Increased T cell trafficking as adjunct therapy for HIV-1
- Publisher: Public Library of Science
PLoS Computational Biology,
(issn: 1553-734X, eissn: 1553-7358)
Microbial Control | Microbial Pathogens | Antivirals | Research Article | Anatomy | Antiretroviral Therapy | Preventive Medicine | T Helper Cells | Pathology and Laboratory Medicine | Antimicrobials | Lymphatic System | Vaccination and Immunization | Immunodeficiency Viruses | Retroviruses | HIV-1 | Viral Persistence and Latency | White Blood Cells | HIV | Pathogens | Antiretrovirals | Lymphoid Tissue | Public and Occupational Health | Pharmacology | Immunology | Antiviral Therapy | Lentivirus | Cellular Types | Viruses | Biology and Life Sciences | Drugs | Blood Cells | Microbiology | Immune Cells | Animal Cells | QH301-705.5 | Viral Replication | Medical Microbiology | Viral Pathogens | Cell Biology | RNA viruses | Virology | T Cells | Organisms | Medicine and Health Sciences | Biology (General)
Author summary Despite the success of potent antiretroviral therapy in suppressing the amount of virus in peripheral blood for long periods of time, a reservoir of infectious virus persists in CD4 T cells, implying the need for long-term treatment. Strategies to control and ultimately eliminate the viral reservoir within specific tissue compartments will need to target virus that persists in both a long-lived reservoir of infectious virus in CD4 T cells as well as low-levels of viral replication that continues despite antiretroviral drug therapy. Using a mathematical model, we describe a hypothetical new therapeutic approach to eliminating HIV-1 persistence in these ‘drug sanctuaries’. Specifically, we show that therapy that increases the rate that the target cells for HIV-1 flow through drug sanctuaries could stop continuous cycles of replication. Used in combination with antiretroviral treatment, such a therapy could contribute to a functional cure for HIV-1.