Eukaryotes Flashcards
explain trypanosomiasis
Trypanosomiasis, also known as sleeping sickness in humans, is a parasitic disease caused by protozoa of the genus Trypanosoma. There are two forms of the disease, depending on the species of Trypanosoma involved: African Trypanosomiasis (caused by Trypanosoma brucei) and American Trypanosomiasis, also known as Chagas disease (caused by Trypanosoma cruzi). Here, I will focus on African Trypanosomiasis:
Nature of the Disease: African Trypanosomiasis primarily affects humans and animals in sub-Saharan Africa. The disease is transmitted through the bite of infected tsetse flies, which carry the Trypanosoma parasites. In humans, it leads to a wide range of symptoms, including fever, weakness, joint pain, headache, and can progress to neurological symptoms, including sleep disturbances, confusion, and in the later stages, severe neurological problems and death if not treated. It is considered a neglected tropical disease.
Structure Related to Function of the Trypanosome Cell: Trypanosoma are unicellular parasites with a complex life cycle. They have a single flagellum, which is crucial for their mobility. The surface of the trypanosome is covered with a dense coat of a glycoprotein called the variant surface glycoprotein (VSG). Trypanosomes are capable of antigenic variation, switching their VSGs to evade the host immune system. This coat of VSGs is critical for their survival in the host.
Immune Evasion: Trypanosomes are masters of immune evasion. As mentioned earlier, they can undergo antigenic variation by switching their VSGs. This allows them to avoid detection by the host’s immune system, as the host antibodies recognize the VSGs on the parasite’s surface. Additionally, trypanosomes can hide in various host tissues, including the central nervous system, where the immune system has limited access.
Life Cycle: The life cycle of Trypanosoma involves both an insect vector (tsetse fly) and a mammalian host. When an infected tsetse fly bites a mammal, it injects the parasites into the host’s bloodstream. Trypanosomes then multiply and move to various tissues. In the tsetse fly, they undergo changes, and the fly becomes infectious. When an infected tsetse fly bites another mammal, the cycle continues.
Anti-Trypanosome drugs, such as suramin and pentamidine, are available for the treatment of African Trypanosomiasis.
explain the causative agents and various forms of trypanosomiasis
Sleeping sickness, or African Trypanosomiasis, is indeed a severe and potentially deadly disease caused by Trypanosoma brucei. The two main subspecies that affect humans are T. brucei gambiense (TbG) and T. brucei rhodesiense (TbR). TbG is responsible for the majority of reported cases and is generally associated with a more chronic and less aggressive form of the disease, while TbR is more acute and aggressive.
Chagas disease, caused by Trypanosoma cruzi, is prevalent in parts of Latin America and has different clinical manifestations compared to African Trypanosomiasis. It can lead to a chronic infection that affects the heart and digestive system and is primarily transmitted by triatomine bugs.
Nagana, caused by T. brucei, is a form of trypanosomiasis that affects cattle and horses, leading to significant economic losses in affected regions.
The clinical symptoms you mentioned for sleeping sickness, including fevers, headaches, joint pain, and later neurological symptoms, are characteristic of the disease. The ability of Trypanosoma brucei to breach the blood-brain barrier (BBB) is a critical aspect of the disease, leading to neurological complications in the late stage.
The high mortality rate if left untreated underscores the importance of early diagnosis and treatment for sleeping sickness. Control measures targeting tsetse flies and raising awareness among at-risk populations are essential in endemic regions.
explain how the presence of a kinetoplast is a distinctive feature of trypanosomatid parasites
The presence of a kinetoplast is a distinctive feature of trypanosomatid parasites, including Trypanosoma species, which are the causative agents of African Trypanosomiasis (sleeping sickness). The kinetoplast is a specialized organelle located at the base of the flagellum and contained inside a single, large mitochondrion, which is often referred to as the kinetoplast mitochondrion.
Here are some key points regarding the kinetoplast:
Unique Structure: The kinetoplast is unique to kinetoplastids, a group of flagellated protozoa. It contains a network of concatenated DNA molecules known as kinetoplast DNA (kDNA).
Composition of kDNA: Kinetoplast DNA is composed of two main types of molecules: maxicircles and minicircles.
