Plasmodium falciparum malaria is a deadly pathogen. The invasion of red blood cells (RBCs) by merozoites is a target for vaccine development. Although anti-merozoite antibodies can block invasion in vitro, there is no efficacy in vivo. To explain this discrepancy we hypothesized that complement activation could enhance RBC invasion by binding to the complement receptor 1 (CR1).

Tumor suppressor p53 is a critical player in the fight against cancer as it controls the cell cycle check point, apoptotic pathways and genomic stability. It is known to be the most frequently mutated gene in a wide variety of human cancers. Single-nucleotide polymorphism of p53 at codon72 leading to substitution of proline (Pro) in place of arginine (Arg) has been identified as a risk factor for development of many cancers, including nasopharyngeal carcinoma (NPC).

Malaria infection poses a serious public health problem in endemic countries. As per World Malaria Report 2015, it is estimated that 3.2 billion people in 97 countries are at risk of being infected with malaria; 214 million cases of malaria with 4,38,000 malaria induced deaths are reported during the year . Clinical consequences of malaria result primarily from parasitic invasion of red blood cells (RBCs). Inside the RBCs, the parasite metabolizes the host haemoglobin in the acidic environment of the parasite’s food vacuole.

It is generally believed that an efficacious vaccine will be a major asset and the most cost-effective intervention in combating malaria. The fact that individuals living in malaria endemic areas develop immunity against the disease and that injection of irradiated sporozoites can protect humans from infection, suggest that it may be possible to develop vaccines against malaria. (Editorial)

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