Varicella zoster virus (VZV) establishes lifelong infection by evading and manipulating the immune system, with natural killer (NK) cells thought to be part of this early response. The authors were therefore interested in how VZV directly interacts with NK cells and found that the virus is capable of infecting human NK cells from peripheral blood in vitro. This VZV infection of NK cells is productive, leading to a full kinetic cascade of viral gene expression and the production of new infectious virus that could then be transmitted to epithelial cells in culture. Using flow cytometry, the authors also found that this NK cell infection with VZV was preferential for the mature CD56dim NK cell subset and also drove acquisition of the terminally-differentiated maturity marker CD57. Culture of NK cells with VZV also induced a potent loss of expression of the low-affinity IgG Fc receptor CD16 on the cell surface and VZV infection of NK cells upregulated surface expression of chemokine receptors associated with trafficking to the skin. Therefore VZV does actively manipulate the NK cell phenotype through productive infection.
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