Maxicircles: Maxicircles are large, circular DNA molecules that contain genes encoding for various mitochondrial functions, particularly those related to energy production and oxidative phosphorylation.
Minicircles: Minicircles are smaller circular DNA molecules that play a crucial role in RNA editing. They serve as templates for the production of guide RNAs (gRNAs) that are used to edit the RNA transcribed from the maxicircles. This editing process is essential for the generation of functional mitochondrial mRNAs, as it corrects the insertion and deletion of uridines (U) in the mRNA sequences.
Energy Production: The maxicircles in the kinetoplast contain genes that are involved in the mitochondrial electron transport chain and ATP production, which are essential for the parasite’s energy metabolism.
RNA Editing: The minicircles produce gRNAs that are responsible for the process of RNA editing. This editing is necessary to correct the information in the maxicircle-encoded transcripts, allowing the parasite to generate functional proteins.
Mitochondrial Role: The kinetoplast and its associated mitochondrion are vital for the survival and energy metabolism of trypanosomatid parasites.
explain Ethidium bromide (EtBr)
Ethidium bromide (EtBr) is a chemical compound commonly used in molecular biology and biochemistry for staining nucleic acids, primarily DNA, and RNA in electrophoresis gels. In the context of trypanosomatid parasites like Trypanosoma brucei, which cause diseases like African Trypanosomiasis in cattle and humans, EtBr is used as a treatment.
Here’s how EtBr works in this context:
Binding to DNA: EtBr is known for its strong affinity for DNA molecules. It intercalates between the base pairs of double-stranded DNA, which results in the insertion of the compound into the DNA helix.
Selective Targeting: Ethidium bromide is particularly effective against kinetoplast DNA (kDNA), which is unique to kinetoplastids like Trypanosoma. Kinetoplast DNA consists of a network of concatenated minicircles and maxicircles. Minicircles are important for RNA editing, and they are released from the kDNA network during replication.
Effect on Minicircles: When EtBr binds to the released minicircles, it has a pronounced effect on their structure. The binding causes the minicircles to become supertwisted, which interferes with their replication and function.
Preventing Replication: The supertwisting of minicircles induced by EtBr prevents their successful replication. Since minicircles are crucial for RNA editing and the production of guide RNAs for mitochondrial mRNA editing, their disruption hampers the parasite’s ability to generate functional mitochondrial mRNAs.
By selectively affecting kinetoplast DNA and minicircles in particular, EtBr can disrupt the unique biology of trypanosomatid parasites like Trypanosoma, ultimately leading to their death. This property makes EtBr a potential treatment for trypanosomiasis in cattle, where the parasites can be a significant threat to livestock health.
explain EtBr is also toxic to mammalian cells - why is this less of a problem?
Ethidium bromide (EtBr) is indeed known to be toxic to mammalian cells, but its use in molecular biology and medical diagnostics is generally considered safe when appropriate precautions are taken. Here are some reasons why EtBr toxicity is less of a problem when used in these contexts:
Concentration: In molecular biology and diagnostic applications, EtBr is typically used at relatively low concentrations. This minimizes the potential for cytotoxicity in mammalian cells.
Short Exposure: When used for DNA staining in agarose or acrylamide gels, EtBr is usually only exposed to cells for a short period during electrophoresis. This limited exposure reduces the risk of harmful effects.
Proper Handling: Laboratory personnel are trained to handle EtBr safely. Standard safety practices include wearing gloves, lab coats, and eye protection, as well as working in a well-ventilated area.
Waste Disposal: Disposal of waste containing EtBr is carefully managed to prevent environmental contamination. EtBr-contaminated materials are often treated as hazardous waste.
Alternatives: In recent years, researchers have developed and adopted alternative DNA stains that are less toxic and potentially safer than EtBr for both researchers and the environment. These alternatives are designed to be more environmentally friendly and have reduced health risks.
In summary, while EtBr is toxic to both trypanosomatid parasites and mammalian cells, its controlled and responsible use in laboratory settings, as well as the use of safety measures and precautions, helps minimize the risks associated with its toxicity to mammalian cells.
explain how the flagellum attachment zone (FAZ) in trypanosomes is indeed a unique and complex structure that plays a crucial role in attaching the flagellum to the cell body.
