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Early SARS strains included many variants of the virus's spike protein, which helps it adhere to host cells.
Streptococcus pneumoniae, like many other Gram-positive bacteria, assembles long filamentous pili on their surface through which they adhere to host cells.
A necessary step in the successful colonization and progression of disease by microbial pathogens is the ability to adhere to host surfaces [8].
To do so requires that the bacterium evade complement-mediated killing and adhere to host cell surfaces and/or extracellular matrices, especially epithelial and endothelial basement membranes.
TAAs are a family of outer membrane proteins that adhere to host cell surfaces, and thus have an important role in virulence of these pathogens [2].
The pathogenesis of the fungus is attributed to a number of virulence factors, including its ability to adhere to host cells, form biofilm, and secrete hydrolytic enzymes such as lipases, aspartic proteinases and phospholipases [2].
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B. bronchiseptica adhered to host cells almost exclusively to GM1-enriched lipid raft microdomains and BteA colocalized to these same sites following T3SS-mediated translocation.
Fluorescent parasites adhered to host cells (in blue) were counted using an Eclipse 80i epifluorescence microscope (Nikon) and the NIS-Elements BR 2.1 software (Nikon) (Table 3).
These structures exhibit adhesive properties and may play a key role in adhering to host cells and tissues, as well as in biofilm formation by pathogens of the Streptococcus species.
Cell-surface pili are important virulence factors that enable pathogens to adhere to specific host tissues and to modulate host immune response [ 63].
Such features could be related to the ability to adhere to the host, persist in tissues other than the gut and to overcome the (debilitated) host immune system.
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