“Infectious diseases have no geographic boundaries.  It doesn’t matter whether a country is rich or poor, developed or developing, these diseases can still arrive.” – Sujan Shresta, Ph.D.

Sujan Shresta joined LIAI in 2005 as an Assistant Member in the Vaccine Discovery Division. Dr. Shresta's research focuses on the interface between immunology and virology, with particular interest in viral immunopathogenesis.

Dr. Shresta obtained her B.A. in Biological Sciences from Smith College and Ph.D. in Immunology from Washington University in St. Louis. She completed her post-doctoral training in Virology at the University of California, Berkeley. She received a Research Scholar Development award from the NIAID in 2005.

Sujan Shresta, Ph.D., and her team study the immunology of dengue virus (DEN), a globally important mosquito-borne human pathogen. DEN causes a spectrum of clinical disease ranging from Dengue Fever (DF), a self-limited febrile illness, to a life-threatening syndrome called Dengue Hemorrhagic Fever/Dengue Shock Syndrome (DHF/DSS).

Studies suggest that DHF/DSS is an immunopathogenic disease; however, the precise role of the immune system in response to DEN infection is presently unclear. Using a mouse model, Dr. Shresta and her team plan to dissect the protective versus pathogenic mechanisms of the immune system in response to this viral infection. Presently, they are identifying immune mediators that control primary and sequential DEN infections using mice that are genetically deficient in specific components of the immune system. A better understanding of the immune response to DEN is critical for developing much-needed anti-viral therapies and vaccines.

A second line of research involves the identification of viral components that modulate the severity of DEN infection. Dr. Shresta and her team have isolated novel DEN strains that cause a severe disease phenotype in mice by adapting viral isolates from humans and mosquitoes into peripheral tissues of mice. They are currently developing a reverse-genetics system, in which specific viral sequences are manipulated within the context of a full-length infectious clone of the virus. Knowledge of the viral determinants of infection should provide novel avenues for developing anti-virals and vaccines.

Cardif-mediated signaling controls the initial innate response to dengue virus in vivo. J Virol. 2009

A protective role for dengue virus-specific CD8+ T cells. J Immunol. 2009

Mouse models of dengue virus infection and disease. Antiviral Research. 2008

A mouse-passaged dengue virus strain with reduced affinity for heparan sulfate causes severe disease in mice by establishing increased systemic viral loads. Journal of Virology. 2008

A murine model for dengue virus-induced lethal disease with increased vascular permeability. Journal of Virology. 2006

Critical roles for both STAT1-dependent and STAT1-independent pathways in the control of primary dengue virus infection in mice. Journal of Immunology. 2005

Interferon-dependent Immunity is essential for resistance to primary dengue virus infection in mice, whereas T and B cell-dependent immunity are less critical. Journal of Virology. 2004

Early activation of natural killer and B cells in response to dengue virus infection in A/J mice. Virology. 2004

ICOS co-stimulatory receptor is essential for T-cell activation and function. Nature. 2001

Granzyme A initiates an alternative pathway for granule-mediated apoptosis. Immunity. 1999

How do cytotoxic lymphocytes kill their targets? Current Opinion in Immunology. 1998

Residual cytotoxicity and granzyme K expression in granzyme A-deficient cytotoxic lymphocytes. Journal of Biological Chemistry. 1997

Mechanisms responsible for granzyme B-independent cytotoxicity. Blood. 1997

Profiles of pulp infiltrating lymphocytes at various times throughout feather regeneration in smyth line chickens with vitiligo. Autoimmunity. 1997

Natural killer and lymphokine-activated killer cells require granzyme B for the rapid induction of apoptosis in susceptible target cells. Proceedings of the National Academy of Science USA. 1995

Granzyme B plays a critical role in cytotoxic lymphocyte induced apoptosis. Immunological Reviews. 1995

Cytotoxic lymphocytes require granzyzme B for the rapid induction of DNA fragmentation and apoptosis in allogeneic target cells. Cell. 1994

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