This question is concerned only with recurrences that are neither reinfections nor recrudescences originating from persisting parasites in the bloodstream.

Given these two exclusions, when a Plasmodium vivax infection recurs clinically or there is renewed parasitaemia in the absence of symptoms, an explanation in terms of contemporary understanding is, then, that there has been a hypnozoite-mediated relapse. Related hereto, some excellent genetic epidemiological research on malaria has been carried out in recent years, and it is ongoing. Consequently, I am vaguely wondering how many (if any) experts in this field think at present that there could be a non-hypnozoite explanation for some of the homologous (as opposed to heterologous, which is a different subject), relapse-like P. vivax recurrences?

This question arises in the light of indirect biological and potential genetic support for the possible existence of (inter alia) quiescent, non-hepatic, non-bloodstream, tissue merozoites in P. vivax malaria. A calculated and semi-evidence-based idea is involved, rather than an uninformed and totally wild, half-baked amateur theory. Technical details can be accessed via:

https://malariaworld.org/blog/vivax-and-non-vivax-malaria-elimination-related-research-agenda-items