About Hyeryun Choe
Hyeryun Choe has done her graduate studies at Pennsylvania State University and received her Ph.D. degree from the Department of Biochemistry, Molelcular Biology, and Cell Biology in erythrocyte membrane lipid bilayer asymmetry in diseases such as sickle cell anemia. During her postdoctoral training at Beth Israel Hospital and Dana Farber Cancer Institute at Harvard Medical School, her research interests broadened to viruses and the mechanisms with which viruses enter cells and cause diseases. In the decade of 2000, as Assistant and Associate Professor at the Department of Pediatrics, Boston Children’s Hospital, Harvard Medical School, Dr. Choe discovered or co-discovered the HIV-1 coreceptors CCR3 and CCR5, the SARS-CoV receptor ACE2 when it emerged in the winter of 2002, and TFR1 as the receptor for all five South American hemorrhagic fever viruses. Of these, the identification of ACE2 as the receptor for SARS-CoV likely accelerated SARS-CoV-2 research because SARS-CoV-2 also uses ACE2 as its entry receptor. In the following decade after her relocation to the Scripps Research, Dr. Choe, as Associate Professor and Professor, studied the entry mechanisms of newly emerging viruses such as West Nile virus, Zika virus, and SARS-CoV-2. Her passion is to develop or contribute to developing effective vaccines or vaccine alternatives against dengue virus that infects hundreds of millions people and causes diseases in tens of millions a year.
Viruses enter cells through common mechanisms. Parallel studies of the entry processes of various viruses can therefore highlight differences among them, as well as their similarities. The Choe laboratory studies a wide range of viruses to better understand their entry pathways and the mechanisms of pathogenesis of viral diseases. In doing so, we identified a number of viral receptor and host factors critical for viral infection and pathogenesis. These include: the HIV-1 coreceptor CCR5, and its post-translational modification tyrosine sulfation critical HIV-1 infection; the SARS-CoV receptor angiotensin-converting enzyme 2 (ACE2) and the lysosomal enzyme cathepsin L as an essential target-cell factors for SARS-CoV infection; transferrin receptor 1 (TFR1) as the receptor for New World hemorrhagic fever arenaviruses, and the intimate association between virus’ ability to use human TFR1 and its tendency to cause hemorrhagic fever. We also study other entry factors such as the TIM family members of phosphatidylserine receptors. By binding the lipids on the virion membrane, they promote the infections of a wide range of enveloped viruses including filoviruses and flaviviruses such as West Nile, dengue and Zika viruses.
In addition to our focus on basic virology, we use our knowledge to discover entry inhibitors and to develop strategies to improve known inhibitors. We have previously identified potent antibodies that inhibited the infection of all five NW hemorrhagic fever arenaviruses. We also employ a novel strategy to improve the potency and breadth of protein inhibitors.
Recently, we extended our studies to adeno-associated virus (AAV), a commonly used gene therapy vector, with the goal of improving its transduction efficiency in specific target cells. We successfully developed AAV vectors that transduce skeletal muscle or CD4+ T cells with markedly improved efficiency and specificity.