This is indeed a strange disease. The epidemiology suggests it to be of relatively low infectivity, but high severity. This in itself is odd, especially if the causative agent is a virus and the principal mode of spread by coughing/droplet. Also odd is the undoubted existence of “superspreaders”, who can infect very many of their contacts—I can’t think of any parallels to this in respiratory virology.

Perhaps the SARS virus obeys the usual rules of droplet transmitted respiratory infections, and is of high infectivity. However, because of shared antigens, a proportion of the population has an acquired resistance to the new virus, having already been exposed to another, relatively innocuous, virus that provides immune protection. It is possible that the proportion of humanity immune or partially immune to SARS could be as high as, say, 95% if the second virus were a very common one, for example, one of the coronaviruses that causes coryza. This would explain the seemingly low, unexpectedly so, infectivity of the SARS agent.

Perhaps this also explains “superspreaders”. Picture humanity divided into two categories:

1. Those who have met a common related coronavirus, and consequently have a degree of immunity to SARS, say for the sake of argument ± 95% of the population.

2. Those who have not met it, and have no immunity, ±5%. If the defences of the first group are overwhelmed by exposure to a huge SARS virus inoculum, perhaps they would contract a modified form of the disease, quickly recruit their immune systems to produce antibodies to a recognised infectious agent, be likely to recover, not shed large amounts of virus, not be all that infectious. The second group would get the disease in an exuberant form, excrete quantities of infectious material, be likely to succumb before their immune system could meet the challenge—the superspreaders—always allowing that other factors may be implicated in superspreader events, such as a pre-existing condition in the initiator, or variation in the likely number of contacts, this greatly increased by hospitalisation before the risk is known.

The invocation of a high (but presumably variable and incomplete) level of acquired immunity to the SARS agent in affected populations explains other apparent anomalies of the 2003 epidemic—Why did some regions (Russia, Japan, Indonesia, Thailand, Malaysia, etc) not have any cases, despite a high intensity of air traffic with the epicentre of the disease? Why did some affected regions (Guangdong, Hong Kong, Toronto) struggle to contain the disease, when others (Singapore, Vietnam) had no such difficulty? Above all, how was a pandemic averted when in the earlier stages of the spread of SARS this outcome appeared very much a probability?

I believe that a coherent mathematical model of the SARS epidemic could be constructed from the above theory. This of course would not necessarily lend it validity, but it may be worth looking at.

Even if this apercu should prove anywhere near the mark, it still would fail to answer another question—Will epidemic SARS recur? On the other hand, the possibility of a pandemic might be seen to recede.