About

Felicia Goodrum is an Interim Associate Department Head in Immunobiology at the University of Arizona. She is associated with the Biochemistry and Molecular & Cellular Biology Graduate Program. Her professional profile is available through the university's website. The page acknowledges her role within the department and her connection to the university, but does not provide specific details about her research focus, background, or key contributions.

Research topics

• Virology
• Immunology
• Political Science
• Pathology
• Medicine
• Biology

Selected publications

• Viral and host network analysis of the human cytomegalovirus transcriptome in latency.

  UNC Libraries · 2026-05-06

  articleOpen accessSenior author

  The human cytomegalovirus (HCMV) <em>UL135</em> and <em>UL138</em> genes play opposing roles regulating latency and reactivation in CD34⁺ human progenitor cells. We designed an RNA sequencing study to compare the transcriptional profile of HCMV infection in the presence and absence of these genes using the Tohoku Hospital Pediatrics-1 (THP-1) monocytic cell line model for latency. Relative to primary cell models, THP-1 cells offer the strength of a homogenous population that uniformly silences gene expression and will synchronously reexpress viral genes following stimulation to differentiate, which models early phases of viral reactivation. The loss of <em>UL138</em> resulted in elevated levels of viral gene expression and in spontaneous adhesion of distinct cell populations that support HCMV gene expression and genome synthesis. The loss of <em>UL135</em> resulted in diminished viral gene expression during an initial burst that occurs as latency is established and in no expression of eleven viral genes from the UL<em>b</em>' region even following differentiation and reexpression of viral genes. Transcriptional network analysis revealed host transcription factors (TFs) with potential to regulate the UL<em>b</em>' genes in coordination with pUL135. We show that the cellular TF peroxisome proliferator-activated receptor gamma binds to the viral genome and influences the expression of <em>UL133-UL138</em> locus genes. Our results define roles for <em>UL135</em> and <em>UL138</em> in regulation of patterns of viral gene expression for the establishment of latency and reexpression of viral genes for reactivation and reveal insights into differentiation-linked mechanisms of transcriptional control of the HCMV genome.

  PublisherDOI

• A call for the United States to continue investing in science

  Journal of Virology · 2025-02-27

  editorialOpen access
  PublisherDOI

• A call for the United States to continue investing in science

  Clinical Microbiology Reviews · 2025-02-27

  reviewOpen access
  PublisherDOI

• A call for the United States to continue investing in science

  ASM Case Reports · 2025-02-27

  articleOpen access
  PublisherDOI

• A call for the United States to continue investing in science

  mSystems · 2025-02-27

  editorialOpen access
  PublisherDOI

• 2024 Acknowledgment of <i>Journal of Virology Ad Hoc</i> Reviewers

  Journal of Virology · 2025-05-20

  articleOpen access1st authorCorresponding
  PublisherDOI

• Human cytomegalovirus regulates host DNA repair machinery for viral genome integrity

  Nucleic Acids Research · 2025-12-05

  articleOpen accessSenior author

  The DNA damage response (DDR) encompasses a multitude of interconnected pathways that serve as a cellular defense to protect genome integrity. Dysregulation or failure of these pathways results in cancers and genetic disease. DNA viruses, including the herpesvirus cytomegalovirus (CMV), activate DDR signaling during their replicative program. The mechanisms by which they commandeer these responses for replication of their genome remain unclear. Here, we define a viral protein, UL138, that modulates the activity of host DDR pathways. The loss of UL138 results in structural variants, including inversions, deletions, and duplications, with signature of homology-directed repair and other DDR pathways. The actions of UL138 are due, in part, to its modulation of pathways regulated by the cellular deubiquitinating complex that targets proliferating cell nuclear antigen (PCNA) and Fanconi Anemia effectors, FANCD2 and FANCI. However, we also show that UL138 accesses pathways independent of USP1-PCNA/FANCD2/FANCI. Disruption of UL138 or these pathways impacted viral genome replication and had consequences for viral genome integrity. This work provides mechanistic insight into the long-standing questions of how DNA viruses recruit, modulate and use cellular DDR pathways. It also puts forth CMV as a model system for further defining these pathways in human cells.

