Early SARS strains included many variants of the virus's spike protein, which helps it 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.
Streptococcus pneumoniae, like many other Gram-positive bacteria, assembles long filamentous pili on their surface through which they adhere to host cells.
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].
Also, a pXO1-encoded S-layer protein (BslA) was recently shown to play a role in the ability of B. anthracis vegetative cells to adhere to host cells [36].
Colonization is crucial to pathogenesis of bacteria, being the earliest stage during onset of the disease and the ability to adhere to host surfaces is by far the most vital step in the successful colonization by microbial pathogens [7], [8].
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].
Var genes are composed of multiple Duffy-binding-like (DBL) and cysteine-interdomain-rich (CIDR) domains that adhere to host tissues to enhance parasite survival and contribute to pathogenesis [14].
Trypomastigotes adhere to host cells using surface receptors.
