Abstract
Background: Malaria remains a major health threat worldwide. Endemic regions for malaria are endemic for other infectious diseases that might affect the malaria infection. Methods: A systematic search was conducted where it included published data about HBV, HCV and malaria. Published data on epidemiology, pathogenesis and consequences of HBV, HCV and malaria, were extracted from relevant studies. Epidemiology of co-infection has not been well studied, and studies in this concern will definitely draw the attention of decision makers towards such problem. Results: Younger age and male gender were risk factors for co-infection. There were no protective effects of HBV vaccine against malaria. The interaction between malaria parasites and HCV among chronic HCV carriers might slow the emergence of the former and that could help in determining new therapeutic approaches to defeat malaria. Conclusion: Strategies to improve currently available diagnostic techniques, researches dealing with therapeutic and prophylactic agents and protocols, vector control procedures, vaccine bringing up evolution, and other operational tools and approaches are needed.
Highlights
MethodsA systematic search was conducted where it included published data about hepatitis B virus (HBV), HCV and malaria
Malaria remains a major health threat worldwide
A study carried in Vietnam illustrated that patients with cerebral malaria had a slightly greater vulnerability to demonstrate hepatitis B virus (HBV) surface antigen (HBsAg) sero-positivity [8]; the aforementioned study failed to show any significant relation between the overall risk of death caused by severe falciparum malaria and positivity for HBs Ag [8]
Summary
Asystematic search was conducted where it included published data about HBV, HCV and malaria. The T cell response appeared earlier in the blood stage than in hepatic stage infection, possibly because parasitemia was detectable earlier in those animals and a T cell–independent phase was not seen, perhaps reflecting that it was induced primarily by infected hepatocytes In both cases, the generated cytokine ripostes were accompanied with a decline in HBV RNA and DNA in the liver [6]. Andrade et al found (among 636 Brazilian patients) that HBV infection was associated with a decreased intensity of malaria infection among individuals in the study [18] They proposed that this effect is due to cytokine balance and control of inflammatory ripostes [18]. The interaction between malaria parasites and HCV among chronic HCV carriers has been found to slow the emergence of the former a thing that could help in determining new therapeutic approaches to defeat malaria [9]
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