Melanie M. Brinkmann

This study uses in vivo single-cell analysis to show that type I IFN signaling and NK cells limit MHV68 infection in lymph nodes, with IFNAR deficiency increasing infected B cell numbers and NK cell depletion enhancing viral spread.

This study identifies UL35 as a viral protein that degrades SLF2, preventing SMC5/6 from silencing HCMV genomes.

The paper identifies TBKBP1 as a key gene whose demethylation enhances cytotoxic activity in CMV-specific CD8+ T cells, suggesting it as a therapeutic target.

This study shows that cytomegalovirus (CMV) inhibitors of programmed cell death restrict antigen cross-presentation, thereby limiting CD8 T-cell priming in mice.

This study identifies a novel function of MCPyV small T antigen in suppressing the type I interferon response by reducing IRF9 levels, impacting immune evasion and tumor progression.

This study investigates how CMV primes CD8 T cells, finding that balanced immune evasion supports optimal antiviral responses despite conflicting evidence on direct antigen presentation's role.

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.

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.