Table 2.

Alphaherpesvirus-host interactions that exploit actin-based myosin.

Virus	Viral Protein	Host-Cell Proteins/System	Role	Reference
HSV-1	Unknown	Myosin Va	Myosin Va is activated during infection, facilitating transport of virion- and glycoprotein-bearing vesicles from TGN to plasma membrane through cortical actin in HeLa cells. It is hypothesised that egressing virions (collected within TGN-derived vesicles) behave in a similar manner to other myosin-dependent cargo: kinesin motors (see Section 4) deliver vesicles to cortical actin and myosin Va “captures” the vesicles and then transports them to the plasma membrane.	[98]
HSV-1	pUL49 (VP22)	Non-muscle myosin heavy chain IIA (NM-IIA)	Affinity chromatography experiments with HSV-1-infected baby hamster kidney (BHK) cell extracts have shown tegument protein VP22 interacts with NM-IIA. HSV-1 infection of Vero cells redistributes NM-IIA but only a subpopulation of NM-IIA colocalises with VP22 in a perinuclear cluster.	[99]
HSV-1	gB	NM-IIA/myosin light chain kinase (MLCK)	NM-IIA is a functional coreceptor for gB in Vero cells. Inhibition of NM-IIA (by blebbistatin) and MLCK (by ML-7 and ML-9) decreased viral entry into corneal epithelial cells. Activation of NM-IIA by MLCK is necessary for the cytoskeletal rearrangements needed for HSV-1 infection of corneal cells. To regulate actin, NM-IIA cross-links and contracts F-actin.	[100,101]
HSV-1	gB	Non-muscle myosin heavy chain IIB (NM-IIB)	Interaction may serve as an entry coreceptor in the CV-1 in origin with SV40 genes (COS) cell line as above. Activation of NM-IIB by MLCK is also necessary for the cytoskeletal rearrangements. Likely to be important in a range of cell types.	[102]