Salk Institute for Biological Studies


John A. T. Young

John A. T. Young

Nomis Foundation Laboratories for Immunobiology and Microbial Pathogenesis
Nomis Foundation Chair



John A. T. Young, a Professor in the Nomis Foundation Laboratories for Immunobiology and Microbial Pathogenesis, studies the cell biology of virus infection and anthrax intoxication. His laboratory is identifying and characterizing cellular factors that contribute to the early steps of infection by HIV and other retroviruses, influenza virus, and filoviruses such as Ebola virus. These studies are giving novel insights into virus-host interactions and are suggesting new therapeutic strategies for combating virus infection. The Young laboratory has also identified both known cellular receptors for anthrax toxin. Current research in the lab is aimed at understanding how these receptors, along with other cellular factors, regulate anthrax toxin entry into cells. Soluble versions of a cellular receptor are also being developed as receptor decoys to efficiently neutralize anthrax toxin.

"A major goal of our work is to reveal how host cell proteins either contribute to or defend against infection by important human microbial pathogens, such as HIV, influenza virus, Ebola virus and the bacterium that causes anthrax. Knowledge of the roles played by this cellular machinery provides new insights into the cell biology of microbial infections and could suggest new broad-spectrum antimicrobial approaches."

A major focus of Young's work is on the HIV virus. HIV/AIDS continues to be a serious global problem. The virus can remain "hidden" in a latent form in infected individuals for years, even after long-term suppression with highly active antiretroviral therapy. Moreover, viral drug resistance represents a formidable problem, creating an urgent need for new classes of antiretrovirals.

HIV begins its assault by injecting its core, which contains single-stranded RNA, into a host cell. Once inside, the viral RNA is converted into double-stranded DNA—a process known as reverse transcription—and the original viral RNA is degraded. Another enzyme, integrase, mediates the final step of the genome conversion, where the viral double-stranded DNA slips into the host's DNA, allowing it to take advantage of the host cell's genetic machinery to replicate and propagate itself. During these early steps of infection, the virus relies heavily on its host cell to lend a helping hand, which makes it particularly vulnerable to antivirals and host defense mechanisms.

To identify cellular processes that either facilitate or defend against HIV-1 infection, Young and his collaborators use systems biology approaches to investigate the roles played by individual genes in the genome of host cells. These experiments have uncovered ZASC1, a new regulator of virus gene expression. They have also revealed that sulfonation—a type of chemical modification— regulates viral gene expression. A number of cellular factors they have identified restrict HIV infection, some of which play known roles in innate immunity, one of the body's defense mechanisms that protect against microbial infections. In addition, virus countermeasures of these host defenses are being identified. Young anticipates that these discoveries will open up new avenues for the development of drugs that specifically interfere with HIV replication.

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