Malaria and COVID-19: unmasking their ties

Abstract

The incidence and mortality of COVID-19, according to the World Health Organization reports, shows a noticeable difference between North America, Western Europe, and South Asia on one hand and most African countries on the other hand, especially the malaria-endemic countries. Although this observation could be attributed to limited testing capacity, mitigation tools adopted and cultural habits, many theories have been postulated to explain this difference in prevalence and mortality. Because death tends to occur more in elders, both the role of demography, and how the age structure of a population may contribute to the difference in mortality rate between countries were discussed. The variable distribution of the ACEI/D and the ACE2 (C1173T substitution) polymorphisms has been postulated to explain this variable prevalence. Up-to-date data regarding the role of hydroxychloroquine (HCQ) and chloroquine (CQ) in COVID-19 have been summarized. The article also sheds lights on how the similarity of malaria and COVID-19 symptoms can lead to misdiagnosis of one disease for the other or overlooking the possibility of co-infection. As the COVID-19 pandemic threatens the delivery of malaria services, such as the distribution of insecticide-treated nets (ITNs), indoor residual spraying, as well as malaria chemoprevention there is an urgent need for rapid and effective responses to avoid malaria outbreaks.

Keywords: ACE2; COVID-19; Hydroxychloroquine and chloroquine; Malaria; Malaria and COVID-19 syndemics; Malaria service.

Fig. 1

It shows the RAAS pathway, mechanism of action of ACEIs and ARBs, and the use of ACE2 receptors by SARS and SARS-COV2 for host cell entry. ARBs angiotensin receptor blockers, ACEIs angiotensin-converting enzyme inhibitors

Fig. 2

Hydroxychloroquine (HCQ) and chloroquine (CQ) interfere with T cell activation and prevent co-stimulatory signals and cytokines release. They inhibit lysosomes, prevent membrane fusion and antigen presentation rendering T cell inactivated. They also inhibit the virus binding to ACE2 receptors and prevent viral entry to the cell. TLRs toll-like receptors, MHC major histocompatibility complex, cGAS cyclic GMP-AMP synthase