The flagellum attachment zone (FAZ) in trypanosomes is indeed a unique and complex structure that plays a crucial role in attaching the flagellum to the cell body. This attachment is essential for the proper function of the flagellum, which is used for motility and other important functions in these parasites.
Here are some key points about the flagellum attachment zone (FAZ) in trypanosomes:
Structural Complexity: The FAZ is a specialized region near the base of the flagellum that consists of a complex network of filaments, microtubules, and other structures. It is responsible for anchoring the flagellum to the cell body.
Attachment to Microtubules: Within the FAZ, there is a quartet of microtubules that are attached to the endoplasmic reticulum (ER). These microtubules are part of the cytoskeleton and provide structural support for the attachment.
Cell Motility: The flagellum is a whip-like structure that extends from the cell body. It is essential for the trypanosome’s motility, enabling it to move through various bodily fluids and tissues. The FAZ ensures that the flagellum remains properly anchored during these movements.
Transport of Material: In addition to anchoring the flagellum, the FAZ is involved in the transport of materials between the cell body and the flagellum. This includes the movement of proteins and other molecules required for the flagellum’s function.
Cell Division: The FAZ is also involved in the process of cell division in trypanosomes. It plays a role in segregating the organelles and other cellular components between daughter cells during cell division.
Understanding the FAZ and its role in attaching the flagellum is important for researchers studying trypanosomes, as it provides insights into the biology and pathogenicity of these parasites. Trypanosomes, including Trypanosoma brucei, are responsible for diseases such as African trypanosomiasis, and a better understanding of their cellular structures and mechanisms can contribute to the development of potential treatments and interventions.
explain the significance of the flagellum attachment zone (FAZ) in Trypanosoma cells
(FAZ) in Trypanosoma cells:
Regulation of Cell Length: The FAZ plays a crucial role in regulating the length of the trypanosome cell. This regulation is important for maintaining the proper structure and function of the cell, and it ensures that the flagellum remains correctly positioned.
Organelle Positioning: The FAZ is involved in determining the positioning of organelles within the trypanosome cell. Proper organelle organization is essential for various cellular functions.
Cell Division: The FAZ is also associated with cell division in trypanosomes. It contributes to the segregation of cellular components between daughter cells during the division process.
Attachment to Tsetse Fly Epithelium: The development of outgrowths on the flagellum that attach to the microvilli of the Tsetse Fly’s salivary gland epithelium is a critical step in the trypanosome life cycle. This attachment is essential for the transmission of the parasite from the fly to a mammalian host. Understanding the molecular mechanisms involved in this attachment process is important for studying the transmission of trypanosomes.
Tissue Migration: The flagellum is essential for trypanosomes to migrate through various tissues in their host, including the central nervous system (CNS). This migration is a key aspect of the pathogenesis of trypanosomiasis.
explain why a drug targeting the flagellum could be a potentially useful therapeutic. Which proteins would you target?
Critical for Motility: The flagellum is essential for the motility of trypanosomes. It allows them to move through various bodily fluids and tissues, which is a key aspect of their life cycle and pathogenicity. Inhibiting flagellar motility could impair the parasite’s ability to migrate and establish infections in their host.
Transmission Block: Targeting the flagellum could potentially block the interaction between the parasite and its vector (such as the Tsetse Fly). If the flagellum is unable to attach to the vector’s salivary gland epithelium, it could prevent the transmission of the parasite to new hosts, disrupting the life cycle.
Disruption of Tissue Migration: Trypanosomes, including Trypanosoma brucei, migrate through various tissues in their mammalian host, including the central nervous system. Targeting the flagellum could disrupt this migration, limiting the damage caused by the parasite within the host.
Reduced Pathogenicity: By impairing the function of the flagellum, a drug could reduce the overall pathogenicity of the parasite, potentially alleviating disease symptoms in infected individuals.
As for which proteins to target, several flagellar proteins may be potential candidates. These could include proteins involved in the assembly and regulation of the flagellum. Specific protein targets could be identified through research and experimentation.
One approach could be to target proteins involved in the attachment of the flagellum to host tissues, such as those responsible for interdigitating with host cell structures or forming adhesive junctions. Disrupting these interactions could prevent the parasite from attaching to host cells and vectors.
