One of the frequently asked questions about the SARS-CoV-2 virus is how long the virus can live outside the body. “Live” is not exactly the appropriate term, as viruses are not really "alive" because they cannot reproduce by themselves. Instead, viruses have to invade a living cell and hijack its genetic machinery in order to reproduce. In this process, they disrupt the cell’s life cycle and it is that cellular damage that results in disease. So instead of asking how long a virus can live outside the body, we can ask how long it remains infectious, that is, how long it retains its ability to invade a living cell and cause mischief. That ability depends on how long the extremely complex structure of a virus stays intact. And extremely complex it is.
A virus is composed of a complex array of nucleic acids, proteins, glycoproteins (proteins with carbohydrates attached), fats and water molecules, all assembled in a three-dimensional network. If this assembly is disrupted, the virus cannot invade a cell. The picture we so often see of the coronavirus features spikes emerging from a ball. Those spikes contain the proteins the virus uses to attach itself to receptors on cells, which is the first step to invading a cell. All proteins are composed of amino acids linked in a chain (primary structure), but those chains are folded in a specific pattern with the folds maintained by various types of “cross-links,” much like rungs of a ladder (secondary structure). Some of these links are “hydrogen bonds” in which a partially positively charged hydrogen atom on one part of the chain is attracted to the negatively charged electrons on an oxygen or nitrogen atom elsewhere on the chain. Water molecules can also take part in such bonding with the two hydrogens being attracted to oxygen or nitrogen atoms on two amino acids located at different positions on the protein chain, forming a bridge.
On top of it all, the folded chains themselves then twist into an even more complex array (tertiary structure), again maintained by more “rungs.” This arrangement has to be maintained for a virus to remain infective. Although somewhat too simplistic, a lock and key model can serve as an analogy. If the proteins in the spike have the right twists and turns, they constitute the right “key” to fit into the cell’s receptor, which is the “lock.” If the shape of the key is altered, it will not fit. However, if there is a fit, then the “door” opens, and the virus will enter the cell and insert its genetic material into the cell’s DNA and trick it into making many copies of itself. But if the virus’s genetic material has been somehow previously compromised, no replication occurs even if it invades the cell successfully. The spikes of the virus are also protected by an “envelope” of fats and glycoproteins, which if disrupted allow the proteins needed to invade cells to leak out.
We now see that there are at least three ways that a virus can become inactive. Any disruption of the structure of key proteins, nucleic acids or the fatty membrane will render it incapable of infecting cells. What then happens to a virus particle, also known as a virion, that lands on a surface? Many possibilities. Heat speeds up molecular motion and the more molecules move around, the greater the chance that the links needed to maintain the secondary and tertiary structure of proteins are broken. This is why temperatures above 60C are lethal to most viruses. (Cold temperatures do not bother viruses, they can remain viable for a long time in refrigerators and freezers.)
Also, with time, the molecules of water embedded in the viral structure evaporate and that can disrupt the folding pattern of the proteins. Air is composed of oxygen and nitrogen molecules that have an affinity for hydrogen atoms on proteins and can cause some of the hydrogen bonds to dissociate. Oxygen can also engage in a chemical reaction with fats, much like it causes rancidity in cooking oils, and impair the protective effect of the fatty envelope. Ultraviolet light, particularly short-wavelength (UV-C), is energetic enough to break chemical bonds and has been shown to alter the structure of nucleic acids. Put all of this together and we can see why the viability of a virus to cause an infection wanes with time. That time, though, depends on several factors. The cleanliness of the surface is important. Viral particles can be embedded in grease, protecting them from outside agents. The composition of the surface can also play a role. Copper, for example, releases copper ions that have antiviral activity. Paper has residues of the chemicals used in pulping that can inactivate viruses. Steel and plastic seem to be more hospitable, but even here survival time is only a couple of days.
Obviously, the viability of viruses can be reduced with disinfectants like soap, alcohol, sodium hypochlorite (bleach), hydrogen peroxide, quaternary ammonium compounds (alkyldimethylbenzyl ammonium chloride) all of which in some way disrupt the chemical bonds that maintain the shape of the virus particles. Like everything else in life, the viability of virions is a function of molecular structure. It is a matter of chemistry.