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Micah Luftig

Associate Professor
Molecular Genetics and Microbiology
919-668-3091
Research Interest: 
Immunology
Microbiology and virology
Signal transduction
Research Summary: 
Mechanisms of viral oncogenesis and host response to oncogenic virus infection
Research Description: 

The laboratory focuses on the mechanisms by which Epstein-Barr virus activates and ultimately subverts the host oncogenic stress response to growth transform primary B lymphocytes into indefinitely proliferating lymphoblastoid cell lines (LCLs). EBV infection of B cells leads to a latent growth program where eight viral proteins and several non-coding RNAs are expressed. Among these gene products, latent membrane protein 1 (LMP1) and Epstein-Barr virus nuclear antigen (EBNA) 2 are the core transforming oncogenes. These proteins are capable of driving B cell proliferation and act to suppress the apoptotic response induced by aberrant S phase induction. The goals of the laboratory include: i) understanding the host pathways that respond to and suppress EBV-mediated growth transformation, ii) understanding the viral gene products important for activating the oncogenic stress response and ultimately overcoming this response, and iii) identifying and characterizing a cell population within the CD21-expressing primary B cell population that has an increased susceptibility to oncogenic stress.

The biochemical and genetic analyses of these pathways will provide valuable insight into our understanding of oncogenes and oncogenic viruses and the host cell response to such insults. Further, detailed understanding of the virus/host interaction may allow for the identification of specific pathways for therapeutic intervention in EBV-associated malignancies and possibly more broadly in malignancies which rely on similar pathways for their proliferation, survival, or self-renewal.

Publications: 
Mitogen-induced B-cell proliferation activates Chk2-dependent G1/S cell cycle arrest.
Nikitin PA, Price AM, McFadden K, Yan CM, Luftig MA.
PLoS One. 2014. 9:e87299.

Epstein-Barr virus induces global changes in cellular mRNA isoform usage that are important for the maintenance of latency.
Homa NJ, Salinas R, Forte E, Robinson TJ, Garcia-Blanco MA, Luftig MA.
J Virol. 2013. 87:12291-301.

Analysis of Epstein-Barr virus-regulated host gene expression changes through primary B-cell outgrowth reveals delayed kinetics of latent membrane protein 1-mediated NF-κB activation.
Price AM, Tourigny JP, Forte E, Salinas RE, Dave SS, Luftig MA.
J Virol. 2012. 86:11096-106.

An ATM/Chk2-mediated DNA damage-responsive signaling pathway suppresses Epstein-Barr virus transformation of primary human B cells.
Nikitin PA, Yan CM, Forte E, Bocedi A, Tourigny JP, White RE, Allday MJ, Patel A, Dave SS, Kim W, Hu K, Guo J, Tainter D, Rusyn E, Luftig MA.
Cell Host Microbe. 2010. 8:510-22.

MDM2-dependent inhibition of p53 is required for Epstein-Barr virus B-cell growth transformation and infected-cell survival.
Forte E, Luftig MA.
J Virol. 2009. 83:2491-9.