Stuart C. Ray

Stuart C. Ray is an American physician. He is Vice Chair of Medicine for Data Integrity and Analytics,[1] Associate Director of the Infectious Diseases Fellowship Training Program at the Johns Hopkins School of Medicine, and a Professor in the Department of Medicine, Division of Infectious Diseases. Ray also holds appointments in Viral Oncology and the Division of Health Sciences Informatics. He is affiliated with the Institute for Computational Medicine[2] at Johns Hopkins and is licensed to practice medicine in Maryland.

Ray researches the influence of viral evolution on viral pathogenesis, concentrating in particular on complex RNA viruses such as hepatitis C virus (HCV) and human immunodeficiency virus (HIV).[3] He has published approximately 100 scientific articles on HIV, HCV, or both.

Education and training

As an undergraduate, Ray studied at the California Institute of Technology and graduated from Vanderbilt University with a B.S. cum laude in molecular biology. He remained at Vanderbilt for medical school and received his M.D. in 1990.

Ray completed a medical residency and both research and clinical fellowships in infectious diseases at the Johns Hopkins Hospital. In 1995, he became the assistant chief of service for the Department of Medicine at Johns Hopkins. Ray was appointed to an assistant professorship in 1997 and was promoted to associate professor in 2003.

HIV research

Ray has studied the ability of HIV to undergo high levels of mutation in its genomic sequence, exploring the health consequences of this mutability.[4] In 1999, Ray and colleagues reported on the sequence diversity of HIV in India. They cautioned that different subtypes could combine, thwarting traditional efforts to develop vaccines.[5][6]

In 2005, along with colleagues including Robert F. Siliciano, Ray examined the phenomenon of viral "blips." HIV-positive patients who have suppressed HIV replication with the help of highly active antiretroviral therapy (HAART) occasionally exhibit apparent transient increases in the amount of virus in their blood, leading some scientists to express concern that these blips could allow the virus to develop drug resistance. The results of the 2005 study indicated that the virus was unable to gain resistance mutations during the blips, and that many of the blips could be attributed to statistical artifact.[7][8]

Ray has also participated in the study of "elite suppressors," rare individuals who control HIV replication naturally and do not progress to AIDS quickly, even in the absence of treatment. With Joel Blankson and others, Ray contributed to a study of a monogamous husband-wife couple who were infected with the same strain of HIV but had very different responses to the virus. This work was published in 2008.[9][10]

HCV research

As HCV evades the immune system, Ray found, its genome not only mutates to escape the body's defenses, but also reverts to its previous, "ancestral" state when possible. This balance helps the virus to retain fitness.[11][12]

Ray's work on HCV has characterized sources of selective pressure on the HCV genome[13] and identified factors leading to HCV immune escape.[14][15]

The interactions between HCV and HIV infections have also been a topic of interest for Ray.[16][17][18][19] He has been interviewed by numerous media outlets, including Newsweek.[20][21][22]

