Michael J. Peluso

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

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 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.

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.

The paper identifies a Neandertal introgressed haplotype in the OAS1 gene associated with increased risk of severe COVID-19 and shows it impairs SARS-CoV-2 clearance through genetic regulation of OAS1 expression.