Table 3.

Epidemiological implications

1.	A substantial proportion of the population in P. vivax endemic areas harbours latent but activatable hypnozoites. Some of these may derive from inoculations which were not followed by any illness.
2.	If relapse rates exceed 50%, then relapse becomes the predominant cause of vivax malaria.
3.	Spontaneous or activated relapse followed by asymptomatic parasitaemia may be an important source of P. vivax transmission.
4.	Reducing P. vivax transmission will have a smaller than currently predicted effect on the incidence and prevalence of vivax malaria initially.
5.	Reducing P.falciparum transmission may reduce the incidence of P.vivax infections and reduce P.vivax transmission. However any effect on the incidence of clinical disease would probably be delayed because reducing falciparum malaria will also reveal vivax malaria by lifting suppression in mixed infections, and a reduction in vivax incidence will reduce immunity. A single radical treatment for all malaria infections may be justified in areas where both parasites are prevalent (i.e. ACT + radical primaquine regimen) [143].
6.	It is very difficult to exclude the presence of long-latency P. vivax phenotypes in studies conducted in vivax endemic areas. Long-latency phenotypes may be prevalent over a much wider area of the tropics than currently thought.
7.	Assessment of the efficacy of interventions requires characterization of the prevalent relapse phenotypes.
8.	Assessments of radical curative activity where long-latency phenotypes are prevalent require one year's follow-up. Genotyping should assist in assessing long-latency relapse.
9.	The proportion of genotypically different (heterologous) relapses will fall as transmission intensity falls