Steven G. Deeks

The paper identifies immune cell activation patterns associated with rapid clearance of infectious SARS-CoV-2 in both unvaccinated and vaccinated individuals.

The paper assesses whether HIV-1 infection confers resistance to CTL-mediated cell death and finds no intrinsic resistance, with survival differences attributed to MHC class I downregulation.

The paper identifies persistently activated virus-specific CD8 T cells in long COVID patients, suggesting chronic antigen stimulation by SARS-CoV-2 or herpesvirus.

The paper identifies a subset of HIV elite controllers with proteomic profiles similar to uninfected individuals, associated with lower viral reservoirs and protective HLA alleles.

The paper develops a mechanistic model linking CD8+ T cell expansion sensitivity to HIV post-treatment control, showing strong correlations with Ki-67 and TCF-1 levels.

This study uses DAb-seq to analyze HIV-infected CD4 T cells on ART, revealing subset-specific differences in provirus maintenance and surface protein expression.

This study uses multiomic and spatial profiling of colorectal tissue and blood to show that Long COVID is linked to immune dysregulation and viral persistence, with stronger signals in tissue than blood.

The paper identifies autologous neutralizing antibodies (aNAbs) as critical determinants of HIV-1 rebound after treatment interruption, defining quantitative limits on rebound-competent reservoirs.

The paper identifies increased mannosylation of extracellular vesicles in Long COVID plasma and shows GNA affinity resin can remove them, potentially rebalancing immune and tissue-repair networks.

This study shows that bNAb-mediated HIV suppression is linked to increased immune activation compared to ART suppression, with unique transcriptional patterns in controllers.

The paper identifies early immune responses preceding HIV rebound and links them to viral control outcomes in individuals discontinuing antiretroviral treatment.

The paper develops HIV-seq to capture HIV transcripts for scRNA-seq, revealing distinct transcriptional features of HIV-transcribing cells in viremic and ART-suppressed HIV patients.

This study uses computational modeling to show that broadly neutralizing antibodies (bnAbs) promote the evolution of diverse autologous antibodies that target multiple HIV spike epitopes, potentially enabling viral control.

This study detects HIV-1 antisense transcripts in vivo, showing higher expression in ART-treated individuals compared to untreated ones, suggesting a regulatory role in viral expression.

The paper identifies increased CD16++ monocytes with anti-viral gene expression before HIV-1 rebound, suggesting early immune signals of viral resurgence.

This study examines how pre-existing neutralizing antibodies affect viral shedding in post-vaccination SARS-CoV-2 infections, finding that higher titers reduce viral load and duration but are less effective against Omicron variants.

This study identifies transcriptomic clusters in HIV patients on ART linked to immune recovery and inflammation markers, revealing novel subgroups with distinct immunological profiles.

The paper shows that cognate antigen engagement in CD4+ T cells on long-term ART increases HIV-1 transcription through T cell activation, suggesting a role in viral rebound.

The paper compares the fraction and total number of HIV-infected cells with unspliced RNA in controllers and non-controllers, finding that viremic control is linked to fewer infected cells, not a lower fraction of infected cells with HIV usRNA.

This study identifies host gene expression patterns associated with HIV reservoir size in treated individuals, linking inflammation, innate immunity, and potassium/gap junction channels to viral persistence.

The paper investigates host genetic variations in MX1, CCR5Δ32, and MHC class I alleles in HIV+ non-controllers on ART and finds associations with HIV reservoir size.