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Biography and Research Information
OverviewAI-generated summary
Eduardo Salinas's research focuses on viral infections and the host immune response, with a significant emphasis on hepatitis C virus (HCV). His work investigates the mechanisms by which the immune system, including T cells and B cells, contributes to viral clearance and the development of immune memory. Salinas has studied the role of specific immune cell populations, such as CD8+ T cells and T follicular helper cells, in controlling viral replication and preventing persistent infection. His research also explores the development of novel animal models for studying viral diseases, including the use of cultured rat hepacivirus to better understand HCV infection. Furthermore, his publications indicate an interest in the long-term immunological consequences of viral infections, such as the persistence of memory B cells after viral cure, and the immune responses to reinfection. He has also contributed to research on SARS-CoV-2 persistence and the immune system's role in nasal compartment control.
Metrics
- h-index: 12
- Publications: 20
- Citations: 270
Selected Publications
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Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment (2025)
Collaboration Network
Top Collaborators
Arash Grakoui
Emory National Primate Research Center
9 shared publications
- Early T follicular helper cell activity accelerates hepatitis C virus-specific B cell expansion
- Resolution of hepatitis E virus infection in CD8+ T cell-depleted rhesus macaques
- Neutralization and receptor use of infectious culture–derived rat hepacivirus as a model for HCV
- Serum neutralization activity declines but memory B cells persist after cure of chronic hepatitis C
- CD4 <sup>+</sup> and CD8 <sup>+</sup> T cells are required to prevent SARS-CoV-2 persistence in the nasal compartment
Showing 5 of 9 shared publications
Elizabeth J. Elrod
Emory University (US)
4 shared publications
- Neutralization and receptor use of infectious culture–derived rat hepacivirus as a model for HCV
- CD4 <sup>+</sup> and CD8 <sup>+</sup> T cells are required to prevent SARS-CoV-2 persistence in the nasal compartment
- Concerted synergy between viral-specific IgG and CD8+ T cells is critical for clearance of an HCV-related rodent hepacivirus
- CD4+ and CD8+ T cells are required to prevent SARS-CoV-2 persistence in the nasal compartment
Nathalie Bédard
Centre Hospitalier de l’Université de Montréal (CA)
2 shared publications
- Early T follicular helper cell activity accelerates hepatitis C virus-specific B cell expansion
- Differential immune transcriptomic profiles between vaccinated and resolved HCV reinfected subjects
Joseph Marcotrigiano
National Institutes of Health (US)
2 shared publications
- Early T follicular helper cell activity accelerates hepatitis C virus-specific B cell expansion
- Concerted synergy between viral-specific IgG and CD8+ T cells is critical for clearance of an HCV-related rodent hepacivirus
Naglaa H. Shoukry
Université de Montréal (CA)
2 shared publications
- Early T follicular helper cell activity accelerates hepatitis C virus-specific B cell expansion
- Differential immune transcriptomic profiles between vaccinated and resolved HCV reinfected subjects
Heather Blasczyk
2 shared publications
- Resolution of hepatitis E virus infection in CD8+ T cell-depleted rhesus macaques
- Contribution of soluble ORF2 viral protein to viral replication and host immune response during acute Hepatitis E virus infection
Zongdi Feng
2 shared publications
- Resolution of hepatitis E virus infection in CD8+ T cell-depleted rhesus macaques
- Contribution of soluble ORF2 viral protein to viral replication and host immune response during acute Hepatitis E virus infection
Christopher M. Walker
2 shared publications
- Resolution of hepatitis E virus infection in CD8+ T cell-depleted rhesus macaques
- Contribution of soluble ORF2 viral protein to viral replication and host immune response during acute Hepatitis E virus infection
Sheetal Trivedi
Nationwide Children's Hospital (US)
2 shared publications
- Neutralization and receptor use of infectious culture–derived rat hepacivirus as a model for HCV
- Concerted synergy between viral-specific IgG and CD8+ T cells is critical for clearance of an HCV-related rodent hepacivirus
Amit Kapoor
Nationwide Children's Hospital (US)
2 shared publications
- Neutralization and receptor use of infectious culture–derived rat hepacivirus as a model for HCV
- Concerted synergy between viral-specific IgG and CD8+ T cells is critical for clearance of an HCV-related rodent hepacivirus
Charles M. Rice
Rockefeller University (US)
2 shared publications
- Neutralization and receptor use of infectious culture–derived rat hepacivirus as a model for HCV
- Concerted synergy between viral-specific IgG and CD8+ T cells is critical for clearance of an HCV-related rodent hepacivirus
Brantley Holland
Emory University (US)
2 shared publications
- Concerted synergy between viral-specific IgG and CD8+ T cells is critical for clearance of an HCV-related rodent hepacivirus
- Contribution of soluble ORF2 viral protein to viral replication and host immune response during acute Hepatitis E virus infection
Shana M. Owens
University of Arkansas for Medical Sciences
2 shared publications
In database
- 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
Jeffrey M. Sifford
University of Arkansas for Medical Sciences
2 shared publications
In database
- 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
Steven Murdock
University of Arkansas for Medical Sciences
2 shared publications
In database
- 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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