M. Emerman

Indels allow antiviral proteins to evolve functional novelty inaccessible by missense mutations

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

A CRISPR screen of HIV dependency factors reveals CCNT1 is non-essential in T cells but required for HIV-1 reactivation from latency

This study uses a CRISPR screen to identify HIV-1 latency reversal factors, finding that CCNT1 is non-essential for T cell activation but critical for HIV reactivation from latency.

Primate TRIM34 is a broadly-acting, TRIM5-dependent lentiviral restriction factor

This study identifies primate TRIM34 as a lentiviral restriction factor that requires TRIM5 for activity, restricting multiple SIV capsids across primate species.

A Virus-Packageable CRISPR System Identifies Host Dependency Factors Across Multiple HIV-1 Strains

The paper identifies host dependency factors for HIV replication across multiple strains using a virus-packageable CRISPR system in human T cells.

A human-specific motif facilitates CARD8 inflammasome activation after HIV-1 infection

The paper identifies a human-specific CARD8 motif that is cleaved by HIV-1 protease, leading to inflammasome activation and pyroptosis after HIV-1 infection.

A modular CRISPR screen identifies individual and combination pathways contributing to HIV-1 latency

This study uses a CRISPR screen to identify pathways involved in HIV-1 latency, finding that ING3 and AZD5582 combination activates proviruses.

HIV-1 Vif gained breadth in APOBEC3G specificity after cross-species transmission of its precursors

The paper explores how HIV-1 Vif evolved to broaden its specificity for APOBEC3G through cross-species transmission, revealing Loop 5 adaptations that enhance its ability to antagonize A3G variants.

Divergence in dimerization and activity of primate APOBEC3C

This study identifies the molecular basis for differences in dimerization and antiviral activity of primate APOBEC3C proteins through biochemical, virological, and computational analyses.

Highly-potent, synthetic APOBEC3s restrict HIV-1 through deamination-independent mechanisms

This paper creates synthetic APOBEC3 proteins with enhanced antiviral activity against HIV-1 through non-catalytic mechanisms, comparable to the most potent natural APOBEC3 variant.

Mutational resilience of antiviral restriction favors primate TRIM5α in host-virus evolutionary arms races

The paper uses deep mutational scanning to assess how mutations in the TRIM5 v1 loop affect retroviral restriction, finding that most mutations enhance or preserve antiviral function.

APOBEC3C tandem domain proteins create super restriction factors against HIV-1

The paper shows that synthetic tandem domain APOBEC3C proteins create more potent antiviral factors against HIV-1 than native A3C, with increased resistance to viral antagonism.

Polymorphisms in human APOBEC3H differentially regulate ubiquitination and antiviral activity

This study shows that polymorphisms in APOBEC3H affect ubiquitination and antiviral activity, with haplotype II being the only active variant.

TRIM34 acts with TRIM5 to restrict HIV and SIV capsids

This study identifies TRIM34 as an HIV-1 capsid-targeting restriction factor that acts with TRIM5alpha to restrict HIV and SIV infection during reverse transcription.

Combinatorial mutagenesis of rapidly-evolving residues yields super-restrictor antiviral proteins

The paper uses combinatorial mutagenesis to generate super-restrictor antiviral proteins against Thogoto virus, finding variants with enhanced restriction activity compared to wild-type MxA.

A Virus-Packageable CRISPR Screen Identifies Host Factors Mediating Interferon Inhibition of HIV

The paper uses a CRISPR screen to identify host factors that mediate interferon inhibition of HIV replication, finding several restriction factors and novel dependencies.

Recurrent Loss of APOBEC3H Activity during Primate Evolution

The paper examines APOBEC3H variation in African green monkeys, finding recurrent loss of function and its potential negative impact on host fitness.