumpacker C.S. 1989. Molecular Targets of Antiviral Therapy. N. Engl. J. Med.; 321:163-172.
  2. Chatis PA, Crumpacker CS 1991. Analysis of the Thymidine Kinase Gene From Clinically Isolated Acyclovir Resistant Herpes Simplex Virus. Virology; 180:793-797.
  3. Japour AJ, Chatis PA, Eigenrauch HA, Crumpacker CS 1991. Detection of Human Immunodeficiency Virus Type 1 Clinical Isolates with Reduced Sensitivity to Zidovudine and Dideoxyinosine by RNA-RNA Hybridization. Proc Nat Acad Sci, USA.; 88:3072-3076.