J. Craig Forrest
Professor
University of Arkansas for Medical Sciences
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Biography and Research Information
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J. Craig Forrest's research program focuses on understanding the pathogenesis of gammaherpesviruses and the immune response to viral infections. He has served as Principal Investigator on multiple NIH-funded grants totaling over $1.2 million, investigating mechanisms of gammaherpesvirus-driven genomic instability in B cells, KSHV LANA functions in viral pathogenesis and immune evasion, and the role of lytic viral genes in oncogenic gammaherpesvirus pathogenesis. He also contributed as a Co-PI on a grant examining how periodontal bacteria enhance oral KSHV pathogenesis and Kaposi's Sarcoma development in HIV+ patients.
His recent publications include work on ACE2 autoantibodies after SARS-CoV-2 infection, the Serological Sciences Network (SeroNet) for COVID-19 assay harmonization and epidemiological cohort studies, and pediatric SARS-CoV-2 seroprevalence in Arkansas. Forrest's laboratory has also published on the protective effects of a replication-deficient gammaherpesvirus vaccine in mice and the role of B cell-intrinsic STAT3 in viral latency and interferon suppression during murine gammaherpesvirus 68 infection.
With a career h-index of 26 and over 2,800 citations across 65 publications, Forrest is recognized as a highly cited researcher. He collaborates extensively with colleagues at the University of Arkansas for Medical Sciences, including Shana M. Owens and Joshua L. Kennedy.
Metrics
- h-index: 26
- Publications: 65
- Citations: 2,893
Selected Publications
- The amplitude of gammaherpesvirus lytic replication dictates adaptive immune activation: Potential implications for KSHV LANA in immune evasion (2026) DOI
- Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment (2025) DOI
- Vaccination with a Replication-Dead Murine Gammaherpesvirus Lacking Viral Pathogenesis Genes Inhibits WT Virus Infection (2024) DOI
- Vaccination with a Replication-Dead Murine Gammaherpesvirus Lacking Viral Pathogenesis Genes Inhibits WT Virus Infection (2024) DOI
- Molecular Mechanisms of KSHV Latency Establishment and Maintenance (2024) DOI
- A replication-deficient gammaherpesvirus vaccine protects mice from lytic disease and reduces latency establishment (2024) DOI
- Multifaceted roles for STAT3 in gammaherpesvirus latency revealed through <i>in vivo</i> B cell knockout models (2024) DOI
- Intrinsic p53 Activation Restricts Gammaherpesvirus-Driven Germinal Center B Cell Expansion during Latency Establishment (2023) DOI
- Replication-dead gammaherpesvirus vaccine protects against acute replication, reactivation from latency, and lethal challenge in mice (2023) DOI
- Uracil-DNA glycosylase of murine gammaherpesvirus 68 binds cognate viral replication factors independently of its catalytic residues (2023) DOI
- A longitudinal study of SARS-CoV-2 antibody seroprevalence and mitigation behaviors among college students at an Arkansas University (2023) DOI
- Uracil-DNA Glycosylase of Murine Gammaherpesvirus 68 Binds Cognate Viral Replication Factors Independently of its Catalytic Residues (2023) DOI
- B cell-intrinsic STAT3-mediated support of latency and interferon suppression during murine gammaherpesvirus 68 infection revealed through an <i>in vivo</i> competition model (2023) DOI
- The Serological Sciences Network (SeroNet) for COVID-19: Depth and Breadth of Serology Assays and Plans for Assay Harmonization (2022) DOI
- Lytic Replication and Reactivation from B Cells Is Not Required for Establishing or Maintaining Gammaherpesvirus Latency <i>In Vivo</i> (2022) DOI
Federal Grants 4 $1,590,316 total
Lytic viral genes in the pathogenesis of oncogenic gammaherpesviruses
Defining KSHV LANA functions in viral pathogenesis and immune evasion
Defining mechanisms of gammaherpesvirus-driven genomic instability in B cells
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