Skip to main content

Melissa E. Kane Ph.D.

  • Assistant Professor, Department of Pediatrics
  • Assistant Professor, Department of Immunology
  • Member, Center for Microbial Pathogenesis
  • PMI Graduate Faculty

    Education & Training

  • Postdoc - Rockefeller University/Aaron Diamond Aids Research Center - Laboratory of Dr. Paul Bieniasz
  • Ph.D. - Microbiology - University of Chicago - Laboratory of Dr. Tatyana Golovkina
  • B.S. - Animal Science - Cornell University
Representative Publications

Kane M, Rebensburg SV, Takata MA, Zang TM, Yamashita M, Kvaratskhelia M and Bieniasz PD. 2018. Nuclear pore heterogeneity influences HIV-1 infection and the antiviral activity of MX2. Elife. 7: e35738.

Kane M, Zang TM, Rihn SJ, Zhang F, Kueck T, Alim M, Schoggins J, Rice CM, Wilson SJ and Bieniasz PD. 2016. Identification of Interferon-Stimulated Genes with Antiretroviral Activity. Cell Host Microbe. 20: 392-405.

Kane M, Yadav SS, Bitzegeio J, Kutluay SB, Zang T, Wilson SJ, Schoggins JW, Rice CM, Yamashita M, Hatziioannou T and Beiniasz PD. 2013. MX2 is an interferon-induced inhibitor of HIV-1 infection. Nature. 502: 563-566.

Kane M, Case LK, Wang C, Yurkovetskiy L, Dikiy S and Golovkina TV. 2011. Innate immune sensing of retroviral infection via Toll-like receptor 7 occurs upon viral entry. Immunity. 35: 135-145.

Kane M, Case LK, Kopaskie K, Kozlova A, MacDearmid C, Chervonsky AV and Golovkina TV. 2011. Successful transmission of a retrovirus depends on the commensal microbiota. Science. 334: 245-249.

Complete List of Publications

Research Interests

The central focus of the Kane Lab is understanding the genetic and immunological basis for protective antiviral immune responses, as well as the molecular details underlying the direct inhibition of retroviral replication by restriction factors. We utilize both in vitro and in vivo tools to investigate intrinsic, innate, and adaptive immune responses to retroviral infection.

Our research is centered around three questions:

  1. What allows some individuals to restrict or control retroviral replication?
  2. How do retroviruses counteract host defenses?
  3. What are the features of successful anti-retroviral immune responses?