Professor of Microbiology
Office: 3-712 Bowen Science Building
51 Newton Rd
Iowa City, IA 52242
Lab: 3-730 Bowen Science Building
51 Newton Rd
Iowa City, IA 52242
Web: Perlman Lab Website
Web: Faculty Focus: Stanley Perlman, MD, PhD
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
Fellowship, Brandeis University
Residency, Children's Hospital Medical Center
Fellowship, Infectious Diseases, Children's Hospital Medical Center
Licensure and Certifications
American Board of Pediatrics
Medical License, Iowa
Medical License, Massachusetts
Education/Training Program Affiliations
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
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. We have begun studies of the coronavirus that causes the Middle East Respiratory Syndrome (MERS-CoV). We have developed a mouse model for studying MERS and begun to evaluate several MERS-CoV specific vaccines and therapies.
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
Airway Memory CD4(+) T Cells Mediate Protective Immunity against Emerging Respiratory Coronaviruses.
2016 June 21. 44(6):1379-91.
Dysregulated Type I Interferon and Inflammatory Monocyte-Macrophage Responses Cause Lethal Pneumonia in SARS-CoV-Infected Mice.
Cell Host Microbe.
2016 February 10. 19(2):181-93.
Critical role of phospholipase A2 group IID in age-related susceptibility to severe acute respiratory syndrome-CoV infection.
J Exp Med.
2015 October 19. 212(11):1851-68.
Middle East respiratory syndrome.
2015 September 5. 386(9997):995-1007.
Passive immunotherapy with dromedary immune serum in an experimental animal model for Middle East respiratory syndrome coronavirus infection.
2015 June. 89(11):6117-20.
Virus-specific regulatory T cells ameliorate encephalitis by repressing effector T cell functions from priming to effector stages.
2014 August 7. 10(8):e1004279.
Receptor variation and susceptibility to Middle East respiratory syndrome coronavirus infection.
2014 May. 88(9):4953-61.
Rapid generation of a mouse model for Middle East respiratory syndrome.
Proc Natl Acad Sci U S A.
2014 April 1. 111(13):4970-5.
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.
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.
Date Last Modified: 06/06/2016 -