Michael Emerman

This study engineered hMxA to restrict multiple human-adapted influenza viruses as effectively as mMx1 by combining nuclear relocalization and specific amino acid changes.

This study identifies structural adaptability in HIV-2 Vif that enables broad antagonism of APOBEC3G through conformational selection.

This study identifies chromatin regulators of HIV latency and reactivation using RelB proximity proteomics and CRISPR screening, revealing key acetyltransferases involved in noncanonical NF-κB pathway activation.

The paper maps mutational landscapes of HIV-1 Vif proteins to understand how they antagonize APOBEC3G, revealing strain-specific epistasis and structural flexibility.

This study shows that an in-frame stop codon in alphaviruses helps evade innate immune defenses in both mosquito and vertebrate hosts.

The paper investigates CARD8 inflammasome activation during HIV-1 cell-to-cell transmission, showing it depends on viral protease activity and not NLRP3.

The paper identifies strategies for MxA to overcome breadth-specificity tradeoffs in antiviral restriction by using heterozygous and generalist super-restrictor variants.

This study shows that the opal stop codon in alphaviruses optimizes protein production and processing at 37°C by balancing polymerase levels and RNA replication transitions.

This study identifies INTS12 knockout as a method to enhance HIV latency reversal by overcoming a transcriptional block, improving reactivation in CD4 T cells from HIV-positive individuals.

This paper identifies ETS1 as a regulator of HIV latency through a CRISPR screen and shows it has opposing roles in actively and latently infected CD4 T cells.

The paper shows that indels, not just missense mutations, enable antiviral proteins like TRIM5 to evolve new functions against viruses.

The paper traces the evolutionary origins of Mx proteins, showing they predate the interferon system and are widespread across eukaryotes, including fungi, plants, and early-branching lineages.

The paper shows that retrocopying generates new APOBEC3 antiviral proteins in primates, expanding their functional repertoire to counteract viral evolution.

Affinity-purification mass spectrometry of 26 SARS-CoV-2 proteins in HEK293T cells yields 332 high-confidence host interactions and 67 druggable human proteins with known compounds.