Understanding HIV-1 latency provides clues for the eradication of long-term reservoirs.
HIV-1 can infect both activated and resting, non-dividing cells, following which the viral genome can be permanently integrated into a host cell chromosome. Latent HIV-1 reservoirs are established early during primary infection and constitute a major barrier to eradication, even in the presence of highly active antiretroviral therapy. This Review analyses the molecular mechanisms that are necessary for the establishment of HIV-1 latency and their relationships with different cellular and anatomical reservoirs, and discusses the current treatment strategies for targeting viral persistence in reservoirs, their main limitations and future perspectives.
Coiras
Mayte
M
AIDS Immunopathology Unit, National Centre of Microbiology, Instituto de Salud Carlos III, 28220 Majadahonda, Madrid, Spain. mcoiras@isciii.es
López-Huertas
María Rosa
MR
Pérez-Olmeda
Mayte
M
Alcamí
José
J
D023241:Antiretroviral Therapy, Highly Active; D003713:Dendritic Cells / Q000821:virology; D015658:HIV Infections / Q000188:drug therapy / Q000276:immunology / Q000821:virology*; D015497:HIV-1 / Q000276:immunology / Q000502:physiology*; D006801:Humans; D007156:Immunologic Memory; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D008213:Lymphocyte Activation; D008264:Macrophages / Q000821:virology; D013601:T-Lymphocytes / Q000276:immunology / Q000821:virology; D017735:Virus Latency / Q000235:genetics / Q000502:physiology
D007166:Immunosuppressive Agents