Thomas Hennig

This study shows that murine cytomegalovirus infection exacerbates inflammation in Pkp2 mutant mice but not in Ttn mutant mice, highlighting the interaction between genetic predisposition and environmental factors in cardiomyopathy.

This study shows HSV-1 infection causes a downstream shift of +1 nucleosomes by depleting RNA Polymerase II from host genes, similar to Pol II depletion in yeast.

Heterogeneity-seq identifies causal factors driving heterogeneous cellular responses by combining single-cell RNA-seq with metabolic labeling and double machine learning.

This study shows HSV-1 inhibits phosphorylation of RNA polymerase II CTD serine-7, affecting viral gene expression and host transcription.

The paper develops computational methods to correct 4sU-induced quantification bias in nucleotide conversion RNA-seq data by addressing mappability and reverse transcription efficiency issues.

This paper develops a reverse genetics platform for SARS-CoV-2 to generate recombinant viruses and study their replication and phenotypic effects.

This study shows that CMTR1-mediated N1-2'O-methylation prevents antiviral recognition and regulates NVL2 mRNA splicing, affecting cell size, division, and ribosome biogenesis.

This study shows HSV-1 infection causes a downstream shift in promoter-proximal Pol II pausing for most host genes, more pronounced than NELF depletion.

This paper identifies M35 as a viral protein that binds DNA and inhibits IRF3-mediated gene expression, including Ifnb1, thereby suppressing the antiviral type I IFN response.

The paper shows HSV-1 and influenza infection induce circular and linear splicing of the NEAT1_2 isoform, independent of vhs and linked to transcription termination disruption.

This study shows that ZAP restricts HCMV infection by destabilizing viral transcripts with low CG content, revealing its role in antiviral defense against DNA viruses.

This study shows HSV-1 infection causes widespread changes in host mRNA alternative polyadenylation, with ICP27 playing a role in shifting polyadenylation to intronic sites and affecting mRNA export and expression.

scSLAM-seq measures transcription dynamics in single cells by distinguishing newly synthesized from pre-existing RNA, revealing stochastic transcription and gene-specific differences.