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Prof. Barry T. Rouse
Distinguished Professor
Biomedical and Diagnostic Sciences

Research Interests

  • My research is in the field of infectious disease and has focused on viral immunology and immunopathology. We have mainly studied herpes simplex virus (HSV) infection in mice both with a view to devising successful vaccines and more particularly to determine how HSV causes tissue damage in critical tissues such as the eye and nervous system. We have worked on both host innate and adaptive immune mechanisms, particularly the T cells responsible for immunity as well as those involved in orchestrating tissue damage. We have defined the role of several subtypes of proinflammatory T cells as well as numerous cytokines and chemokines. Our group was the first to show a role of regulatory T cells (Treg) in the host response to a virus infection. We demonstrated that Treg responses could act to inhibit the efficiency of immunity, but that Treg were valuable to modulate the severity of immunopathological responses, such as those that occur in the corneal stroma after HSV infection of the eye. My group has studied the important blinding lesion herpes stromal keratitis (SK) for >30 years and has demonstrated how multiple events set off by ocular HSV infection culminate in SK. We have paid particular attention to the non specific inflammatory cells, particularly neutrophils, that are recruited to the eye and which appear to be mainly responsible for the tissue damage that occurs. We were also the first to show a critical role for corneal neovascularization (CV) during SK pathogenesis, identified several angiogenic factors and studied how such factors are generated following HSV infection. We have also investigated how to diminish the extent of CV and have shown that controlling CV represents a valuable means of therapy, particularly if combined with approaches that control other critical events in lesion pathogenesis. Recently, we have also investigated various ways of modulating the extent of proinflammatory T cell involvement during SK with a view to understanding how to optimally achieve lesion resolution. We have shown that host derived factors such as Galectin 9 and Galectin 1 can be manipulated to achieve control of lesion severity as can be approaches that modulate Treg numbers and activity. We have also shown how molecules derived from Omega-3 polyunsaturated fatty acids, such as some synthetic resolvins and protectins, participate in the control of lesions. Our therapeutic studies have also manipulated levels of multiple microRNA species that are involved in SK as well as encephalitis caused by HSV. Most recently the main direction of our research has turned toward characterizing and manipulating the metabolic requirements of immune cells involved in SK with a view to changing the balance of responses to minimize tissue damage.

Education

  • University of Bristol, England -1965 - Bachelor of Veterinary Science with honors
  • University of Guelph, Canada -1967 - M.Sc.
  • University of Guelph, Canada - 1970 - Ph.D.
  • Walter and Eliza Hall Institute of Medical Research, Australia – 1970-72 – Postdoctoral research
  • University of Bristol, England - 1997 - D.Sc.

Teaching

  • Immunology

Funding

  • Two RO1 grants from National Institutes of Health

Professional Activities

  • Trained > 75 graduate students and postdoctoral fellows
  • Received several awards for research accomplishments most notably Alcon Award for outstanding contributions to vision research, 2000 and Medal of Merit, Warsaw University of Life Sciences, 2014.
  • Recipient of Fogarty Senior International Fellowship and Alexander Von Humboldt Fellowship
  • Been extensively involved in reviewing NIH grants since 1978 which includes 3 times as a permanent member of study section and once as chairman
  • Member of Faculty of 1000 since its inception
  • Coorganizer of several conferences
  • Member of editorial board and reviewer of many journals
  • Member of AAI and ASM for >30 years
  • 2017 UTIA Institute Professer - UT Institute of Agriculture

