Retrovirus infection of resting cells
Completion of the early stages of retrovirus infection depends on the cell cycle. While gammaretroviruses, such as murine leukemia virus, require mitosis for provirus integration, lentiviruses such as HIV are able to replicate in post-mitotic non-dividing cells. Resting cells such as resting T lymphocytes from peripheral blood cannot be productively infected by retroviruses, including lentiviruses, but the molecular basis of this restriction remains poorly understood. In G0 resting cells (primary fibroblasts or peripheral T cells), incoming foamy retroviruses accumulate in close proximity to the centrosome, where they lie as structured and assembled capsids for several weeks. Under these settings, virus uncoating is impaired, but upon cell stimulation, gag proteolysis and capsid disassembly occur, which allows viral infection to proceed. The data imply that foamy virus uncoating is the rate-limiting step for productive infection of primary G0 cells. Incoming foamy retroviruses can stably persist at the centrosome, awaiting cell stimulation to initiate capsid cleavage, nuclear import, and viral gene expression. Maintenance of incoming viral capsids at the centrosome in resting cells could be a strategy that viruses have evolved to rapidly respond to stimuli received by the cell. The cellular signal triggering the uncoating process upon cell stimulation remains unclear, but is likely linked to the centrosome cycle.
Centrosomal Latency of Incoming Foamy Viruses in Resting Cells
PLoS Pathogens Vol. 3, No. 5, e74
So why does this matter? Because most retrovirus vectors cannot infect resting cells, i.e. most of the cells in your body, so are unable to correct genetic defects in somatic cells. Since gene therapy vectors based on lentiviruses can infect resting cells, they offer much more potential.
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