Scientists Discover New Target to Prevent Malaria Infection

New Study Reveals Potential Clues to Prevent Malaria Infection

With the declaration of the COVID-19 pandemic, the number of overseas travelers has been increasing, leading to a rise in malaria cases worldwide. Recent reports have shown that Korea is not a malaria-safe zone, as a malaria warning was issued. In response to this public health crisis, scientists have been actively searching for targets that can prevent malaria infection. A recent study published in Nature has identified the inhibition of a specific protein as a key mechanism to prevent malaria infection.

The study, led by the National Center for Scientific Research in France, found that malaria infection can be prevented by inhibiting Plasmodium falciparum myosin A. Malaria is a deadly disease, causing over 500,000 deaths annually. While there are various antibiotics available to prevent and treat malaria, the parasite Plasmodium falciparum has been developing resistance to these drugs over time.

Plasmodium falciparum is the most problematic strain of malaria worldwide. Its resistance to existing antibiotics, coupled with the expanding epidemic area, has intensified the severity of the problem. To understand the mechanism of malaria infection, researchers focused on the gliding motility of the parasite. Gliding motility is a form of movement in which the parasite moves on a solid surface by consuming energy. Through this process, the infectious worms reach host tissues and cells.

The gliding motility of the parasite is facilitated by the glideosome protein, a macromolecular complex composed of adhesive proteins. The core of this complex’s action is the interaction between actin (PfAct1) and myosin A (PfMyoA). Actin is a major protein that constitutes muscle myofibrils, while myosin A is a motor protein responsible for muscle contraction. The research team identified PfMyoA, a class XIV myosin motor, as a potential target for therapeutic drugs to prevent malaria infection.

The National Center for Scientific Research in France discovered a new small-molecule drug candidate called ‘KNX-002’ that inhibits PfMyoA. Among approximately 50,000 substances in the compound repository, ‘KNX-002’ showed inhibitory activity against PfMyoA. In contrast to the currently used malaria vaccine ‘RTS, S’, which targets proteins on the cell envelope of the parasite, ‘KNX-002’ blocks the migration of infectious insects to the host by inhibiting the glidosome’s PfMyoA protein. This prevents host infection, while ‘RTS, S’ prevents in vivo infection after host cell migration.

Preclinical in vitro experiments were conducted to evaluate the efficacy of ‘KNX-002’. The results showed that ‘KNX-002’ effectively inhibited PfMyoA adenosine triphosphatase activity and blocked asexual reproduction during the life cycle of Plasmodium. However, further research is needed to determine the wide-ranging effects of ‘KNX-002’ on the human body. The currently licensed malaria vaccine, ‘RTS, S’, has a preventive efficacy of less than 50%, highlighting the need for more research in the future.

The research team stated, “The combination of ‘KNX-002’ and PfMyoA prevents the activation of efficient hydrolase and blocks gliding motility, providing a clue to prevent malaria infection.” This breakthrough discovery offers hope in the fight against malaria and may pave the way for the development of more effective preventive measures and treatments.

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How does inhibiting the motor protein myosin A disrupt the gliding motility of the parasite and prevent its ability to invade host tissues and cells?

Is the motor protein myosin A, which generates the force for the parasite’s movement. By inhibiting myosin A, researchers were able to disrupt the gliding motility of the parasite, preventing its ability to invade host tissues and cells.

The study used a combination of genetic and pharmacological approaches to inhibit myosin A in the parasite. They found that when myosin A was inhibited, the parasite was unable to undergo gliding motility and its infection capabilities were significantly reduced. This suggests that targeting myosin A could be a promising strategy for preventing malaria infection.

In addition to its role in gliding motility, the researchers also found that myosin A plays a crucial role in the parasite’s ability to multiply within host cells. By inhibiting myosin A, they were able to effectively prevent the replication of the parasite, further reducing its ability to cause infection.

These findings open up new possibilities for the development of anti-malarial drugs that target myosin A. By specifically targeting this protein, scientists may be able to develop drugs that are not only effective against the drug-resistant Plasmodium falciparum, but also prevent the spread of the disease in the first place.

While further research is needed to fully understand the mechanism of myosin A inhibition and its potential as a therapeutic target, these findings provide important insights into the development of new strategies to combat malaria infection. With the continued rise in malaria cases worldwide, the need for effective prevention and treatment options is more pressing than ever. The discovery of myosin A as a potential target is a step forward in the fight against this deadly disease.