Eduardo Salinas
Molecular Biologist III
Also affiliated: Oregon National Primate Research Center (2021); Centers for Disease Control and Prevention (2024); Emory University (2020–2024); Emory and Henry College (2022); Cherokee Nation (2024); Atlanta VA Medical Center (2022); Emory National Primate Research Center (2022–2024); The Ohio State University (2021)
Faculty Researcher
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Eduardo Salinas's research focuses on the immune response to viral infections, particularly hepatitis C virus (HCV) and SARS-CoV-2. His work investigates the roles of T cells and B cells in viral clearance and persistence. Salinas has published on how CD8+ T cell depletion affects hepatitis E virus resolution in macaques and the acceleration of HCV-specific B cell expansion by T follicular helper cells. His recent publications also explore the neutralization and receptor use of rat hepacivirus as an HCV model, the decline of serum neutralization activity and persistence of memory B cells after HCV cure, and the requirement of CD4+ and CD8+ T cells to prevent SARS-CoV-2 persistence in mice. He has also examined differential immune transcriptomic profiles in HCV-reinfected subjects and the intrinsic p53 activation restricting gammaherpesvirus-driven B cell expansion. Salinas has an h-index of 12, with 20 total publications and 276 citations. He collaborates with several researchers at the University of Arkansas for Medical Sciences, including Jason S. Stumhofer, J. Craig Forrest, Mark Manzano, and Shana M. Owens.
Metrics
- h-index: 12
- Publications: 20
- Citations: 286
Selected Publications
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Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment (2025)
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p53 Controls Murine Gammaherpesvirus Latency and Prevents Infection-Associated <i>IgH/c-Myc</i> Translocations (2020)
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Conditional mutagenesis in vivo reveals cell type- and infection stage-specific requirements for LANA in chronic MHV68 infection (2018)
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Murine Gammaherpesvirus 68 Expressing Kaposi Sarcoma-Associated Herpesvirus Latency-Associated Nuclear Antigen (LANA) Reveals both Functional Conservation and Divergence in LANA Homologs (2017)
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Identification of Viral and Host Proteins That Interact with Murine Gammaherpesvirus 68 Latency-Associated Nuclear Antigen during Lytic Replication: a Role for Hsc70 in Viral Replication (2015)
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Murine Gammaherpesvirus 68 LANA and SOX Homologs Counteract ATM-Driven p53 Activity during Lytic Viral Replication (2015)
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Tiled Microarray Identification of Novel Viral Transcript Structures and Distinct Transcriptional Profiles during Two Modes of Productive Murine Gammaherpesvirus 68 Infection (2012)
Collaboration Network
Top Collaborators
- Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment
- Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment
- Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment
- Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment
- Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment
- Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment
- Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment
- Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment
- Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment
- Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment
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