Werner J. D. Ouwendijk

The paper uses nanopore sequencing to show herpesvirus mRNAs have longer poly(A) tails than cellular or other viral transcripts, suggesting a unique mechanism for enhancing gene expression.

This paper introduces DRAP3R, a method for analyzing Pol III transcribed RNAs and their modifications, revealing new transcripts and epitranscriptomic changes in infected cells.

This paper establishes HD10.6 neurons as an in vitro model for studying VZV latency and reactivation, showing they support viral infection, persistence, and reactivation with capsaicin.

The paper reanalyzes scRNA-Seq data and finds that HSV-1 latency in non-neuronal ganglionic cells is not supported, attributing the previous findings to technical artifacts.

The paper identifies and characterizes a unique VZV latency transcript (VLT) that represses the viral transactivator gene ORF61 during latency, unifying VZV latency with other herpesviruses.