Area of research
Epidemiology · Dermatology
Research interest
Research interests include Biology, Herpes simplex virus, Virology, Capsid, Viral tegument, and Infectivity.
Human IFITM3 restricts chikungunya virus and Mayaro virus infection and is susceptible to virus-mediated counteraction
Absence of cGAS-mediated type I IFN responses in HIV-1–infected T cells
Herpes Simplex Virus Type 1 Propagation, Titration and Single-step Growth Curves
Importin α1 is required for nuclear import of herpes simplex virus proteins and capsid assembly in fibroblasts and neurons
Autophagic degradation of lamins facilitates the nuclear egress of herpes simplex virus type 1
The ATP-Dependent RNA Helicase DDX3X Modulates Herpes Simplex Virus 1 Gene Expression
Inner tegument proteins of Herpes Simplex Virus are sufficient for intracellular capsid motility in neurons but not for axonal targeting
Herpes simplex virus 1 interferes with autophagy of murine dendritic cells and impairs their ability to stimulate CD8<sup>+</sup> T lymphocytes
Conserved Tryptophan Motifs in the Large Tegument Protein pUL36 Are Required for Efficient Secondary Envelopment of Herpes Simplex Virus Capsids
Primary Biliary Acids Inhibit Hepatitis D Virus (HDV) Entry into Human Hepatoma Cells Expressing the Sodium-Taurocholate Cotransporting Polypeptide (NTCP)
Herpes Simplex Virus Internalization into Epithelial Cells Requires Na <sup>+</sup> /H <sup>+</sup> Exchangers and p21-Activated Kinases but neither Clathrin- nor Caveolin-Mediated Endocytosis
A Proteomic Perspective of Inbuilt Viral Protein Regulation: pUL46 Tegument Protein is Targeted for Degradation by ICP0 during Herpes Simplex Virus Type 1 Infection
Cytosolic herpes simplex virus capsids not only require binding inner tegument protein pUL36 but also pUL37 for active transport prior to secondary envelopment
Improper Tagging of the Non-Essential Small Capsid Protein VP26 Impairs Nuclear Capsid Egress of Herpes Simplex Virus