  PublisherDOI

• Human cytomegalovirus promotes <i>de novo</i> PC synthesis during early virus replication

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-03-06

  preprint

  ABSTRACT Human cytomegalovirus (HCMV) infection reprograms metabolism, including lipid synthesis. While several metabolite-related pathways have been demonstrated to have altered activity in infected cells, the alteration of lipid-related pathways by HCMV has not been examined beyond fatty acid synthesis and elongation. In this study, we addressed this lack of understanding by focusing on phosphatidylcholine (PC), a class of lipids we previously showed is increased by HCMV infection in human foreskin fibroblasts. Here, we found that HCMV infection increases the abundance of PCs in several different fibroblasts and, similarly, in endothelial and epithelial cells. Additionally, HCMV elevates PC levels regardless of the level of confluency, type of growth medium, and presence of serum. Next, we investigated if HCMV alters the activity in the three PC synthesis pathways. We demonstrate that HCMV infection promotes the activity in the de novo PC synthesis pathway using a 13 C-choline isotopic tracer and liquid chromatography high resolution tandem mass spectrometry (LC-MS/MS). Infection did not alter the activity in the other two pathways. Moreover, we examined the kinetics of PC remodeling by HCMV and found that the de novo synthesis pathway is promoted and the PC lipidome shifts 24 hours post infection. That led us to examining if the early stages of replication are sufficient to alter PC levels. After inhibiting late virus replication, we found that HCMV alters the PC lipidome independent of late gene expression. Overall, this work suggests that an immediate-early or early viral protein promotes the reprogramming of host lipid metabolism to ensure the synthesis of a lipidome necessary to support HCMV replication. IMPORTANCE Human cytomegalovirus (HCMV) is a common herpesvirus that establishes a lifelong and persistent infection in its human host (1). HCMV infection in most people does not cause overt disease (1). However, in immunocompromised individuals, severe CMV-associated disease can lead to permanent disabilities and even death (1, 2). Additionally, congenital CMV is the leading infectious cause of birth defects (3, 4). Viruses have evolved to hijack host metabolic pathways to facilitate their replication cycle. In this study, we determine that HCMV promotes the activity in the de novo pathway of phosphatidylcholine (PC) synthesis. We demonstrate that the activity in the other PC synthesis pathways, the PEMT and Lands cycle, is unaltered by HCMV infection. Moreover, we found that HCMV infection alters metabolic activity to increase the PC lipidome before 48 hpi. Additionally, we demonstrate that changes in PC lipids during virus replication is independent of late gene expression. Together, our findings demonstrate that infection promotes the de novo PC pathway to increase PC lipids during the early stages of virus replication.

  PublisherDOI

• A call for the United States to continue investing in science

  Journal of Bacteriology · 2025-02-27

  editorialOpen access
  PublisherDOI

• A call for the United States to continue investing in science

  mSphere · 2025-02-27 · 1 citations

  editorialOpen access
  PublisherDOI

Recent grants

• Molecular Switch Regulating Human Cytomegalovirus Replicative and Latent States

  NIH · $2.7M · 2018–2024

• Mechanisms of Human Cytomegalovirus Latency in Primary Human Hematopoietic Cells

  NIH · $2.9M · 2025–2029

• CMV Control of Host Membrane Trafficking

  NIH · $2.1M · 2018–2024

• Antagonistic Viral Determinants Regulating the Outcome of Infection

  NIH · $380k · 2013–2015

• NIH Grant K01CA111343

  NIH · $723k · 2010

Frequent coauthors

• Thomas Shenk

  Princeton University

  34 shared

• Kevin P. High

  Cincinnati Children's Hospital Medical Center

  27 shared

• Craig T. Jordan

  26 shared

• Jason Buehler

  21 shared

• Jeremy P. Kamil

  Louisiana State University Health Sciences Center Shreveport

  20 shared

• Michael Rak

  University of Arizona

  19 shared

• Donna Collins-McMillen

  University of Arizona

  18 shared

• Nathaniel J. Moorman

  University of North Carolina at Chapel Hill

  17 shared