Heparan Sulfates and Coxsackievirus-Adenovirus Receptor: Each One Mediates Coxsackievirus B3 PD Infection

Heparan sulphate mediates swine vesicular disease virus attachment to the host cell

“…However, taking into account the high rate of mutation in this group of viruses, the possibility of this adaptation cannot be ruled out. Several studies have pointed out the flexibility in picornavirus receptor usage (Baranowski et al, 2000;Zautner et al, 2003). It seems a common characteristic of these viruses to easily adapt to bind a different receptor by replacing a few or even a single amino acid residue of a surface protein.…”

“…Also, the decay-accelerating factor (DAF), used as co-receptor for coxsackievirus A21, B1, B3, B5, echovirus 6, 7, 11, and enterovirus 70 appears to have a role in SVDV entry into cells (Martino et al, 2000). However, it has been shown that HS can be used as an alternative receptor for some picornaviruses, such as FMDV (Baranowski et al, 2000) and CVB3 (PD strain) (Zautner et al, 2003), in some conditions or when the 'classic' receptor is absent, a fact that supports the flexibility in picornavirus receptor usage. To investigate whether HS plays a role in SVDV infection, we have analysed the interaction of SVDV with HS and other glycosaminoglycans (GAGs).…”

“…Among the Picornaviridae family, it has been shown that foot-and-mouth disease virus (FMDV) binds to HS, although it reflects an adaptation to in vitro cultures (Fry et al, 1999;Jackson et al, 1996;Sa-Carvalho et al, 1997). Within this family, there is evidence that coxsackie virus B3 (CVB3) (Zautner et al, 2003), Theiler's murine encephalomyelitis virus (Reddi & Lipton, 2002) and certain echovirus serotypes (Goodfellow et al, 2001) also bind cell-surface HS. However, many others (poliovirus 3, coxsackie B2 viruses and most echovirus serotypes) do not seem to interact at all with these compounds (Goodfellow et al, 2001).…”

Islet Endothelium: Role in Type 1 Diabetes and in Coxsackievirus Infections

“…CAR is a 46kD adhesion molecule and all tested clinical and laboratory isolates bind to this receptor (Bergelson, 2002;Kallewaard et al, 2009). A large subset of CVB isolates also binds to DAF, a complement regulatory protein (Coyne & Bergelson, 2006) which appears to act as a receptor for cell attachment (Shafren et al, 1995), and some CVB3 isolates have been shown to use a third receptor, heparan sulfate, to infect CAR-deficient cells in vitro (Zautner et al, 2003). These receptor molecules do not simply bind viruses, but may activate a series of events influencing the organ-specific outcome of disease (Ito et al, 2000;Selinka et al, 2004 ).…”

Initial evidence on differences among Enterovirus 71, Coxsackievirus A16 and Coxsackievirus B4 in binding to cell surface heparan sulphate

“…The possible role of cell surface HS in mediating infection of Human Enteroviruses (HEVs) has mostly been reported for serotypes of HEV group B, including Echovirus [8], Coxsackievirus B3 (CVB3) [24], swine vesicular disease virus (SVDV) [6], and Coxsackievirus A9 (CVA9) [11]. Recently, we demonstrated that several soluble HS mimetic compounds, including heparin (Hep), pentosan polysulphate (PPS) and HS, exhibited potent antiviral activities against a cloned strain of EV71 through interfering with the viral attachment in Vero cells [16] suggesting a role for cellular HS in mediating early move of the EV71 infection.…”