Jeremy Luban

This study identifies PR, RT, and cleavage-site interactions as determinants of KoRV-A replication efficiency and reveals unusual extracellular particle organization.

The paper assesses subtype-specific neutralization resistance of RSV-A and RSV-B isolates to mAbs and vaccines, finding RSV-A more resistant and bivalent vaccines more effective.

The paper models SARS-CoV-2 evolution during the pandemic, finding that immune escape became more important than infectivity as variants evolved.

The paper designs SARS-CoV-2 Spike proteins with novel mutations to evaluate vaccine effectiveness against future viral variants using a deep learning model.

This study identifies how the A82V mutation in Ebola virus GP enhances membrane fusion through conformational changes, using simulations and experiments.

This study shows that Cyclophilin A promotes HIV-1 integration by enhancing preintegration complex activity, revealing a new role for CypA in the viral life cycle.

This study identifies mutations to improve prime editing efficiency in low-dNTP environments by enhancing MMLV-reverse transcriptase and reducing SAMHD1 activity.

The paper identifies PRC1.6 as a partner of the HUSH complex in promoter-specific provirus silencing through chromatin colocalization and functional assays.

This study identifies IFIH1 (MDA5) as essential for innate immune detection of intron-containing RNA from the HIV-1 provirus, linking it to chronic inflammation in HIV-1 patients.

This study optimizes the nuclear localization signal (NLS) of Cas12a to enhance editing efficiency in human primary cells without compromising specificity.

The paper identifies causal 3'UTR variants linked to human disease and evolution using a new high-throughput assay and functional analysis.

This study shows HIV-1-induced cytokines deplete homeostatic ILCs and drive the expansion of TCF7-dependent memory NK cells.

The paper analyzes the piRNA response to retroviral invasion in koalas, finding that KoRV piRNAs are sense-biased and derived from unspliced transcripts, suggesting a conserved innate immune mechanism.

This study identifies Vpx and Vpr as viral proteins that counteract the HUSH complex to activate provirus transcription in primate immunodeficiency viruses.