Abstract
Low-affinity CD46-binding isolates can be converted to the high-affinity CD46-binding phenotype by a substitution of Tyr instead of Asn at position 481 (Hsu et al., 1998). Likewise, a substitution of Gly instead of Ser at site 546 has been shown to confer both the properties of CD46 binding and haemadsorption to isolates that were previously defective for these traits (Li et al., 1999).