Nadia Roan, PhD

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Nadia Roan, PhD

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Senior Investigator, Gladstone Institutes
Professor, School of Medicine
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Biography

Dr. Roan has had a long-standing interest in understanding the effect of host factors on microbial pathogens of the genital mucosa. Her research as a graduate student led to new insights into the nature of the mucosal immune response directed against the most common sexually transmitted bacterium C. trachomatis. She created and characterized C. trachomatis-specific TCR transgenic and retrogenic mice, and used these mice as tools to understand the inflammatory response to C. trachomatis within the upper female reproductive tract (FRT). During her postdoctoral years, Dr. Roan continued her studies on sexually transmitted microbes, but transitioned to studying HIV-1, a viral pathogen with a devastating effect on global health. She focused on understanding the effect of semen components on HIV-1 infection. She identified and characterized amyloid fibrils made up of peptides derived from the major components of the semen coagulum. These amyloids markedly enhance HIV infection, in part by promoting the attachment of HIV-1 to their cellular targets.

Dr. Roan’s current research interest focuses on two major areas. First, she is investigating the mechanisms by which semen components such as coagulum-derived amyloids promote HIV transmission, and the effects of these components on the effectiveness of currently available anti-HIV microbicides. This understanding will help the development of a new class of “combination microbicides” that contain components targeting both HIV-1 and naturally-occurring factors that promote HIV-1 infectivity. In parallel, a high-throughput screen is currently being conducted to identify compounds that inhibit the activity of viral-enhancing factors in semen. Dr. Roan’s second line of research is to understand the physiological functions of semen amyloids and their effects on cells present in the genital mucosa. This understanding will reveal insights into the roles of these semen factors in reproduction, which can lead to novel ways to enhance fertility or to the development of a new class of contraceptives.

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  1. Roan NR, Sowinski S, Münch J, Kirchhoff F, Greene WC. Aminoquinoline surfen inhibits the action of SEVI (semen-derived enhancer of viral infection). J Biol Chem. 2010 Jan 15; 285(3):1861-9.
  2. Gondek DC, Roan NR, Starnbach MN. T cell responses in the absence of IFN-gamma exacerbate uterine infection with Chlamydia trachomatis. J Immunol. 2009 Jul 15; 183(2):1313-9.
  3. Roan NR, Münch J, Arhel N, Mothes W, Neidleman J, Kobayashi A, Smith-McCune K, Kirchhoff F, Greene WC. The cationic properties of SEVI underlie its ability to enhance human immunodeficiency virus infection. J Virol. 2009 Jan; 83(1):73-80.
  4. Starnbach MN, Roan NR. Conquering sexually transmitted diseases. Nat Rev Immunol. 2008 Apr; 8(4):313-7.
  5. Grotenbreg GM, Roan NR, Guillen E, Meijers R, Wang JH, Bell GW, Starnbach MN, Ploegh HL. Discovery of CD8+ T cell epitopes in Chlamydia trachomatis infection through use of caged class I MHC tetramers. Proc Natl Acad Sci U S A. 2008 Mar 11; 105(10):3831-6.
  6. Roan NR, Greene WC. A seminal finding for understanding HIV transmission. Cell. 2007 Dec 14; 131(6):1044-6.
  7. Roan NR, Starnbach MN. Immune-mediated control of Chlamydia infection. Cell Microbiol. 2008 Jan; 10(1):9-19.
  8. Roan NR, Starnbach MN. Antigen-specific CD8+ T cells respond to Chlamydia trachomatis in the genital mucosa. J Immunol. 2006 Dec 01; 177(11):7974-9.
  9. Roan NR, Gierahn TM, Higgins DE, Starnbach MN. Monitoring the T cell response to genital tract infection. Proc Natl Acad Sci U S A. 2006 Aug 08; 103(32):12069-74.
  10. Balsara ZR, Roan NR, Steele LN, Starnbach MN. Developmental regulation of Chlamydia trachomatis class I accessible protein-1, a CD8+ T cell antigen. J Infect Dis. 2006 May 15; 193(10):1459-63.
  11. Hess D, Liu B, Roan NR, Sternglanz R, Winston F. Spt10-dependent transcriptional activation in Saccharomyces cerevisiae requires both the Spt10 acetyltransferase domain and Spt21. Mol Cell Biol. 2004 Jan; 24(1):135-43.
  12. D'Orazio SE, Velasquez M, Roan NR, Naveiras-Torres O, Starnbach MN. The Listeria monocytogenes lemA gene product is not required for intracellular infection or to activate fMIGWII-specific T cells. Infect Immun. 2003 Dec; 71(12):6721-7.