Table 3.

Entry mechanism and/or cellular receptors used by viruses. The cell types used in entry assay are mentioned whenever possible; otherwise, multiple cells might be used. “∞” means “interacts with”

Virus	Cells	Entry method and/or attachment receptors
Adenoviruses
Ad-2/5	–	Clathrin, myeloid, and αvβ3- and αvβ5-integrins-mediated endocytosis [36, 90]
Ad-2	–	Macropinocytosis [90]
Ad-5	Afferent lymph DCs	Actin-dependent macropinocytosis [39]
Ad-3/35	EpC and haematopoietic	PI3K, Rho GTPases and dynamin-dependent macropinocytosis [37, 91]
Egg drop syndrome virus	Duck embryonic FbCs	Low pH, clathrin-mediated endocytosis [38]
Herpesviruses
HSV-1	HeLa, CHO and keratinocytes, but not neuroblastoma	Low-pH endocytosis [92–94]
	Vero cells	Fusion [92]
	CHO	Viral gB and gD, and cellular Nectin-1, HVEM and PILR-α are required for infection; gD ∞ Nectin-1 and gB ∞ PILR-α [95]; gD ∞ Nectin-1 and gB ∞ PILR-α [96–99]
	EpC, neuron and keratinocytes	gH/gL (RGD motif) ∞ αvβ6- and αvβ8-integrins [100]; gH/gL binds to αvβ3-integrin activating IFN-I and NF-κB [101]
	CHO, HeLa, Vero	gD ∞ HVEM [102, 103]
	HeLa	Syndecan-1 and syndecan-2 [104]
	Nectin-1 or HVEM-deficient murine dermal FbCs	Delayed virus entry; HS could be an alternative receptorl; dynamin and cholesterol could be involved [105]
	Murine cornea	HVEM and nectin-1 are crucial for infection [106]
	Human oligodendrocytic cells	Proteolipid protein is required in entry [107]
	–	gD triggers fusion by forming complexes with gB or gH/gL [108]; gB ∞ non-muscle myosin heavy chain IIA [109]
	CHO and fibroblasts	gC, gB and gD are required for entry [110]; gD ∞ 3-O-sulfated HS [111]
HSV-2	Retinal EpCs	Nectin-1, HVEM and PILR-α [95]; gD ∞ Nectin-1 and PILR-α and gB ∞ PILR-α [96–99]
HSV-6	–	gH/gL/gQ ∞ CD46 [112–114]; gB and the gH/gL/gQ complex are required for cell-cell fusion [115]
HSV-7	CHO	gB ∞ HS [116]
CMV	Fibroblast, EnC and retinal EpC	Fusion or endocytosis [78, 117]
	Multiple cells, e.g. CHO, myeloid, EpC, EnC and FbC	gB ∞ epidermal growth factor receptor [118] or integrins (does not depend on RGD motif) [119]; gH ∞ αvβ3 integrin as a co-receptor [120]; gB or gH/gL are required for syncytium [121, 122]. gH/gL/UL128/130/131 and gH/gL/gO complexes are essential for fusion [123]
EBV	B lymphocytes	Endocytosis [124, 125]; gp350/220 ∞ complement receptor 2 (CR2, CD21) [126, 127]. gH/gL (KGD motif) ∞ αvβ6- and αvβ8-integrins [128, 79]; gp42 ∞ HLA to induce membrane fusion through gH/gL and gB [, 80, 81, 110, 126].
	EpCs	Fusion [125]; macropinocytosis and lipid raft-dependent endocytosis [82]
	B cells, but not EpC	gp42/gH/gL complex mediates fusion [83]
	Nasopharyngeal EpC	gB ∞ Neuropilin-1 [82]
	Polarized cells	BMRF2 protein ∞ integrins [84]
KSHV (HHV-8)	EnC and FbC	DC-SIGN, pH and clathrin mediated endocytosis [85–87]
	Endothelial cells	Macropinocytosis [88]
	Monocytic THP-1 cells	Endocytosis; clathrin, caveolin, HS, DC-SIGN, integrins, NF-κB, Src, and PI3K signaling are involved [89].
