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Michael Gale Jr., Ph.D.

Email: 
Office: 
750 Republican Street, E383 Seattle WA 98109
Phone: 
(206) 543-8514

Lab Staff

Aimee Sekine
Alison Kell
Amina Negash
Amy Stone
Andrey Shuvarikov
Connor Driscoll
Emily Hemann
Elise Smith
Elyse Dewey
Frank Fernandez
Jackie Berhorst
Jean Chang
Jen Rathe
Jenny Go
Justin Roby
Katharina Esser-Nobis
Kathleen Voss
Kathryn Wuertz
Kwan Chow
Lauren Aarreberg
Lynn Law
Marian Fairgrieve
Megan Knoll
Michael Davis
Michelle Noval
Nanette Crochet
Rebecca Olson
Renee Ireton
Richard Green
Sunil Thomas
Tien-Ying Hsiang
Yueh-Ming Loo
CIIID Leadership
CIIID Member
Michael Gale Jr., Ph.D.
CIIID Director | Signaling and PAMP Cores Leader | Professor, Immunology | Adjunct Professor, Microbiology & Global Health | Member, FHCRC/UW Cancer Consortium | Affiliate Investigator, Clinical Research Division & Virus and Infectious Disease Division, Fred Hutchinson Cancer Research Center | CERID Co-Director

Research in the Gale laboratory is focused on understanding innate immunity to virus infection, and the intracellular immune processes and virus-host interactions that govern viral replication and infection outcome. The laboratory is a component of the Hepatitis C virus Cooperative Research Centers supported by the NIH, and also conducts programs of study focused on understanding immune control of West Nile virus infection, HIV infection, and the immunomodulatory/antiviral actions of interferons and small molecule inhibitors of virus replication.

Virus infection of mammalian cells triggers an intracellular immune response, termed the “innate immune response” that functions to suppress replication and spread of the virus. During infection specific motifs within viral products are recognized as pathogen associated molecular patterns (PAMPs) by cellular factors called pathogen recognition receptors (PRRs). Studies in the Gale laboratory have defined the retinoic acid-inducible gene I (RIG-I) as the major PRR that triggers immunity against hepatitis C virus and a variety of pathogenic RNA viruses. Accumulating evidence now indicates that immunity against RNA viruses is largely triggered through the PRR actions of RIG-I and/or a related protein called MDA5. RIG-I and MDA5 are cytosolic RNA helicase and are expressed at a low levels in most cells. During virus infection RIG-I or MDA5 bind to RNA PAMP motifs of viral genome or viral RNA replication products generated by specific viruses. RIG-I binding of viral RNA triggers its downstream signaling to induce the activation of latent transcription factors and the eventual production of alpha/beta interferons and expression of interferon-stimulated genes. These processes induce the innate immune response that serves to limit virus replication and spread. Many viruses direct actions of immune evasion through regulation of innate immune signaling and function. Our studies have linked the course of virus infection to regulation of innate immune processes, and have identified novel interactions as therapeutic targets for the intervention of infection.

Hepatitis C virus

Description: The figure depicts hepatitis C virus.
Innate Immune signaling by RNA viruses. Michael Gale Jr. et al. (2005) Nature 436: 939-940)

University of Washington
Kineta
Fred Hutchinson Cancer Research Center
UW Immunology