Area of research
Epidemiology · Genetics
Research interest
Research interests include Herpesvirus Infections and Treatments, Virus-based gene therapy research, Cytomegalovirus and herpesvirus research, and Toxin Mechanisms and Immunotoxins.
Statement in support of the scientists, public health professionals, and medical professionals of China combatting COVID-19
hnRNPA2B1 Associated with Recruitment of RNA into Exosomes Plays a Key Role in Herpes Simplex Virus 1 Release from Infected Cells
Herpes Simplex Virus 1 MicroRNA miR-H28 Exported to Uninfected Cells in Exosomes Restricts Cell-to-Cell Virus Spread by Inducing Gamma Interferon mRNA
miRNAs Targeting ICP4 and Delivered to Susceptible Cells in Exosomes Block HSV-1 Replication in a Dose-Dependent Manner
Innate responses to gene knockouts impact overlapping gene networks and vary with respect to resistance to viral infection
PUM1 is a biphasic negative regulator of innate immunity genes by suppressing LGP2
The SP100 component of ND10 enhances accumulation of PML and suppresses replication and the assembly of HSV replication compartments
miR-H28 and miR-H29 expressed late in productive infection are exported and restrict HSV-1 replication and spread in recipient cells
PML plays both inimical and beneficial roles in HSV-1 replication
The 3 facets of regulation of herpes simplex virus gene expression: A critical inquiry
Role of activating transcription factor 3 in the synthesis of latency-associated transcript and maintenance of herpes simplex virus 1 in latent state in ganglia
Cells infected with herpes simplex virus 1 export to uninfected cells exosomes containing STING, viral mRNAs, and microRNAs
HSV-1 degrades, stabilizes, requires, or is stung by STING depending on ICP0, the US3 protein kinase, and cell derivation
RIG-I–like receptor LGP2 protects tumor cells from ionizing radiation
Patterns of accumulation of miRNAs encoded by herpes simplex virus during productive infection, latency, and on reactivation
An Inquiry into the Molecular Basis of HSV Latency and Reactivation
Selective degradation of mRNAs by the HSV host shutoff RNase is regulated by the U <sub>L</sub> 47 tegument protein
Modulation of reactivation of latent herpes simplex virus 1 in ganglionic organ cultures by p300/CBP and STAT3
The Virion Host Shutoff RNase Plays a Key Role in Blocking the Activation of Protein Kinase R in Cells Infected with Herpes Simplex Virus 1
The Herpes Simplex Virus Host Shutoff RNase Degrades Cellular and Viral mRNAs Made before Infection but Not Viral mRNA Made after Infection
The Role of the CoREST/REST Repressor Complex in Herpes Simplex Virus 1 Productive Infection and in Latency
HSV carrying WT REST establishes latency but reactivates only if the synthesis of REST is suppressed
Molecular Pathways: Interferon/Stat1 Pathway: Role in the Tumor Resistance to Genotoxic Stress and Aggressive Growth
Induction of apoptosis accelerates reactivation of latent HSV-1 in ganglionic organ cultures and replication in cell cultures