Another approach could involve targeting proteins that are critical for flagellar motility. Proteins involved in flagellar movement, coordination, and control could be potential drug targets. Inhibiting these proteins could impair the parasite’s ability to move and navigate through host tissues.
explain the flagellar pocket in trypanosomes
The flagellar pocket in trypanosomes is a unique and crucial structure in the life of these parasites. It serves as the sole site of endocytosis and secretion, meaning it is where the parasite takes in nutrients and eliminates waste. The flagellar pocket is intimately linked to the parasite’s survival and pathogenicity.
One of the notable functions of the flagellar pocket is its role in immune evasion. Trypanosomes have developed various strategies to evade the host immune system, and the flagellar pocket plays a part in this. A key mechanism involves the movement of a specific surface protein, the Variant Surface Glycoprotein (VSG), which is essential for the parasite’s immune evasion.
Here’s how it works:
Trypanosomes have a dense layer of VSG on their surface, which serves as a protective shield against the host’s immune response. VSG is highly immunogenic, and the host immune system produces antibodies against it.
To escape immune recognition and clearance, the trypanosome utilizes the flagellar pocket. The beating of the flagellum creates hydrodynamic forces that push the antibodies bound to VSG back into the flagellar pocket.
Once inside the flagellar pocket, the immune complexes (VSG bound to antibodies) are endocytosed and processed. This allows the trypanosome to remove the antibodies and change its VSG coat. The endocytosis process effectively “hides” the VSG and antibodies from the host’s immune system.
The trypanosome can then express a different VSG variant on its surface. This process is known as antigenic variation, and it enables the parasite to continually change its surface proteins to evade the host’s immune response. This is why trypanosomes are often referred to as “masters of immune evasion.”
explain glycosomes
Glycosomes are specialized organelles found in certain single-celled organisms, such as trypanosomes and other kinetoplastid parasites. They are membrane-bound vesicle-like organelles, classified as microbodies, and play a crucial role in the energy metabolism of these organisms, particularly in glycolysis.
Here are some key features and functions of glycosomes:
Compartmentalization of Glycolysis: Glycosomes are dedicated compartments for glycolytic enzymes. Glycolysis is a metabolic pathway that breaks down glucose into pyruvate, producing energy in the form of adenosine triphosphate (ATP). In trypanosomes and related parasites, glycolysis is essential for energy production, as they lack mitochondria for oxidative phosphorylation. Glycosomes serve as specialized regions within the cell where glycolysis occurs.
Enzyme Storage: Glycosomes contain various enzymes involved in glycolysis, including hexokinase, phosphofructokinase, and pyruvate kinase, among others. These enzymes are stored within the glycosomes, ensuring that the glycolytic pathway proceeds efficiently and independently within this organelle.
Compartmentalized Metabolism: The presence of glycosomes allows for compartmentalized metabolism. By keeping glycolytic enzymes within a separate organelle, the cell can regulate and control glycolysis without interfering with other cellular processes. This organization is especially important for trypanosomes, as it helps them adapt to changing conditions in their host’s bloodstream.
Unique Enzyme Structures: Some of the glycolytic enzymes found in glycosomes have unique structures or properties that make them well-suited for their roles in this organelle. For example, they may have specialized domains or modifications that enhance their function in glycolysis.
In summary, glycosomes are organelles that play a vital role in the energy metabolism of trypanosomes and related organisms. They compartmentalize glycolytic enzymes, ensuring efficient energy production in the absence of mitochondria. This adaptation allows these parasites to thrive in their host environments, where they face varying nutrient conditions.
Q.3 Explain why glycosomes are a suitable target for anti-Trypanosome drugs (Suramin is one such drug)
Glycosomes are a suitable target for anti-Trypanosome drugs because they play a critical role in the energy metabolism of trypanosomes and other kinetoplastid parasites. Targeting glycosomes can disrupt the parasites’ ability to produce energy, ultimately leading to their death. Here are several reasons why glycosomes make suitable targets for anti-Trypanosome drugs:
Essential Role in Energy Metabolism: Glycosomes are the primary site for glycolysis in trypanosomes. Glycolysis is the central metabolic pathway responsible for the breakdown of glucose into pyruvate and the production of ATP, which is vital for the parasites’ survival and growth. Inhibition of glycolysis within glycosomes can lead to a severe energy crisis for the parasites.
