Jack A. Collora

ORCID: 0000-0002-6423-2316
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About
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Research Areas
  • HIV Research and Treatment
  • Immune Cell Function and Interaction
  • T-cell and B-cell Immunology
  • CRISPR and Genetic Engineering
  • interferon and immune responses
  • HIV/AIDS drug development and treatment
  • Cytomegalovirus and herpesvirus research
  • RNA modifications and cancer
  • SARS-CoV-2 and COVID-19 Research
  • HIV/AIDS Research and Interventions

Yale University
2020-2023

HIV-1 integration introduces ectopic transcription factor binding sites into host chromatin. We postulate that the integrated provirus serves as an enhancer recruits additional factors to locus, increases chromatin accessibility, changes 3D interactions, and enhances both retroviral gene expression. used four well-characterized HIV-1-infected cell line clones having unique low high levels of Using single-cell DOGMA-seq, which captured heterogeneity expression we found correlated with...

10.1101/gr.277698.123 article EN cc-by-nc Genome Research 2023-06-01

HIV-1-infected cells, which can survive drug treatment and immune cell killing, prevent an HIV-1 cure. Immune recognition of infected cells requires protein expression; however, expression is limited in after long-term therapy.

10.1128/jvi.00577-22 article EN Journal of Virology 2022-06-22

Abstract Despite antiretroviral therapy (ART), HIV-1 persists in proliferating T cell clones that increase over time. To understand whether early ART affects persistence vivo , we performed single-cell ECCITE-seq and profiled 89,279 CD4 + cells paired samples during viremia after immediate versus delayed six people the randomized interventional Sabes study. We found partially reverted TNF responses while did not. Antigen persisted despite shaped transcriptional landscape of cells, RNA...

10.1101/2021.01.27.428491 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2021-01-28
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