The first thing about malaria – especially the part of cure – that we can think of is Quinine. Quinine can cure malaria but at the same time, it is one hell of a distasteful liquid. However, there is no way to avoid having it considering how it is the only option that we have for situations such as these. A survey has recently stated that all around the world more than 4 lakh people die each year due to this dreaded disease. The same survey has also revealed that there are occasions when the anti-malarial drugs do not work as well.
What does the survey say?
The survey has been published in a journal named Nature Microbiology. The publication has also brought to the fore interesting facts that scientists have come up with such a way so that the parasite of malaria – Plasmodium falciparum – leave the red blood cells (RBC) of your body and go make their home in another cell. According to Mike Blackman, a researcher with the Francis Crick Institute of the United Kingdom, this would make treating malaria a lot easier than before. Blackman and his co-researchers have found out a couple of proteins – SERA6 and SUB1 – that actually helps the malarial parasite proliferate in your body.
Efforts are now being made to come up with medicines that can help destroy those proteins.
The importance of medicines
It has already been said that in many cases anti-malarial drugs do not work and this is why this development – Blackman and his team coordinating with the pharmaceutical companies in order to come up with medicines to destroy said proteins – can be regarded as such a groundbreaking development. It is also pretty critical from a health perspective.
What did the research focus on?
Blackman has said that his team focused on Plasmodium falciparum, which can easily be called the deadliest among all the parasites that cause malaria. The aim was to find fresh drug goals that could work in a way that was different to the treatments that exist right now. For the study, the team also worked with Proteomics Science Technology Platform of Francis Crick Institute, London School of Hygiene & Tropical Medicine, and scientists of the Birkbeck College of King’s College London.
In fact, the team has already started to work with GlaxoSmithKline (GSK) in order to verify if the designing drugs, which are able to target the two proteins, can be used to create the basis for new anti-malarial drugs or not. This was revealed by Dr. James Thomas, who is a postdoctoral scholar at the Francis Crick Institute and happens to be a first joint author of this paper as well.
How do malarial parasites function?
When RBCs are invaded by malarial parasites they create an internal section as such. Here they replicate on plenty of occasions before they finally burst out of the compartment and start to infect the other cells as well. The parasites will have to burst through the internal section as well as the membrane of the RBC so that they can escape the RBCs.
The methods followed
The team of researchers employed genetic knockout tests in order to reveal how important SUB1 was for the malarial parasite to escape the internal section. It is also SUB1 that activates SERA6 that is necessary for parasites to escape the RBC membrane. The group then used analytical tools in order to show the way SERA6 does its work. Michele Tan, a Ph.D. student and a joint author of the said paper, explained how this happened. She says that underneath our RBC membrane there is a meshwork that is really strong and resembles a chicken wire.
Its main responsibility is to provide support and strength to the structure. The researchers found out that SERA6 cuts through this chicken wire. This causes the membrane to get ripped open after collapsing. This lets the parasites escape. The paper is named “A protease cascade regulates the release of the human malaria parasite Plasmodium falciparum from host red blood cells”.
Given how most diseases – communicable in this case – are becoming resistant to medicines built to counter them such developments are heartwarming indeed because they show that not all is lost and there is hope for all.