	Human dermal microvascular EnC	gB ∞ ESCRT-0 component Hrs (hepatocyte growth factor-regulated tyrosine kinase substrate) promoting macropinocytosis [129]
	–	gB (RGD motif) ∞ integrins [130, 57]. gB, gH/gL and K8.1 ∞ HSPG induces fusion [58, 59, 60].
VZV	B cells	Endocytosis [61]
	VZV-permissive human melanoma cells expressing integrins	gB and gH-gL ∞ αV integrins [62]
Ovine herpesvirus 2	–	gB and gH/gL induce cell-cell fusion [131]
Poxviruses
VV MV / EV	HeLa	Low-pH, dynamin, actin, and cholesterol-dependent macropinocytosis [132–137]
VV MV	HeLa cells	Bind to CD98 and enters via endocytosis [138]
VV MV / EV	DCs	Dynamin and pH-independent macropinocytosis [139], cholesterol (lipid raft), PS, actin, kinases, GTPases, integrins and Na+/H+ exchangers are required [134, 140, 141].
VV-MV	HeLa or A549	Low-pH, and serine/threonine kinase PAK1 and tyrosine kinase [142].
VV	Human pancreatic carcinoma cell lines	Entry enhanced by vascular endothelial growth factor A and Akt signaling pathway [143].
VV	Leukocytes	Attach to heparin and laminin [144, 145]
VV	Fibroblast or HeLa	Tumor necrosis factor receptor associated factor 2 [146]
VV	Drosophila DL1 cells	Macropinocytosis [147]
VV	Drosophila S2 cells	Low-pH endocytic pathway that requires EFC proteins [148]
Myxoma virus	Leukocytes	Attach to heparin [144]
VV and myxoma virus	FbCs BSC-40	Inhibition of HS affects entry, but laminin blocks binding of VV [144].
WR and IHD-J	HeLa	PS, kinases and actin macropinocytosis; IHD-J MV induces filopodia; WR utilizes tyrosine kinase, PI3K and Rac1 to activate blebs [136].
	HeLa, B78H1 and L cells	Inhibited by soluble heparin [149, 150]
	B78H1 and BSC-1	Require endosomal acidification [149, 150]
WR, monkeypox virus and cowpox virus	–	Low-pH [150, 151]
IHD-J, Copenhagen and Elstree strains	–	A pH-independent fusion [150, 151]
WR EV	–	Gas6 protein enhances entry by bridging viral PS to TAM (Tyro3/Axl/Mer) receptor tyrosine kinases [152].
EVs	–	Expression of A33 and A36 at plasma membrane of the infected cells mediates the repulsion between EVs toward uninfected cells leading to rapid spread of virus [153]. A56 (hemagglutinin) interact with K2 (serine proteinase inhibitors) forming A56-K2 complex that co-localizes at the cell surface blocking the superinfection and fusion [154–157]. A56-K2 complex interacts with A16 and G9 subunits and prevents the superinfection [158].
Iridoviruses
Tiger frog virus, Ranavirus genus	HepG2 cells	pH, cholesterol, dynamin, actin and caveolin-mediated endocytosis [159]
Frog virus 3, Ranavirus genus	BHK-21 cells	Low pH and clathrin-mediated endocytosis [160]
ISKNV, Megalocytivirus	Mandarin fish fry cells	Major capsid protein ∞ caveolin-1 and induces caveolin-endocytosis [161, 162]
SGIV	Grouper spleen cell line	pH-dependent clathrin-endocytosis and macropinocytosis [163]; the deletion of VP088 envelope protein inhibits viral entry [164].
Large yellow croaker iridovirus	Bluegill fry (BF-2) cells	037L (RGD motif) ∞ integrins inducing fusion [165, 166]