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Aclose relative of Lassa fever virus (LFV) may sneak into cells by displacing the extracellular matrix molecule laminin from its normal binding partner, α-dystroglycan, according to Kunz et al. (page 301). A mutant virus with a lower binding affinity for α-dystroglycan fails to displace laminin and cannot infect the same cell types. This changes the course of the disease.
High affinity (left), but not low affinity (center), virus can compete with laminin (red).
The infection with the mouse virus, lymphocytic choriomeningitis virus (LCMV), is played out primarily in the spleen. The high affinity virus infects mostly α-dystroglycan–producing dendritic cells, which normally migrate from the peripheral zone into the white pulp, where they present antigen to naive B and T cells. An infection of the dendritic cells with high affinity LCMV interferes with antigen presentation and causes immunosuppression.
To infect dendritic cells and establish a persistent...
The Rockefeller University Press
2001
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