G. J. Towers

Type I IFN expression is inhibited during cell division by CDK4/6

The paper shows that CDK4/6 inhibition enhances DNA- or cGAMP-induced IFN and ISG expression by limiting IFNβ mRNA production during cell division.

A maturation defective HIV-1 activates cGAS

The paper shows that a maturation-defective HIV-1 variant activates the cGAS pathway, leading to an IFN response due to exposed viral DNA.

Karyopherin mimicry explains how the HIV capsid penetrates nuclear pores

This paper shows how the HIV capsid mimics karyopherins to penetrate nuclear pores by interacting with FG-motifs, enabling it to bypass the size limit of the nuclear pore complex.

Pharmacologic hyperstabilisation of the HIV-1 capsid lattice induces capsid failure

This study shows Lenacapavir's antiviral effect comes from hyperstabilizing the HIV-1 capsid lattice, leading to loss of compartmentalization and capsid failure.

Evolution of enhanced innate immune suppression by SARS-CoV-2 Omicron subvariants

This study shows that later Omicron subvariants of SARS-CoV-2, such as BA.4 and BA.5, have evolved enhanced innate immune suppression compared to earlier subvariants like BA.1 and BA.2.

SARS-CoV-2 Spike evolution influences GBP and IFITM sensitivity

This study shows that SARS-CoV-2 variants differ in their sensitivity to GBP and IFITM restriction factors, with Omicron uniquely restricted by these factors due to changes in its spike protein.

Macrophage activation of cGAS and TRIM5 distinguish pandemic and non-pandemic HIV

The paper compares pandemic HIV-1(M) and non-pandemic HIV strains, finding that non-pandemic strains activate cGAS and TRIM5 in myeloid cells, leading to antiviral responses and poor replication.

Induction of transposable element expression is central to innate sensing

The paper shows that exogenous PAMPs epigenetically activate LINE1 TEs, which engage cGAS to enhance innate immune responses.

Evolution of enhanced innate immune evasion by the SARS-CoV-2 B.1.1.7 UK variant

This study identifies that the B.1.1.7 SARS-CoV-2 variant enhances innate immune evasion through increased Orf9b and Orf6 expression and activity.

SARS-CoV-2 convergent evolution cannot be reliably inferred from phylogenetic analyses

This paper develops a method to detect homoplasy in SARS-CoV-2 phylogenetic trees and finds that phylogenetics provides limited support for convergent evolution.

Characterisation of B.1.1.7 and Pangolin coronavirus spike provides insights on the evolutionary trajectory of SARS-CoV-2

This study characterizes the B.1.1.7 and Pangolin coronavirus spike proteins, revealing how NTD mutations enhance viral entry and provide insights into SARS-CoV-2 evolution.

Host-directed therapies against early-lineage SARS-CoV-2 retain efficacy against B.1.1.7 variant

This study evaluates the efficacy of host-directed therapies against the B.1.1.7 SARS-CoV-2 variant and finds similar antiviral activity compared to early-lineage SARS-CoV-2.

SARS-CoV-2 sensing by RIG-I and MDA5 links epithelial infection to macrophage inflammation

This study shows SARS-CoV-2 activates RNA sensors in lung epithelial cells, driving macrophage inflammation, which can be mitigated by inhibiting RNA sensing or downstream signaling.

STING Nuclear Partners Contribute to Innate Immune Signalling Responses

The paper identifies nuclear STING partners that contribute to innate immune signaling by interacting with IRF3/7 transcription factors and enhancing antiviral responses.

HIV-1 Vpr antagonizes innate immune activation by targeting karyopherin-mediated NF-kB/IRF3 nuclear transport

This study shows HIV-1 Vpr inhibits IRF3 and NF-κB nuclear transport by interacting with karyopherins, thereby evading innate immune activation and promoting HIV-1 replication in macrophages.

In Vivo Emergence of a Novel Protease Inhibitor Resistance Signature in HIV-1 Matrix

The paper identifies a novel protease inhibitor resistance signature in HIV-1 matrix through genotypic and phenotypic analysis of patients failing PI therapy.

Disrupting HIV-1 capsid formation causes cGAS sensing of viral DNA

The paper shows that disrupting HIV-1 capsid formation exposes viral DNA to cGAS, triggering an IFN response in macrophages.