G. J. Towers

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

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

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.

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

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.

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.

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.

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

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.

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

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.

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.

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.

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

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.

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

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