Increased T cell trafficking as adjunct therapy for HIV-1

Helen R. Fryer*, Steven M. Wolinsky, Angela R. McLean

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

2 Scopus citations


Although antiretroviral drug therapy suppresses human immunodeficiency virus-type 1 (HIV-1) to undetectable levels in the blood of treated individuals, reservoirs of replication competent HIV-1 endure. Upon cessation of antiretroviral therapy, the reservoir usually allows outgrowth of virus and approaches to targeting the reservoir have had limited success. Ongoing cycles of viral replication in regions with low drug penetration contribute to this persistence. Here, we use a mathematical model to illustrate a new approach to eliminating the part of the reservoir attributable to persistent replication in drug sanctuaries. Reducing the residency time of CD4 T cells in drug sanctuaries renders ongoing replication unsustainable in those sanctuaries. We hypothesize that, in combination with antiretroviral drugs, a strategy to orchestrate CD4 T cell trafficking could contribute to a functional cure for HIV-1 infection.

Original languageEnglish (US)
Article numbere1006028
JournalPLoS computational biology
Issue number3
StatePublished - Mar 2018

ASJC Scopus subject areas

  • Genetics
  • Ecology, Evolution, Behavior and Systematics
  • Cellular and Molecular Neuroscience
  • Molecular Biology
  • Ecology
  • Computational Theory and Mathematics
  • Modeling and Simulation


Dive into the research topics of 'Increased T cell trafficking as adjunct therapy for HIV-1'. Together they form a unique fingerprint.

Cite this