I’ve heard that HIV developed from SIV, etc.

I’ve also heard that most species (including most monkeys) can’t get a common cold like humans.

So then what causes infections to be able to travel across species, or vice-versa?

For the sake of the question, I’ll narrow the scope. Let’s say we have a virus that can infect humans but not infect close human relatives, like Chimpanzees. What about that virus biology or animal biology causes that difference?

I know with some animals it’s about body temperature or skin composition, etc. But humans and chimps are physically pretty similar. Is it all about the immune differences?


2 Answers 2


Viruses evolve alongside their hosts. If you swapped a human chromosome into a chimp cell for the matching chimp chromosome, there would be a lot of genetic similarities but you would also surface a bunch of incompatibilities because the genes on each chromosome have been evolving independently from the rest of the genome.

Viruses interact with their host genome at many stages. First, they need a way to identify their target hosts (cells) in the environment and gain access to the cells. They do this by recognizing markers on the cell surface. For something like HIV, this identification is far more specific than identifying just humans even: they are identifying particular immune cells.

Once inside, viruses interact with the host to express viral genes, produce and assemble new virions, and get transmitted to subsequent hosts. If an incompatibility occurs at any of these stages, the virus won't be able to replicate.

However, because there is a lot of homology across related species, it is feasible for a virus to infect more than one host. If a virus evolves in a context where it commonly infects multiple hosts, there can be selective pressures for it to maintain those abilities across all the hosts. Alternatively, selective pressures might cause the virus to evolve into separate lineages, one infecting ducks and another infecting sparrows, for example.

For a virus that is specific to a certain host (or range of hosts), it is likely that it will have difficulty in another host outside the context in which it evolved. However, there is also variability in viral genomes, and if many viral copies are exposed to a novel host, there is chance that some of them can survive in that host. This will select for those particular viral genes, and subsequent viral generations will be further selected for traits that help replicate in that host.

Immune reactions could also play a role, but in most cases it is the specialization of the viruses themselves that hold the key to host specificity.

Ahlquist, P., Noueiry, A. O., Lee, W. M., Kushner, D. B., & Dye, B. T. (2003). Host factors in positive-strand RNA virus genome replication. Journal of virology, 77(15), 8181-8186.

Hao, L., Sakurai, A., Watanabe, T., Sorensen, E., Nidom, C. A., Newton, M. A., ... & Kawaoka, Y. (2008). Drosophila RNAi screen identifies host genes important for influenza virus replication. Nature, 454(7206), 890.

Schild, G. C., Oxford, J. S., De Jong, J. C., & Webster, R. G. (1983). Evidence for host-cell selection of influenza virus antigenic variants. Nature, 303(5919), 706.

  • $\begingroup$ Great answer and concise, thank you!! One question I have that I may address if I have time (or if you/someone else wants): so your answer says that one possible reason why rhinovirus doesn’t infect mice is that the receptors are different. So (1) what are the receptors that rhinovirus binds to in humans and (2) can we do an alignment between those receptors in mice and humans? Do we know which misaligned residues/change in structure leads to the mismatch? $\endgroup$ Commented Oct 11, 2018 at 15:50
  • 2
    $\begingroup$ @CalendarJ That would be an excellent separate question. Not my area of expertise but I am almost certain that rhinovirus cell specificity has been studied, though I'm less certain that specific residues involved in human/mouse differences would be understood. In any case it's a good question that should produce a well-referenced answer. $\endgroup$
    – Bryan Krause
    Commented Oct 11, 2018 at 15:54

The biggest key to understanding viruses and their hosts (more specifically, host cells) is external (membrane and ECM) protein structure.

As a general rule of thumb, viruses need to latch on to their host cells. Some viruses abuse transport mechanisms to trick host cells into "eating them" and running their contents. Other types of viruses have nasty-looking clamps (most prominent example that comes to mind are bacteriophages) that grab specific structures on host cells while the central piece of the virus punches a hole in the host cell's membrane to feed it malicious DNA/RNA and enzymes.

Cross-species infections usually abuse structures common to many species. For example, sialic acid receptors are commonly abused as viral entry points (see https://www.ncbi.nlm.nih.gov/pubmed/23873408). If humans had genomic support just like computer operating systems receive updates for vulnerable components, sialic acid receptors would have been labeled a critical risk millennia ago and patched.

Obviously there are other factors that can thwart cross-species infection. A successful cross-species virus needs to use a minimum supported operation subset of cell functions common to its hosts. If a potential (by external structure match) host cell is unable to make a piece required for viral replication, it fails. If a potential host cell (or the host itself, in the case of multi-celled life forms) is built with some oddball anti-infection measures (for example: tamper-detection, integrity check before producing protein from RNA, or unexpectedly robust immunity), then the infection could fail anyway.


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