Selected Publications out of > 400. Current H index 78

  1. Zheng, M., S. Deshpande, S. Lee, N. Ferrera, and B. T. Rouse.  2001.  Contribution of       VEGF in the neovascularization process during the pathogenesis of herpetic stromal keratitis.  J. Virol.  75:9828-9835. (136 CITATIONS)
  2. Zheng, M., D. M. Klinman, M. Gierynska, and B. T. Rouse.  2002.  Angiogenesis caused by bioactive CpG motifs and herpesvirus DNA.  Proc. Nat. Acad. Sci (USA).  99: 8944-8949.  (105 CITATIONS)
  3. Lee, S., M. Zheng, B. Kim, and B. T. Rouse.  2002.  Matrix metalloproteinase-9 plays a major role in angiogenesis caused by ocular infection with herpes simplex virus.  J. Clin. Invest.  110: 1105-1111.  (130 CITATIONS)
  4. Suvas, S., Kumaraguru, U., Pack, C. D., Lee, S., and Rouse, B. T.  2003.  CD4+ CD25+ T cells regulate virus-specific primary and memory CD8+ T cell responses.  J. Exp. Med.  198: 889-901. (545 CITATIONS) PMID: 12975455
  5. Suvas, S., Kim, B.S., Azkur, K., Kumaraguru, U., and Rouse, B.T.  2004.  CD4+CD25+ regulatory T cells control the severity of viral immunoinflammatory lesions.  J. Immun.  172: 4123-4129. (290 CITATIONS) PMID: 15034024
  6. Kim, B., Tang, Q.Q., Xu, J., Biswas, P.S., Schiffelers, R., Xie, F.Y., Ansari, A.M., Scaria, P.V., Woodle, M.C., Lu, P.Y., Rouse, B.T.  2004.  Inhibition of ocular angiogenesis by siRNA targeting vascular endothelial growth factor – pathway genes; therapeutic strategy for herpetic stromal keratitis.  Am. J. Path.  165: 2177-85. (217 CITATIONS)
  7. Belkaid, Y., and Rouse, B.T.  2005.  Natural regulatory T cells in infectious disease.  Nature Immunol.  6: 353-360. (977 CITATIONS) PMID: 15785761
  8. Rouse, B.T., Sarangi, P., and Suvas, S. 2006. Regulatory T cells in virus infections. Immun. Revs. 212: 272-286. (245 CITATIONS) PMID: 16903920
  9. Sehrawat S., Suryawanshi, A., Hirashima M and Rouse, B.T. 2009. Role of Tim3/Galectin-9 inhibitory interaction in viral induced immunopathology: Shifting the Balance towards regulators. J.Immunol. 182 3191-3201  (78 CITATIONS) PMID: 19234217
  10. Rouse,B.T. and Sehrawat,S. 2010 Immunity and immunopathology to viruses- what decides the outcome?  Nature Revs Immunology. 10 514-526 (71 CITATIONS) PMID: 20577268
  11. Rajasagi NK ,  Reddy PB, Suryawanshi A, Mulik S,  Gjorstrup, P  and Rouse B.T. (2011) Controlling herpes simplex virus induced ocular inflammatory lesions with the lipid derived mediator Resolvin E1. J Immunol.  186(3): 1735-1746 (55 Citations) doi: 10.3389. PMID: 21187448
  12. Suryawanshi A, Veiga-Parga T, Rajasagi N, Reddy PBP, Sehrawat S, Sharma S and Rouse BT. 2011. Role of IL-17 and Th17 Cells in HSV Induced Corneal Immunopathology. J. Immunol.  187 1919-1930. (39 CITATIONS) PMID: 21765013
  13. Veiga-Parga T., Sehrawat S., and Rouse B.T. 2013 Role of Regulatory T Cells during Virus Infections. Immunol Revs. 2013 Sep; 255(1): 182-96. (27 CITATIONS) PMID: 23947355
  14. Bhela S, Mulik S, Reddy P BJ, Richardson RL, Gimenez F, Rajasagi NK, Veiga-Para T, Osmand AP, Rouse BT. 2014. Critical Role of MicroRNA-155 in Herpes Simplex Encephalitis. J. Immunol.192:2734-2743 PMCID:3951608
  15. Sehrawat S and Rouse BT (2017) Interplay of Treg and Th17 cells during infectious diseases in humans and animals. Front Immunol 8:341. doi: 10.3389. PMCID: 5377923
  16. Bhela,S Varanasi,SK,Jaggi,U Sloan,SS and Rouse,BT (2017) The plasticity and stability of regulatory T cells during viral induced inflammatory lesions. J Immunol. doi: 10.4049 PMID:28710254.
  17. Rajasagi, N. K., Bhela, S., Varanasi, S. K., Rouse, B. T. (2017). Aspirin triggered resolvin D1 controls herpes simplex virus induced corneal immunopathology. J. Leukoc. Biol. DOI:10.1189 PMID: 28554076.
  18. Varanasi, S. K., Reddy, P. B., Bhela, S., Jaggi, U., Gimenez, F., & Rouse, B. T. Azacytidine treatment inhibits the progression of Herpes Stromal Keratitis by enhancing regulatory T cell function. (2017). J Virol 13;91(7). Doi: 10.1128.
  19. Varanasi, S. K., Donohoe, D. R., Jaggi, U., Rouse, B. T. Metabolic reprogramming of CD4 T cells during Herpes Stromal Keratitis. J Immunol (in press).