Malaria Parasites: Immunity Evasion Mechanism: The malaria parasite’s ability to hide from the human immune system is an important discovery in understanding malaria infection. The parasite can “switch” between red blood cells undetected, and therefore escape detection.
This process allows the malaria parasite to reproduce “itself” inside another red blood cell and produce a new wave of daughter parasites. This discovery is described in a study published in the journal Cell Host & Microbe.
Malaria Parasites: Immunity Evasion Mechanism
Immune System Invasion
The immune system of humans is a powerful defense mechanism against malaria parasites. During dry season, the malaria parasite can persist in the human host, but the high splenic clearance of this condition leads to low levels of infection.
These low levels will not trigger host immune factors. When the rainy season arrives, however, the parasite can infect more mosquitoes, leading to more malaria infections. Understanding this mechanism could help develop better treatments.
The Mechanism of Invasion
While the immune response to malaria parasites is less well understood than that of other intracellular pathogens, certain findings indicate that the innate system may provide rapid protection against the malaria parasite.
Specifically, the innate response limits parasite replication during the initial wave of parasitaemia, allowing the host time to develop more adaptive immune responses to clear the infection.
This, in turn, reduces the virulence of the infection. However, the innate immune response may also increase the risk of malaria transmission.
The innate immune response
The innate immune response to malaria parasites is a complex process. In order to effectively eliminate malaria parasites, the human body must first recognize the parasite.
This requires repeated exposure to the parasite. This process may take several months, even years, but the human body can build up immunity to malaria by repeated infections.
A new model for malaria immune response
A new model for malaria immune response highlights the role of innate immune responses and CD4+ T-cells in innate immune responses.
In addition, the immune response to malaria is dependent on IL-12, an inflammatory cytokine that regulates the body’s immune response. It also has adjuvant properties, allowing it to promote protective immunity against the parasite.
Researchers have discovered that malaria parasites have an effective way of hiding from the human immune system. The parasites have the ability to switch between different coats, which allows them to avoid detection.
The early life stages of malaria parasites circulate in the blood and thrive in red blood cells that stick to blood vessels. Hence, the immune system produces antibodies that recognize these parasites, but they are not able to find them in their green-coated counterparts.
Specific Molecule Sensing
The new research demonstrates that malaria parasites can sense a molecule produced by immune cells and use it as an effective way of hiding.
This discovery is significant because it reveals a previously unknown, reversible malaria mechanism. Malaria is a terrible disease that kills 1.2 million people every year, but vaccines and other treatments have been ineffective.
Molecular sensing of malaria parasites allows researchers to find ways to combat the disease before it becomes an issue.
By identifying the specific way the parasites hide from the human immune system, scientists can develop new vaccines that can target the parasites and prevent them from spreading.
To find out how the parasites hide from the human immune system, researchers have analyzed data from more than 600 people in Mali. They found that the disease occurs most often during the rainy season, when mosquitoes are abundant and the malaria parasite reproduces.
The discovery also helps researchers understand how the parasites have evolved over time. By studying the var gene’s structure, they can track the genetic changes of a malaria parasite.
This helps them understand their evolution and how they have adapted to their hosts. While the process of sequencing malaria genomes took more than a decade, the research has led to the discovery of new ways to combat malaria.
Blocking Blood Flow
Plasmodium parasites can hide from the human immune system by blocking blood circulation through the bloodstream.
This can be done through a sticky new strategy that the parasite uses to infect red blood cells. The parasite makes a protein that sticks to the surface of infected blood cells and attaches itself to the inner walls of blood vessels. This allows the parasite to reproduce in the sick blood cell while restricting blood flow.
The parasites communicate with each other using tiny sac-like nanovesicles that are less than one micron in size. These sacs contain a small segment of the parasite’s DNA.
These nanovesicles help the parasites learn when to transform. These tiny particles are carried by mosquitoes, which are able to carry both male and female parasites.
The development of the different sexual stages of the parasite is critical to the transmission of malaria. The development of these stages can be blocked by the use of vaccines and drugs.
This way, the transmission of malaria is prevented. However, the molecular mechanisms surrounding this switch remain elusive.
When the parasite enters the human bloodstream, it hides from the human immune system. It reproduces within hepatocytes and multiplies exponentially.
Once inside the bloodstream, hundreds of thousands of merozoites are released. These are the merozoites responsible for the pathology and clinical features associated with malaria.
Activation of Antibodies
The human immune system has many mechanisms that can fight against the parasite. Antibodies play an important role in this process.
The antibodies help in the immune response by recognizing the parasites and preventing them from spreading throughout the body. They also act as opsonin’s, preventing erythrocytes from adhering to the endothelial tissue.
Infection with Plasmodium parasites causes red blood cells to become infected with PfEMP1s. These PfEMP1s act like ‘knobs’, allowing the parasite to interact with the host from inside the red blood cell.
This recombination process occurs in 0.2 per cent of malaria parasite cells every 48 hours. Since an average malaria patient has billions of parasites inside their bodies, 0.2 per cent equates to two million newly-created var gene sequences. During the dry season, this means that millions of new PfEMP1 variants are produced inside one infected person.
Children with low-grade immune system may be at risk of developing endémic BL, a severe form of malaria. Children with endémic BL often exhibit attenuated reactivity to PfEMP1 antigens. They are also predisposed to recurrent low-grade malaria.
The findings have important implications for malaria-control programs. With a large number of strains of malaria parasites, each with different surface coat proteins, many children may remain infected despite aggressive interventions. Because of the wide variety of PfEMP1s, many malaria parasites may not respond to the same treatment as others.
The molecule PfEMP1 is a large sticky protein that is produced by the malaria parasite. It causes the red blood cells to stick to the blood vessels, and prevents the parasite from making its way to the spleen, which is the organ that filters blood.
This knowledge can be used to improve vaccine design, as well as adjunct interventions for malaria.
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