Lack of Mitochondria: Unlike most eukaryotic cells, trypanosomes lack mitochondria and oxidative phosphorylation. Instead, they rely exclusively on glycolysis for their energy needs. Disrupting glycolysis in glycosomes is particularly detrimental for trypanosomes because they lack an alternative energy production mechanism.
Unique Enzymes: The glycolytic enzymes within glycosomes often have unique structures and properties that make them distinct from their counterparts in mammalian cells. These differences provide opportunities to develop drugs that selectively target the trypanosomal enzymes without affecting host cell enzymes.
Compartmentalized Metabolism: Glycosomes allow for compartmentalized metabolism. This means that drugs targeting glycosomes can specifically interfere with the trypanosomes’ energy production while leaving other cellular processes in the host cell unaffected. This selectivity is crucial for minimizing potential side effects on the host.
Essentiality for Trypanosome Survival: Inhibition of glycolysis within glycosomes results in an inability to produce ATP, causing a metabolic crisis for trypanosomes. Without sufficient energy, the parasites cannot maintain their vital functions, and their survival is compromised.
Suramin is one such drug that targets glycosomes in trypanosomes. It interferes with the function of enzymes within glycosomes, disrupting glycolysis and leading to a depletion of ATP production. As a result, trypanosomes are unable to maintain their essential cellular functions, leading to their eventual death, making glycosomes a crucial target for the development of effective anti-Trypanosome drugs.
explain the life cycle of Trypanosoma brucei
The life cycle of Trypanosoma brucei, the parasite responsible for African trypanosomiasis (sleeping sickness), involves various stages in both the tsetse fly vector and mammalian host. Here’s a step-by-step explanation of the key stages in this complex life cycle:
Tsetse Fly Feeding (Infection Stage): The tsetse fly, a blood-feeding insect, takes a blood meal from an infected mammal. During this feeding, the fly injects metacyclic trypomastigotes into the host’s bloodstream. These trypomastigotes are the infective stage of the parasite.
Transformation in Mammalian Host: Once inside the mammalian host, the injected metacyclic trypomastigotes transform into bloodstream trypomastigotes. These parasites enter the host’s bloodstream, where they can be carried to various sites throughout the body.
Multiplication in Body Fluids: Trypomastigotes multiply within different body fluids, such as blood, lymph, and spinal fluid. They undergo binary fission to increase their numbers.
Presence in the Blood: Trypomastigotes are present in the host’s bloodstream, and they can be detected there during the acute phase of the infection.
Tsetse Fly Feeding (Transmission to Fly): When an infected tsetse fly takes a blood meal from a host, it ingests bloodstream trypomastigotes. This event marks the transmission of the parasite back to the fly.
Transformation in Tsetse Fly Midgut: Inside the tsetse fly’s midgut, the bloodstream trypomastigotes transform into procyclic trypomastigotes. These procyclic forms are adapted to the conditions in the fly’s midgut and can multiply through binary fission.
Migration and Transformation: The procyclic trypomastigotes leave the midgut and move to other parts of the fly’s body, including the salivary glands. During this migration, they transform into epimastigotes.
Multiplication in Salivary Gland: In the salivary gland, the epimastigotes multiply. They undergo division and differentiation, eventually giving rise to metacyclic trypomastigotes, which are the infective stage for humans and other mammals.
Infective Stage in Salivary Gland: The metacyclic trypomastigotes reside in the salivary glands of the tsetse fly. When the fly takes another blood meal from a mammal, it can transmit these metacyclic trypomastigotes to the host, thus completing the life cycle of Trypanosoma brucei.
explain Tsetse flies
Tsetse flies, members of the Glossina genus, are significant vectors of African trypanosomes, including the parasite responsible for sleeping sickness (African trypanosomiasis) in humans. These flies have several distinctive features and characteristics that make them important in the transmission of this disease:
Blood-Feeding: Tsetse flies are obligate blood-feeding insects. They primarily feed on the blood of vertebrates, which includes mammals like humans and livestock. This blood-feeding behavior is essential for their own nutrition and reproduction.
