What is different between species that makes many viruses unable to infect multiple species? Is it their immune systems, or the structure of the cell whose DNA it is trying to hijack? Or a combination of both? Or something altogether different?
To be simplistic about it, it has to do with the proteins on the surface of the cells. These proteins tell the virus whether the cell it is “looking” at is the right type. Viruses don’t know or care about species or tissue type, they only “know” to infect cells bearing a particular protein configuration. More often than not, this results in the virus only infecting cells of a specific tissue of a single species, or small gropup of closely-related species.
This question seems to get asked at least once a month. If you do an archive search you will find numerous previous responses. I’m too lazy to bother retyping a real answer, but there is much more to it than just an inability of viruses to infect alternative host cells, although that is probably the most important reason.
Blake, I did searches for threads in GD with “virus” or “disease” in the title, going back a year, finding no thread on this particular subject. Those monthly threads on this issue must have abysmal titles.
But why does is look for a particular protein configuration? Wouldn’t a more successful strategy be to infect the cell regardless? Seems like it’s doing work to be less successful.
Actually, the premise is incorrect. Most viruses can cross species.
They simply can’t do it indiscriminately. In fact, this is why smallpox is the only viral disease we have truly eradicated, and one of the few we can reasonably hope to truly eradicate: it has no (known) animal reservoir. Various recent flu viruses, for example, can infect certain avian or porcine species, and indeed, reassortment of the “chromosomes” of influenza viruses [which happen to have a multi-partite genome) in birds, with wild strains carried by birds to regions where birds and humans live in close proximity (e.g. Chinese and Southeast Asian farms) sontributes very heavily to the annual “flu strain” changes.
The cell surface receptors or opportunistic binding sites where many viruses first attach to a cell are only part of the story. While it’s true that cells have evolved protections against generic invasion by virons, the initial binding and endocytosis (being taken into the cell) is only the first hurdle. The cell has to be sufficiently similar on all the key enzymes for the viral genome (which is very limited by the amount of genetic material it can carry) to successfully subvert the host cell’s functions to manufacture new virions.
If the virion can’t subvert the cell’s mechaisms, it won’t replicate. That’s not infection. A nonreplicating virus in a cell is no more dangerous (in fact it’s probably much less dangerous) to us or it’s animal host than a virus that’s left sitting on a table.
Interestingly, there are some cases when a species that is not susceptible to a certain infection is susceptible to a coinfection. For example, Virus A that can enter some cells in Species 1, but can’t infect Species 1 because its genes can’t subvert pathway X (e.g. a pathway to synthesize viral lipids, etc.) might well be able to infect a cell with the help of Virus B - which may or may not be able to infect Species 1 either but can subvert Pathway X.
That may seem to be a trivial distinction, but I think it illustrates a point: there are several rodblock, so your flu might not be able to infect your lemur ferret or dog, but might happen to be able to infect your duck (and inter breed with another strain to come back at you, meaner than ever). Coinfection has actually been used in several molecular biology experiments.
Viruses are limited by the amount of genetic material they carry, their structure, etc. They can actually pick up a surprising degree of “sophistication” from their hosts. (That’s a sloppy statement, like many statements about “evolving” but I hope you get the idea) , but every step or chemical process in their life cycle or replication relies on the host having compatible pathways. Viruses have absolutely no metabolism of their own. Without the “unwilling cooperation” of a host, they are as dead as concrete or a silicon chip – intricate and sophisticated, but completely unalive.
Actually, I’d say they’re not alive, period. Though I cringe every time I hear an uneducated comparison to computer viruses, the truth is: the analogy is quite apt in many ways. If you don’t have a compatible OS, or don’t have certain services enabled, or are running an older or newer patch version, or aren’t on a network that is configured a certain way (etc. etc.) a computer virus may not be able to infect you, replicate, and spread [which is as close to ‘life’ as it gets]. The same applies for a virus in a biological system.
Interesting info, thanks KP.