Rebecca Hoh

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

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.

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 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.

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.