Virology Faculty Member - Igor Koralnik

Igor Koralnik

Professor of Neurology

Beth Israel Deaconess Med Ctr
Neurology, Research, E/CLS - 1005
330 Brookline Ave
Boston, MA 2215
Tel: 617/735-4460
Fax: 617/735-4527
Email: ikoralni@bidmc.harvard.edu



The Koralnik laboratory is studying the pathogenesis of the polyomaviruses JC, BK, and SV40. Current areas of investigations include:

Cellular immunity to JC virus in AIDS-associated Progressive Multifocal Leukoencephalopathy (PML):

PML is a deadly demyelinating disease of the central nervous system caused by JC virus (JCV) in immunosuppressed individuals. JCV infects most healthy adults without causing any disease, but its reactivation leads to a productive and lytic infection of oligodendrocytes, the myelin producing cells in the central nervous system. We are currently studying the cellular immune response against JCV mediated by both CD8+ and CD4+ T lymphocytes in patients with PML, and we are characterizing genetic markers of the host associated with favorable outcome of PML. We are studying how this immune response cross-reacts with BK virus, the etiologic agent of polyomavirus nephropathy. Since there is no cure for PML, our laboratory is now developing a dendritic cell-based immunotherapy for this disease.

Latency and reactivation of JC virus:

We are studying the molecular and cellular mechanisms leading to the reactivation of JCV in bone marrow and peripheral blood samples, as well as the phenotype of JCV-infected cells in immunosuppressed individuals including patients with AIDS, leukemias, transplant recipients and multiple sclerosis patients treated with novel immunomodulatory medications.

Characterization of a granule cell neuron-tropic JC virus variant:

Our laboratory has shown that JC virus could also infect and destroy granule cell neurons of the cerebellum, and cause cerebellar atrophy and associated neurological dysfunction. This granule cell neuron tropic JCV variant has a unique mutation in the gene encoding the major capsid protein of JCV. We are now characterizing the phenotype of this JCV variant in vitro.

A nonhuman primate model of AIDS-associated PML:

Since JCV does not infect animals, we are developing an animal model of PML and neuronal infection using the JCV-related simian virus 40 (SV40) in SHIV immunosuppressed rhesus macaques.



Last Update: 10/22/2013



Publications

Chen Y, Trofe J, Gordon J, Autissier P, Woodle ES, Koralnik IJ. BKV and JCV large T antigen-specific CD8+ T cell response in HLA A*0201+ kidney transplant recipients with polyomavirus nephropathy and patients with progressive multifocal leukoencephalopathy. J Clin Virol 2008, 42:198-202. PMCID: PMC2678795

Dang X, Wüthrich C, Axthelm M, Koralnik IJ. Productive SV40 infection of neurons in immunosuppressed rhesus monkeys. J Neuropath Exp Neurol 2008, 67:784-792. PMCID: PMC2745603 (this article was listed as in press)



© 2013 by the President and Fellows of Harvard College