"The Edge of Evolution" by Michael Behe

Heterozygous sickle cell carriers make up around 10% of the population, they are not completely immune to Plasmodium*, and the mechanism of resistance is that infected blood cells are destroyed before the parasite has time to complete it's life cycle meaning that most resistance strategies would require a remodelling of the parasites life cycle.In contrast, chloroquine was introduced into the vast majority of the population, induced near 100% Plasmodium mortality in already present populations and the mechanism of resistance have taken the form of simple alterations to existing intergral membrane proteins to export chloroquine from the cell** and no major lifecycle changes.So, you see, there's a pretty sharp distinction between the two cases. In one you have a mild selective pressure, and no apparent simple means of resistance; in the other you have extreme selection pressure and a simple means of resistance.I say 'apparent' because there's a big flaw in Behe's argument anyway: the assumption that there have been no adaptions in Plasmodium in response to Sickle Cell. We don't know this. For all we know Sickle Cell used to be much more effective against Plasmodium but changes to the parasite now make it more effectively able to infect such hosts.* - in fact, the resistance of Sickle Cell heterozygotes to Plasmodium may not be disadvantageous to the parasite at all. Often reduced mortality among hosts is of benefit to parasites.** - please note that while the mechanism I describe here is the current preferred model of how anti-chloroquine resistance works it has not yet been conclusively demonstrated.

As I understand it, malarial infection of sickle cell trait individuals does occur but the levels of infection are sufficently low as to be largely asymptomatic in most cases.But thinking about it, it is considerably more likely to be disadvantageous.