Page 9 - Abacoa Community News - March '23
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      The Scripps Research Institute                     drugs.” When HIV infects an immune cell, it can remain   Three Symposium Poster Presenters Take
                                                         dormant for years. If untreated, viral loads eventually   Home Awards
                                                         increase  and  weaken  the  immune  system  to  the  point      Conferences hold poster sessions to foster science
                                                         where it cannot ward off infection and disease. This final,   communications and presentation skills among scientific
                                                         terminal stage is AIDS.                           trainees. At “RNA: From Biology to Drug Discovery,” trainees
      Potential Target For HIV Advances Block-              Antiretroviral therapy, or ART, can keep HIV loads   had the opportunity to showcase their work to some of the field’s
      And-Lock Strategy To Stop AIDS                     low so the patient does not progress to AIDS. But this   leading scientists. Three trainees took home awards.
         Researchers  at  The                            requires a daily drug regimen that lasts a lifetime. HIV,
      Herbert W ertheim                                  however, still lingers in cells and causes low-level
      University of Florida                              inflammation. This can potentially put patients who have
      (UF) Scripps Institute for                         HIV at greater risk for diseases of the cardiovascular
      Biomedical Innovation                              system, kidney, bones or liver as well as for diabetes,
      & Technology  have                                 cognitive disorders and some types of cancer, even when
      discovered a protein  that                         they do not progress to AIDS. ART is not a cure for
      appears to play a key role                         HIV but allows it to be controlled as a chronic disease.
      in helping HIV replicate                           However, if therapy is interrupted, viral loads will again
      in human immune cells,                             climb to dangerous levels. Some HIV researchers have
      providing more clues about     An HIV-infected T cell  focused on a “shock and kill” strategy to eradicate the
      how cellular machinery             Photo by NIAID  virus and move beyond ART. This involves using drugs
      allows the virus to create                         to awaken dormant HIV-infected cells, where they had   Dr. Herbert Wertheim presents poster awards to Jessica
      new copies of itself. The insight is more than scientific   been invisible to the immune system. Once activated, the   Bush, Ryan Hildebrandt, Ph.D., and Ebba Blomqvist.
      curiosity – the protein,                           immune system can then attack and destroy cells carrying
      called p32, might provide                          the virus.                                           Ryan Hildebrandt, Ph.D., a postdoctoral researcher
      a potential target for drugs                          That goal, however, remains elusive, Valente said,   with associate professor Eric T. Wang, Ph.D., at the
      that keep HIV dormant                              because it has proved difficult to reawaken and destroy   University of Florida in Gainesville, took home a poster
      and harmless.  The goal                            every copy of the virus in the body without severe   award for his studies of how RNA moves within cells
      is to achieve what would                           side effects. All it  takes  is one  infected  cell for HIV   by riding other molecules, kinesins, enabling localized
      essentially be a cure for                          to propagate  anew.  Valente  has instead  pioneered  a   protein construction in cells.
      HIV and thus AIDS. “p32                            “functional cure” strategy called “block and lock,” an      Ebba Blomqvist, an FAU graduate and research
      is one piece of the puzzle,”                       approach that blocks  reactivation  of  HIV  in  dormant   technician  with  professor  Katrin  Karbstein,  Ph.D.,  of
      said  Susana  Valente,                             cells without eradicating them, then locks them in that   The Wertheim UF Scripps Institute, described discovery
      Ph.D., a professor at The                          quiescent state. This is where another important protein,   of how an assembly factor helps make ribosomes, the
      Wertheim UF Scripps                                Tat, comes into play. Tat is a regulatory protein that can   cellular organelles that build proteins.
      Institute and chair of its                         boost the cellular assembly line that replicates the virus      Jessica Bush, a doctoral student working in the Disney
      department of immunology   Susana Valente, Ph.D    so it can, in turn, spread and infect additional cells.   lab, won a poster award for her work designing a small,
      and microbiology. She is                           Eliminate Tat, Valente said, and you might lock HIV into   drug-like molecule to degrade an RNA that causes ALS
      the senior author of a paper on p32 published Dec. 30 in   a perpetual state of dormancy. Without Tat, you have a   and frontotemporal dementia.
      the Proceedings of the National Academy of Sciences, a   very weak virus,” she said. p32 also interacts with Tat,      Institute benefactor Dr. Herbert Wertheim presented
      peer-reviewed scientific journal.                  helping to stabilize it, which might make p32 as good a   their certificates, praising them for hard work and
         “This adds another layer of complexity to understanding   target as Tat, Valente said. p32 might serve as a hub where   dedication to expanding knowledge, as they work for the
      HIV,” she added. “We need to identify all of these   other proteins associated with HIV replication can dock.   betterment of humanity.
      unknown factors that help HIV replicate itself, and   “It basically stabilizes the whole complex,” she said.
      ultimately some of them can be targeted in the future by                                             The Scripps Research Institute on page 10


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