How Human Herpesviruses Subvert Dendritic Cell Biology and Function

In the last decades, a multitude of distinct herpesvirus-mediated immune evasion mechanisms targeting dendritic cell (DC) biology were uncovered. Within this chapter, we summarize the current knowledge how herpesviruses, especially the α-herpesviruses HSV-1, HSV-2, varicella-zoster virus (VZV), and the β-herpesvirus HCMV, shape and exploit the function of myeloid DCs in order to hamper the induction of potent antiviral immune responses. In particular, the main topics covering herpesvirus-mediated immune evasion will involve: (i) the modulation of immature DC (iDC) phenotype, (ii) modulation of iDC apoptosis, (iii) the inhibition of DC maturation, (iv) degradation of the immune-modulatory molecule CD83 in mature DCs (mDCs), (v) interference with the negative regulator of β2 integrin activity, cytohesin-1 interaction partner (CYTIP), (vi) resulting in modulation of adhesion and migration of mDCs, (vii) autophagic degradation of lamins to support productive HSV-1 replication in iDCs, (viii) the release of uninfectious L-particles with immune-modulatory potential from HSV-1-infected mDCs, and (ix) the implications of DC subversion regarding T lymphocyte activation.