Key result
Physiological concentrations of serum albumin reversibly blocked echovirus 7 infection by inhibiting viral uncoating.
Serum albumin reversibly inhibits echovirus 7 uncoating, potentially acting as an extracellular determinant for viral tropism in vivo.
May limit echovirus 7 spread in vivo; leaves open its role as a host determinant of human enteroviral tropism.
Echoviruses induce a wide spectrum of diseases in man, the most severe being meningitis. In neonates, however, a severe systemic infection can be observed, leading to death. Serum albumin is the most abundant protein in plasma and most interstitial fluids, and its functions include osmoregulation and transport and delivery of hydrophobic molecules such as fatty acids and steroids. The results of cold-synchronized one-step growth analysis of echovirus 7 infection and sucrose-gradient analysis of A-particles suggest that physiological concentrations of albumin block echovirus 7 infection by inhibiting uncoating. The blockage was reversible and was still effective when albumin was added 30 min after virus adsorption. Inhibition of uncoating was confirmed by using rhodanine, a known specific inhibitor of echovirus uncoating. After removal of the albumin blockage, addition of rhodanine perpetuated the inhibition. Serum and interstitial albumin concentrations may limit echovirus infection in vivo and thereby act as an extracellular determinant for echovirus tropism.
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Ward et al. (1999) studied Echovirus 7 infection. Serum albumin was evaluated on Echovirus 7 uncoating and infection. Physiological concentrations of serum albumin reversibly blocked echovirus 7 infection by inhibiting viral uncoating.