| Autor: |
Kim M; 1] Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. [2] Howard Hughes Medical Institute, Baltimore, Maryland, USA., Hosmane NN; Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA., Bullen CK; Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA., Capoferri A; 1] Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. [2] Howard Hughes Medical Institute, Baltimore, Maryland, USA., Yang HC; Department of Microbiology, National Taiwan University College of Medicine, Taipei, Taiwan., Siliciano JD; Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA., Siliciano RF; 1] Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. [2] Howard Hughes Medical Institute, Baltimore, Maryland, USA. |
| Abstrakt: |
A mechanistic understanding of HIV-1 latency depends on a model system that recapitulates the in vivo condition of latently infected, resting CD4(+) T lymphocytes. Latency seems to be established after activated CD4(+) T cells, the principal targets of HIV-1 infection, become productively infected and survive long enough to return to a resting memory state in which viral expression is inhibited by changes in the cellular environment. This protocol describes an ex vivo primary cell system that is generated under conditions that reflect the in vivo establishment of latency. Creation of these latency model cells takes 12 weeks and, once established, the cells can be maintained and used for several months. The resulting cell population contains both uninfected and latently infected cells. This primary cell model can be used to perform drug screens, to study cytolytic T lymphocyte (CTL) responses to HIV-1, to compare viral alleles or to expand the ex vivo life span of cells from HIV-1-infected individuals for extended study. |
