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Sankar Swaminathan, M.D.

Division Chief, Division of Infectious Diseases

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Specialties

Languages

  • English

Clinical Details

Phone Number Clinical Office Address
(801) 585-2031
University Hospital
Infectious Diseases, Clinic 1A
50 N Medical Dr
Salt Lake City, UT 84132
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Specialties

Bio

Sankar Swaminathan, MD has specialized expertise in the treatment of infectious diseases. He is board certified in Internal Medicine and Infectious Diseases. His main clinical focus is in the diagnosis and treatment of infections in immunocompromised patients, including cancer patients and transplant recipients. He has integrated a research program funded by the National Cancer institute on the role of viruses in cancers into his clinical practice.

Board Certification and Academic Information

Academic Departments Internal Medicine - Professor
Pathology - Adjunct Professor
Academic Divisions Infectious Diseases
Microbiology and Immunology
Board Certification American Board of Internal Medicine
American Board of Internal Medicine (Sub: Infec Disease)
American Board of Internal Medicine (Sub: Infec Disease)
Cancer Center Programs Nuclear Control of Cell Growth & Differentiation

Academic Profile

Research Interests

  • Epstein-Barr Virus Infections
  • Herpesvirus 1, Human

Board Certification and Academic Information

Academic Departments Internal Medicine - Professor
Pathology - Adjunct Professor
Academic Divisions Infectious Diseases
Microbiology and Immunology
Board Certification American Board of Internal Medicine
American Board of Internal Medicine (Sub: Infec Disease)
American Board of Internal Medicine (Sub: Infec Disease)
Cancer Center Programs Nuclear Control of Cell Growth & Differentiation

Academic Office Locations

Academic Office Phone Number Academic Office Address
(801) 587-7216 School of Medicine
Infectious Disease
30 N 1900 E
Salt Lake City, UT 84132
University Hospital
50 N Medical Dr
Salt Lake City, UT 84132

Academic Bio

Dr. Sankar Swaminathan comes from the University of Florida, where he was professor of internal medicine in infectious diseases and director of that university’s Tumor Virology Program. In his new role as Chief of Infectious Diseases at the University of Utah, he plans to make both basic-science and clinical research priorities in his division. This will include expanding the collaborative virology research between the infectious diseases division and other departments and divisions at the medical school as well as promoting more clinical research in HIV, infections in immunocompromised patients, and travel medicine.

Dr. Swaminathan did his medical residency at the University of Chicago Medical Center followed by Infectious Diseases fellowship and research training at Harvard Medical School.

Dr. Swaminathan is a Huntsman Cancer Institute investigator and a member of the Nuclear Control of Cell Growth and Differentiation program. Dr. Swaminathan's research focuses on the regulation of gene expression in two viruses associated with lymphoma and other cancers: Epstein-Barr virus (EBV) and Kaposi’s sarcoma-associated herpes virus. He has been funded by the National Institute of Health for over 20 years. Dissecting the innate immune response and understanding the mechanisms that control these viruses’ replication is a major aspect of Swaminathan’s research.

In addition to his clinical and research duties, Dr. Swaminathan is a member of the editorial board of the Journal of Virology, works on NIH study sections, and serves as treasurer of the International Association for Research on EBV and Associated Diseases, among numerous other activities.

Research Statement

The major long-term goal of my research studies is to understand the mechanisms by which human cancer-causing herpesviruses interact with the host cell. We study Epstein-Barr virus (EBV) and Kaposi’s sarcoma-associated virus (KSHV). EBV has been identified as a cause of Burkitt’s lymphoma, Hodgkin’s lymphoma, lymphomas in transplant recipients, gastric cancer and nasopharyngeal carcinoma. KSHV causes lymphoma in addition to Kaposi’s sarcoma, a malignancy of the blood vessels. Both of these viruses maintain latent infections in their human host but intermittently lead to uncontrolled cellular proliferation that results in cancer. We apply molecular techniques to identify how specific viral gene products modulate cell functions. We introduce targeted genetic changes into the viral DNA, altering or deleting the gene of interest. Prior to 1990, it was not possible to do this with EBV. We developed techniques which allowed the generation of viable EBV viruses (genetic recombinants) that could be used to determine the role of virtually any EBV gene.

We have applied these and other methods to study a unique EBV gene, known as the SM gene, that regulates not only EBV genes, but also those of the host cell. The SM protein acts by pirating components of the host cell to facilitate expression of EBV genes and also modulates host gene expression. Our most recent research accomplishments include the following:

1) We have shown why the SM gene is essential for EBV replication by using an EBV microarray we developed. Specifically, SM is required for production of EBV DNA polymerase, and therefore for replication of the viral DNA, establishing the potential utility of SM as a therapeutic target for novel treatment modalities.

2) We have shown that SM affects host cell RNA splicing. This effect of EBV on host cell splicing, by altering the levels of signaling in the interferon signaling pathway, is predicted to have an inhibitory effect on IFN gamma signaling. Thus the EBV protein downregulates the host immune response to virus replication at the level of mRNA processing.

3) We have shown that several cellular genes induced by interferon (ISGs) are also induced specifically by SM protein. We have found that three of these cellular proteins potently inhibit growth of tumor cells. We are expressing these proteins in adeno-associated virus (AAV) vectors to determine if they could be used as gene therapy vectors with limited toxicity to normal cells.

4) We discovered and cloned the homolog of the SM gene in KSHV. By specifically deleting the gene from the virus, we showed that this gene is essential for KSHV replication. This work is currently funded by two NIH RO1 grants from the National Cancer Institute and we have been consistently funded by the NIH in the field of gammaherpesvirus research for over 18 years.

