Richard Brad Jones

This paper studies HIV superinfection to show how immune responses shape rebound dynamics and reservoir reactivation during treatment interruption.

The paper designs a bispecific CD4-CD4i fusion protein that broadly neutralizes diverse HIV-1 subtypes with potency comparable to broadly neutralizing antibodies.

This study characterizes HIV reservoir clones and shows they can be culled by sustained CTL pressure, with some displaying intrinsic resistance linked to low oxidative stress.

The paper introduces HIV SMRTcap, a method for characterizing HIV-1 reservoirs by identifying integration sites and proviral integrity using long-read sequencing, and validates its performance across subtypes and tissue samples.

This study shows HIV Nef induces a soft phenotype in infected CD4+ T cells, reducing their susceptibility to cytotoxic T lymphocyte killing through cytoskeletal remodeling and intrinsic heterogeneity.

This study shows HIV increases sialoglycan expression to engage Siglecs on myeloid cells, promoting immune evasion, and demonstrates that disrupting these interactions enhances immune killing of infected cells.

This study shows that atorvastatin reduces HIV and ART-induced cardiac fibrosis and dysfunction in mice by blocking platelet TGFβ1, independent of cholesterol changes.

This study examines transcription of HIV-1 at sites of intact latent provirus integration in T cells, finding that latent proviral promoters are significantly less active than in productively infected cells and have minimal impact on neighboring gene expression.

This study identifies that HIV reservoirs consist mainly of genetically younger, clonally enriched proviruses from the pre-ART period, with defective proviruses persisting longer.

The paper evaluates the Intact Proviral DNA Assay (IPDA) for HIV reservoir quantification, finding that HIV diversity leads to a 28% failure rate and underestimation of reservoir size.

Telescope accurately estimates transposable element expression in RNA-seq data by resolving ambiguously mapped fragments using a Bayesian model, revealing cell-type specific retrotranscriptome differences.