“…Within biological membranes, they further exhibit lateral heterogeneity through the formation of specialized microdomains and by establishing asymmetry across bilayers. The overall structural and topological diversity of lipids and their aggregates results in a wide range on specific protein-lipid interactions and electrostatic considerations, which (Coil and Miller, 2005b;Coil and Miller, 2005a) Annexins are hijacked as co-receptors by PS expressed in the virus envelope Influenza virus (Huang et al, 1996), HBV (Hertogs et al, 1993), HCMV (Raynor et al, 1999), RSV a (Malhotra et al, 2003), HIV (Callahan et al, 2003;Ma et al, 2004) Molecular mimicry of apoptotic bodies facilitates macropinocytosis/virus entry VACV (Mercer and Helenius, 2008) Sterols/Sterol Esters Association with apolipoproteins facilitates virus docking and subsequent entry steps HCV (Prince et al, 1996;Agnello et al, 1999;Molina et al, 2007) Virus surface glycoproteins and receptors are clustered in "lipid rafts" HCV (Kapadia et al, 2007;Burlone and Budkowska, 2009), HIV (Sorice et al, 2000(Sorice et al, , 2001Nguyen and Taub, 2002;Popik et al, 2002;Bhattacharya et al, 2004;Nguyen et al, 2005), RSV a (Fleming et al, 2006), influenza virus (Takeda et al, 2003) Sphingolipids Glycan-glycan interactions between host and virus stabilize virus attachment Influenza virus (Huang, 1976;Leskawa et al, 1986;Kasson and Pande, 2008) GalCer, GM3 and Gb3 serve as auxiliary receptors for virus entry HIV (Fantini et al, 1993;Seddiki et al, 1996;Hammache et al, 1999;Hug et al, 2000;Magerus-Chatinet et al, 2007) GSLs aggregate viral receptors which have low endogenous cellular levels EBOV, Marburg virus, VACV, HSV (reviewed in…”