Our current research agenda consists of further discovery of the molecular interactions between EBV and KSHV and the host cell. Specifically, we are performing experiments to determine exactly how these RNA binding proteins recognize their target messenger RNAs. By defining the structure and sequence of the target, we will be able to fully understand how the virus modulates cellular gene expression. The second major area of research is to understand the role of the proteins produced by the host cell in response to interferon and viral infection (the ISGs). These proteins are the primary response of the cell to infection, yet surprisingly little is known about their function. By using affinity purification and mass spectroscopy, we are identifying the protein partners of the ISGs to map the pathways that they regulate, and how these protect against virus infection. Understanding the mechanism of action of these proteins has the potential to lead to discovery of protective mechanisms against viral infection.

Education

Education History

Type School Degree
Research Fellow Beth Israel Hospital, Brigham & Women's Hospital, Dana Farber Cancer Institute
Infectious Disease
Research Fellow
Research Fellow Harvard Medical School
Microbiology and Molecular Genetics
Research Fellow
Fellowship Beth Israel Hospital, Brigham & Women's Hospital, Dana Farber Cancer Institute
Infectious Disease
Clinical Fellow
Fellowship Harvard Medical School
Medicine
Clinical Fellow
Residency University of Chicago Medical Center
Internal Medicine
Resident
Internship University of Chicago Medical Center
Internal Medicine
Intern
Professional Medical Emory University School of Medicine
Medicine
M.D.
Graduate Training Emory University School of Medicine
Microbiology and Immunology
M.S.
Undergraduate Harvard College
Biochemistry and Molecular Biology, magna cum laude
A.B.

Publications

Selected Provider Publications

Journal Article

  1. Li DJ, Verma D, Mosbruger T, Swaminathan S (01/2014). CTCF and Rad21 Act as Host Cell Restriction Factors for Kaposi's Sarcoma-Associated Herpesvirus (KSHV) Lytic Replication by Modulating Viral Gene Transcription. PLoS Pathog, 10(1371).
  2. Verma D, Kim EA, Swaminathan S (2013). Cell-based screening assay for antiviral compounds targeting the ability of herpesvirus posttranscriptional regulatory proteins to stabilize viral mRNAs. J Virol, 87(19), 10742-51.
  3. Li DJ, Verma D, Swaminathan S (2012). Binding of cellular export factor REF/Aly by Kaposi's sarcoma-associated herpesvirus (KSHV) ORF57 protein is not required for efficient KSHV lytic replication. J Virol.
  4. Verma D, Bais S, Gaillard M, Swaminathan S (2010). Epstein-Barr Virus SM protein utilizes cellular splicing factor SRp20 to mediate alternative splicing. J Virol, 84(22), 11781-9.
  5. Verma D, Ling C, Johannsen E, Nagaraja T, Swaminathan S (2009). Negative autoregulation of Epstein-Barr virus (EBV) replicative gene expression by EBV SM protein. J Virol, 83(16), 8041-50.
  6. Han Z, Verma D, Hilscher C, Dittmer DP, Swaminathan S (2009). General and target-specific RNA binding properties of Epstein-Barr virus SM posttranscriptional regulatory protein. J Virol, 83(22), 11635-44.
  7. Verma D, Swaminathan S (2008). Epstein-Barr virus SM protein functions as an alternative splicing factor. J Virol, 82(14), 7180-8.
  8. Han Z, Marendy E, Wang YD, Yuan J, Sample JT, Swaminathan S (2007). Multiple roles of Epstein-Barr virus SM protein in lytic replication. J Virol, 81(8), 4058-69.
  9. Nekorchuk M, Han Z, Hsieh TT, Swaminathan S (2007). Kaposi's sarcoma-associated herpesvirus ORF57 protein enhances mRNA accumulation independently of effects on nuclear RNA export. J Virol, 81(18), 9990-8.
  10. Han Z, Swaminathan S (2006). Kaposi's sarcoma-associated herpesvirus lytic gene ORF57 is essential for infectious virion production. J Virol, 80(11), 5251-60.
  11. Swaminathan S (2005). Post-transcriptional gene regulation by gamma herpesviruses. J Cell Biochem, 95(4), 698-711.

Review

  1. Swaminathan S (2008). Oncogenic herpesvirus noncoding RNAs. [Review]. Journal of Cellular Physiology, 216(2), 321-6.

Book Chapter

  1. Swaminathan S (2010). The role of noncoding RNAs in EBV-induced cell growth and transformation. In Robertson ES (Ed.), Epstein-Barr Virus Latency and Transformation. Caister Academic Press.
  2. Swaminathan S, Kenney S (2009). Lytic EBV DNA Replication. In Damania B, Pipas J (Eds.), DNA Tumor Viruses. Springer Science.
  3. Swaminathan S (2008). Unusual Infections. In Layon A, Gabrielli A, Yu M (Eds.), Civetta, Taylor, & Kirby’s Critical Care (4th). Lippincott Williams & Wilkins.
  4. Swaminathan S (2007). Serious viral infections in adults. In Southwick F (Ed.), Infectious Diseases in thirty days (2nd). McGraw Hill.
  5. Swaminathan S (2005). Post-transcriptional Gene Regulation by EBV SM Protein. In Robertson E (Ed.), Infection, Pathogenesis, Molecular Biology and Control of Epstein - Barr virus. Horizon Press.

Commentary

  1. Swaminathan S (2009). Gamma-secretase inhibitors - Do they have a role in the treatment of B cell lymphoma? Cancer Biol Ther, 8(22), 2126-43.

Clinical Trials

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