Microbiology

Stanley Perlman, MD, PhD

Portrait

Professor of Microbiology
Professor of Pediatrics

Contact Information

Office: 3-712 BSB
Iowa City, IA 52242
Office Phone: 319-335-8549

Lab: 3-730 BSB
Iowa City, IA 52242
Phone: 319-335-7576

Email: stanley-perlman@uiowa.edu
Web: Perlman Lab Website
Web: Faculty Focus: Stanley Perlman, MD, PhD

Education

AB, Physics, University of Rochester
PhD, Biophysics, Massachusetts Institute of Technology
MD, Medicine, University of Miami School of Medicine

Fellowship, Massachusetts Institute of Technology
Fellowship, Harvard University
Fellowship, University of Edinburgh, Scotland
Fellowship, Brandeis University
Residency, Children's Hospital Medical Center, Boston
Fellowship, Infectious Diseases, Children's Hospital Medical Center, Boston

Licensure and Certifications

Medical License, Iowa
Medical License, Massachusetts
American Board of Pediatrics

Education/Training Program Affiliations

Biosciences Graduate Program
Department of Microbiology Graduate Program
Interdisciplinary Graduate Program in Immunology
Interdisciplinary Graduate Program in Neuroscience
Interdisciplinary Graduate Program in Translational Biomedicine
Medical Scientist Training Program

Research Summary

My laboratory has been interested in the pathogenesis of murine coronavirus infections for several years. Now, we also study three respiratory human coronavirus infections: SARS(Severe Acute Respiratory Syndrome)-coronavirus, human coronavirus-OC43 and human coronavirus-NL63.

Mice infected with mouse hepatitis virus develop a demyelinating disease with many similarities to the human disease, multiple sclerosis. Research in my laboratory is aimed at determining the immunological and viral factors involved in the demyelinating process. Previously, we determined the CD4 and CD8 T cell epitopes recognized in the central nervous system (CNS) of infected mice. We showed that in mice infected chronically with the virus, cytotoxic T cell escape mutants arise. These mutations completely abrogate recognition by CD8 T cells and thereby facilitate persistence. We have also identified mutations in a subdominant epitope that enhance immune recognition by CD8 T cells (heteroclitic epitopes) and are studying the structural basis of heteroclitic effects. We have developed a reverse genetics system for introducing these and other mutations into the murine coronavirus genome. We also study the anti-inflammatory components that are needed to diminish immunopathological disease, with specific focus on regulatory CD4 T cells and IL-10. The ultimate goal of our work is to understand the interplay of pro and anti-inflammatory factors that result in myelin destruction.

The SARS-coronavirus causes the most significant disease of any of the human coronaviruses. The disease is especially severe in aged populations. We are using mice infected with murine adapted strains to understand the basis of this severe disease. We are also developing vaccines that might be useful if SARS were to recur, or more likely, as a model approach if another severe disease caused by a coronavirus were to emerge in human populations.

Center, Program and Institute Affiliations

Center for Immunology and Immune-based Diseases
Helen C. Levitt Center for Viral Pathogenesis
Holden Comprehensive Cancer Center
Institute for Clinical and Translational Science
NIH Vaccine Treatment and Evaluation Unit

Selected Publications

Show All

Trujillo J, Fleming E, Perlman S.  Transgenic CCL2 Expression in the Central Nervous System Results in a Dysregulated Immune Response and Enhanced Lethality after Coronavirus Infection.  J Virol.  2013 March. 87(5):2376-89.
[Link]

Zhao J, Wohlford-Lenane C, Zhao J, Fleming E, Lane T, McCray P, Perlman S.  Intranasal treatment with poly(I•C) protects aged mice from lethal respiratory virus infections.  J Virol.  2012 November. 86(21):11416-24.
[Link]

Zhao J, Zhao J, Legge K, Perlman S.  Age-related increases in PGD(2) expression impair respiratory DC migration, resulting in diminished T cell responses upon respiratory virus infection in mice.  J Clin Invest.  2011 December. 121(12):4921-30.
[Link]

Zhao J, Zhao J, Fett C, Trandem K, Fleming E, Perlman S.  IFN-γ- and IL-10-expressing virus epitope-specific Foxp3(+) T reg cells in the central nervous system during encephalomyelitis.  J Exp Med.  2011 August 1. 208(8):1571-7.
[Link]

Trandem K, Zhao J, Fleming E, Perlman S.  Highly activated cytotoxic CD8 T cells express protective IL-10 at the peak of coronavirus-induced encephalitis.  J Immunol.  2011 March 15. 186(6):3642-52.
[Link]

Zhou H, Zhao J, Perlman S.  Autocrine interferon priming in macrophages but not dendritic cells results in enhanced cytokine and chemokine production after coronavirus infection.  MBio.  2010 October 19. 1(4):pii: e00219-10.
[Link]

Trandem K, Anghelina D, Zhao J, Perlman S.  Regulatory T cells inhibit T cell proliferation and decrease demyelination in mice chronically infected with a coronavirus.  J Immunol.  2010 April 15. 184(8):4391-400.
[Link]

Zhao J, Zhao J, Perlman S.  De novo recruitment of antigen-experienced and naive T cells contributes to the long-term maintenance of antiviral T cell populations in the persistently infected central nervous system.  J Immunol.  2009 October 15. 183(8):5163-70.
[Link]

Zhao J, Zhao J, Van Rooijen N, Perlman S.  Evasion by stealth: inefficient immune activation underlies poor T cell response and severe disease in SARS-CoV-infected mice.  PLoS Pathog.  2009 October. 5(10):e1000636.
[Link]

Butler N, Theodossis A, Webb A, Nastovska R, Ramarathinam S, Dunstone M, Rossjohn J, Purcell A, Perlman S.  Prevention of cytotoxic T cell escape using a heteroclitic subdominant viral T cell determinant.  PLoS Pathog.  2008 October. 4(10):e1000186.
[Link]

Date Last Modified: 08/22/2013 - 11:27:19