Elected memberships

References

  1. ↑
  2. ↑ ICM affiliated faculty
  3. ↑ Stuart Ray's CV, JHU ICM website
  4. ↑ "HIV's Success Might Lie in Its Mutations," United Press International, November 5, 2002.
  5. ↑ "Sequencing of HIV from India Waves a Red Flag for Vaccine Developers," Gene Therapy Weekly, January 25, 1999.
  6. ↑ Lole, K. S.; Bollinger, R. C.; Paranjape, R. S.; Gadkari, D.; Kulkarni, S. S.; Novak, N. G.; Ingersoll, R.; Sheppard, H. W.; Ray, S. C. (1999). "Full-length human immunodeficiency virus type 1 genomes from subtype C-infected seroconverters in India, with evidence of intersubtype recombination". Journal of Virology. 73 (1): 152–160. PMC 103818Freely accessible. PMID 9847317.
  7. ↑ "Small increases or 'blips' in HIV levels do not signal mutations leading to drug-resistant HIV"
  8. ↑ Kieffer, T.; Finucane, M.; Nettles, R.; Quinn, T.; Broman, K.; Ray, S.; Persaud, D.; Siliciano, R. (2004). "Genotypic analysis of HIV-1 drug resistance at the limit of detection: virus production without evolution in treated adults with undetectable HIV loads". The Journal of Infectious Diseases. 189 (8): 1452–1465. doi:10.1086/382488. PMID 15073683.
  9. ↑ "Rare Case Explains Why Some Infected with HIV Remain Symptom Free without Antiretroviral Drugs" Newswise, August 12, 2008.
  10. ↑ Bailey, J.; O'Connell, K.; Yang, H.; Han, Y.; Xu, J.; Jilek, B.; Williams, T.; Ray, S.; Siliciano, R.; Blankson, J. N. (2008). "Transmission of human immunodeficiency virus type 1 from a patient who developed AIDS to an elite suppressor". Journal of Virology. 82 (15): 7395–7410. doi:10.1128/JVI.00800-08. PMC 2493308Freely accessible. PMID 18495769.
  11. ↑ "Johns Hopkins Team Finds 'Ancestral' Hepatitis-C Virus at Root of Evolution in Acute and Chronic Infections. AScribe, June 9, 2005.
  12. ↑ Ray, S.; Fanning, L.; Wang, X.; Netski, D.; Kenny-Walsh, E.; Thomas, D. (2005). "Divergent and convergent evolution after a common-source outbreak of hepatitis C virus". The Journal of Experimental Medicine. 201 (11): 1753–1759. doi:10.1084/jem.20050122. PMC 2213258Freely accessible. PMID 15939791.
  13. ↑ Dowd, K.; Netski, D.; Wang, X.; Cox, A.; Ray, S. (2009). "Selection pressure from neutralizing antibodies drives sequence evolution during acute infection with hepatitis C virus". Gastroenterology. 136 (7): 2377–2386. doi:10.1053/j.gastro.2009.02.080. PMC 2895772Freely accessible. PMID 19303013.
  14. ↑ Wölfl, M.; Rutebemberwa, A.; Mosbruger, T.; Mao, Q.; Li, H. M.; Netski, D.; Ray, S. C.; Pardoll, D.; Sidney, J.; Sette, A.; Allen, T.; Kuntzen, T.; Kavanagh, D. G.; Kuball, J.; Greenberg, P. D.; Cox, A. L. (2008). "Hepatitis C virus immune escape via exploitation of a hole in the T cell repertoire". Journal of immunology (Baltimore, Md. : 1950). 181 (9): 6435–6446. doi:10.4049/jimmunol.181.9.6435. PMC 2742502Freely accessible. PMID 18941234.
  15. ↑ Rutebemberwa, A.; Ray, S. C.; Astemborski, J.; Levine, J.; Liu, L.; Dowd, K. A.; Clute, S.; Wang, C.; Korman, A.; Sette, A.; Sidney, J.; Pardoll, D. M.; Cox, A. L. (2008). "High-programmed death-1 levels on hepatitis C virus-specific T cells during acute infection are associated with viral persistence and require preservation of cognate antigen during chronic infection". Journal of immunology (Baltimore, Md. : 1950). 181 (12): 8215–8225. doi:10.4049/jimmunol.181.12.8215. PMC 2773824Freely accessible. PMID 19050238.
  16. ↑ Mao, Q.; Ray, S.; Laeyendecker, O.; Ticehurst, J.; Strathdee, S.; Vlahov, D.; Thomas, D. (2001). "Human immunodeficiency virus seroconversion and evolution of the hepatitis C virus quasispecies". Journal of Virology. 75 (7): 3259–3267. doi:10.1128/JVI.75.7.3259-3267.2001. PMC 114119Freely accessible. PMID 11238852.
  17. ↑ Balagopal, A.; Ray, S.; De Oca, R.; Sutcliffe, C.; Vivekanandan, P.; Higgins, Y.; Mehta, S.; Moore, R.; Sulkowski, M.; Thomas, D. L.; Torbenson, M. S. (2009). "Kupffer cells are depleted with HIV immunodeficiency and partially recovered with antiretroviral immune reconstitution". AIDS (London, England). 23 (18): 2397–2404. doi:10.1097/QAD.0b013e3283324344. PMC 3092442Freely accessible. PMID 19773633.
  18. ↑ Netski, D.; Mao, Q.; Ray, S.; Klein, R. (2008). "Genetic divergence of hepatitis C virus: the role of HIV-related immunosuppression". Journal of acquired immune deficiency syndromes (1999). 49 (2): 136–141. doi:10.1097/QAI.0b013e3181869a6f. PMC 3071283Freely accessible. PMID 18769357.
  19. ↑ Balagopal, A.; Philp, F.; Astemborski, J.; Block, T.; Mehta, A.; Long, R.; Kirk, G.; Mehta, S.; Cox, A.; Thomas, D. L.; Ray, S. C. (2008). "Human immunodeficiency virus-related microbial translocation and progression of hepatitis C". Gastroenterology. 135 (1): 226–233. doi:10.1053/j.gastro.2008.03.022. PMC 2644903Freely accessible. PMID 18457674.
  20. ↑ "Hepatitis C: The Insidious Spread Of A Killer Virus" Newsweek, Geoffrey Cowley, April 22, 2002.
  21. ↑ "The Insidious Spread of a Killer Virus" Newsweek, Anna Kuchment, May 20, 2002.
  22. ↑ "Johns Hopkins Team Finds 'Ancestral' Hepatitis-C Virus At The Root Of Evolution In Infections" ScienceDaily, June 10, 2005.
  23. ↑ Stuart Ray's profile at the American Society for Clinical Investigation
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