This question probably has a really obvious answer but it’s been bugging me for years.
In textbooks, at least the high school ones I remember, they always show diagrams of viruses and cells battling it out as if they were playing Tetris. Specifically, virus cells are shown with these legs or appendages in specific shapes, and they fit these legs into slots on our regular cells and that’s how they attack them.
White blood cells are shown as being able to morph themselves to make them compatible with the virus or something like that. Then they are able to attach themselves to a virus, thus making those legs unable to attach to our regular cells and killing or rendering the virus harmless.
Is it really that simple? Are cells shaped and function in a way that’s much like a game of jigsaw?
Those schematic illustrations of course are greatly simplified. However, the interactions between a virus and the cell surface receptor the virus utilizes to enter the cell is in part dependent on shape complementarity between virus surface protein and receptor. However, the shapes involved are more roundish blobs as depicted here, and the interacting surfaces not only show complementary shapes, but also complementary surface properties, for example electric charges.
Nitpick: “virus cells” are a contradiction in terms. Viruses are essentially massive protein macromolecules will no cellular structure i.e. they have no differentiation of functions, nor any internal support or repair capability. (This is somewhat oversimplified, as viruses do have some kind of genome and many have a protective lipid wall in addition to the protein coat, but they don’t meet anyone’s definition of cellular structure essential to life as we understand it.)
As Anaglyph has said, the illustrations in textbooks are necessarily highly simplified; in reality, viruses interact on a molecular level, not a biomechanical one, so when they attack a receptor site on the cell, they’re replicating the same interaction as a legitimate ligand (a peptide “designed” to interface with that site for some functional purpose). This interaction is via complex intermolecular forces; that is, ionic bonds, covalent bonds, hydrogen bonds, and van der Waals forces (mostly the latter two). This results in a change of the conformal state (shape) of both the ligand and the receptor, so rather than like being a key in a lock, it is more like two octopuses making love. (Okay, I know that octopuses don’t engage in intercourse, but you get the image.) The shapes of the ligand and receptor site change in very complex ways that are extremely difficult to calculate even with sophisticated computer simulations, are are way too complicated to illustrate literally.
A classic virus particle, with legs like you are describing is the T4 bacteriophage. It uses its legs to attach to the bacteria, punctures the cell wall like a needle, and then injects its genetic material into the bacterial cell. See this website for actual pictures of this type of virus: http://www.mirrorservice.org/sites/www.virology.net/Big_Virology/BVDNAmyo.html
Actually, they do, after a fashion. Male octopuses have one of their tentacles modified as a mating arm, which they insert into the mantle of the female in order to transfer sperm.
Receptor binding is a detailed field of study in itself. In general, yes, the receptor and the viral nucleocapsid/membrane proteins do fit together in a lock-and-key fashion, but it’s not as if every surface molecule of the receptor is in close proximity to every surface molecule of the ligand.
It’s also important to note that both the receptor and ligand may have a particular native conformation, but upon binding there may be an inducement of altered morphology.
