Helicobacter pylori infects only gastric type epithelium, to which it adheres closely and forms attaching-effacing lesions. Similar lesions are also seen in ferrets infected with Helicobacter mustelae, the only other host in which peptic ulcer occurs during the course of infection. These observations imply a specific interaction between bacterial adhesin(s) and host receptor(s). They account for the adherence of H. pylori to the gastric epithelium and suggest that adherence is an important virulence factor. Numerous experimental methods, each with their own advantages or disadvantages, are available to study the interaction and characterize the nature of bacterial adhesins and their receptors. Many studies have shown that H. pylori is able to agglutinate red blood cells. Amongst several bacterial lectins, at least one adhesin has a sialic acid receptor specificity. However, the gene encoding this putative adhesin is larger than originally thought, whilst the function and location of its product is unclear. Adherence of H. pylori to a wide variety of cell lines (gastric and non-gastric) has also been shown, and is necessary for the induction of pro-inflammatory responses. However, there is little evidence to support an association between haemagglutination and extent or pattern of adherence to gastric epithelium or gastric-derived cell lines.