OHSU

Klaus Früh, Ph.D.

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Background

Our immune system is extremely efficient at fighting off viruses, yet some viruses are able to overcome innate or adaptive immune response mechanisms and create disease. We study the molecular mechanisms used by viruses to evade host immune responses. Most acute viral infections are eventually cleared by the immune system and generate long-lasting immunity. However, such viruses might cause significant morbidity, or even death in some instances. Examples of such viruses are flaviruses (Dengue, West Nile and Yellow Fever virus) and poxviruses (smallpox and monkeypoxvirus). However, other viruses establish a chronic infection whereby a balance is established in which the host's immune system controls, but is unable to eradicate the virus. Such viruses are often asymptomatic in immune competent individuals but cause disease upon immune suppression, e.g. in AIDS patients. Examples of such chronic infections are viruses of the herpesvirus family, e.g. cytomegalovirus and Kaposi’s sarcoma herpesvirus. Large DNA viruses, such as poxviruses and herpesviruses, encode numerous, often host-related, modulators of the host’s immune response whereas small RNA viruses, such as flaviviruses, have a limited set of immune modulators but might additionally escape immune control by mutation. Our research aims at identifying the function of such viral gene products as well as their related host gene products. We are particularly interested in human and rhesus cytomegalovirus (CMV), Kaposi’s sarcoma herpesvirus (KSHV), West Nile Virus and the orthopoxviruses Cowpoxvirus and Monkeypoxvirus. To characterize how these viruses manage to escape or delay immunity we apply the whole arsenal of modern molecular biology, functional genomics, genetics, cell imaging and in vivo models. Stripping viruses of their stealth mechanisms will be a new approach to anti-viral therapy and vaccine development. Additionally, viral immune modulatory protein can be used to modulate unwanted auto-immune responses.


Summary of Current Research

Following undergraduate studies at the University of Konstanz and the University of Heidelberg, Dr. Klaus Früh received his Ph.D. from the University of Heidelberg in 1990 studying the immune response to the malaria parasite. He then spent four years as a postdoctoral fellow: one year at the Center for Molecular Biology in Heidelberg and three years at the Scripps Research Institute in La Jolla, CA where he studied molecular pathways of antigen presentation. Dr. Früh then became a Senior Scientist at the R.W. Johnson Pharmaceutical Research Institute, eventually becoming the Group Leader for Molecular Virology at the same company. During this time he developed research programs in viral immune modulation and in antiviral drug discovery. He joined OHSU in 2000 as an Associate Scientist at the VGTI and as Director of the Gene Microarray Shared Resource. Dr. Früh became full Professor for Microbiology and Immunology in 2006.


Selected Publications

"Cowpox virus protein CPXV012 eludes CTLs by blocking ATP binding to TAP," Journal of Immunology (Vol: 193, Issue: 4, Page 1578-1589) - 2014

"Cytomegalovirus pp65 limits dissemination but is dispensable for persistence," Journal of Clinical Investigation (Vol: 124, Issue: 5, Page 1928-1944) - 2014

"Inhibition of dengue virus replication by a class of small-molecule compounds that antagonize dopamine receptor d4 and downstream mitogen-activated protein kinase signaling," Journal of Virology (Vol: 88, Issue: 10, Page 5533-5542) - 2014

"T Cell Inactivation by Poxviral B22 Family Proteins Increases Viral Virulence," PLoS Pathogens (Vol: 10, Issue: 5, ) - 2014

"Comprehensive analysis of varicella-zoster virus proteins using a new monoclonal antibody collection," Journal of Virology (Vol: 87, Issue: 12, Page 6943-6954) - 2013

 

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Contact

  Email Klaus Früh

503 494-8311

Memberships & Associations

American Association for the Advancement of Science; American Society for Microbiology; Deutsche Gesellschaft für Virologie