Unique Proboscis: Tsetse flies have a specialized proboscis, which is a long, needle-like structure they use to pierce the skin of their host and feed on their blood. This proboscis allows them to access the blood vessels of their host.
Obligate Parasites: Tsetse flies are obligate parasites because they rely on blood meals for their survival and reproduction. They cannot complete their life cycle without blood-feeding.
Disease Vectors: Tsetse flies are notorious vectors of trypanosomes, particularly Trypanosoma brucei, which causes African trypanosomiasis in humans. When an infected tsetse fly feeds on a mammal, it can transmit the trypanosome into the bloodstream of the host, leading to infection.
Glossina Species: There are different species of Glossina flies, and they may have different habitats and preferences. The two most well-known species associated with sleeping sickness transmission are G. morsitans, which is often found in woodland areas, and G. palpalis, which is typically found in streamside habitats.
Disease Transmission: Tsetse flies play a crucial role in the life cycle of the trypanosomes they transmit. When they bite an infected host, they ingest trypanosomes, which then develop within the tsetse fly’s midgut. These mature parasites can later be transmitted to another host when the fly feeds again.
Sleeping Sickness: Tsetse flies are responsible for transmitting the parasites that cause sleeping sickness in humans. This disease can have severe neurological and systemic effects if not treated promptly.
explain Trypanosoma brucei
Trypanosoma brucei, the causative agent of African trypanosomiasis (sleeping sickness), is known for its ability to undergo antigenic variation, a clever strategy to evade the host’s immune system. Here’s how this process works:
Variable Surface Glycoprotein (VSG): Trypanosomes are covered with a dense layer of surface glycoproteins called Variable Surface Glycoproteins (VSGs). These VSGs form a monolayer on the parasite’s surface.
Antigenic Variation: Antigenic variation is the key mechanism employed by trypanosomes. Each trypanosome expresses one specific VSG at a time. The parasite population contains a large repertoire of different VSG genes, and these genes can be switched on and off to express different VSGs.
Molecular Switch: Trypanosomes have the ability to switch from expressing one VSG to another. This switch is not instantaneous but occurs spontaneously over time. On average, about 1 in every 100 cell divisions results in a change from one VSG to another.
Silent Archives: Trypanosomes maintain a “silent archive” of VSG genes. There are two types of silent archives:
a. Silent Archive 1: This archive includes approximately 1,000 VSG genes that are organized in tandem on the main chromosomes. These genes are typically silent.
b. Silent Archive 2: In addition to the primary VSG genes, there is another archive with around 200 VSG genes located on approximately 100 minichromosomes. These genes are also mostly silent.
Copy and Paste: The mechanism of antigenic variation involves copying a silent VSG gene from the archive and pasting it into an actively transcribed region known as the Bloodstream Expression Site (BES). This allows the trypanosome to switch from expressing one VSG to another.
The process of antigenic variation is a critical survival strategy for Trypanosoma brucei. By frequently changing the VSG on their surface, trypanosomes can evade the host’s immune system, which has difficulty keeping up with the rapidly changing antigenic profile of the parasite. This ability to switch VSGs allows the trypanosome population to persist and continue the infection even in the presence of host immune responses. It’s an excellent example of host-pathogen coevolution.
how does this antigenic variation enable the trypanosome to evade humoral immunity?
Antigenic variation in Trypanosoma brucei plays a crucial role in evading humoral immunity, which is the branch of the immune system that involves the production of antibodies. Here’s how antigenic variation enables trypanosomes to escape the host’s humoral immune response:
VSG Switching: Trypanosomes, the causative agents of African trypanosomiasis, have a vast repertoire of VSG genes. Each trypanosome expresses only one specific VSG on its surface at a time. When the host’s immune system generates antibodies against the current VSG (often referred to as the “variant antigen”), the trypanosome can switch to a different VSG from its silent archive.
Rapid Changes: Antigenic variation allows trypanosomes to change the VSG displayed on their surface rapidly. This means that the immune system’s production of antibodies targeting the previous VSG becomes ineffective against the new variant. In this way, trypanosomes can continuously evade the antibodies circulating in the host’s bloodstream.
Production of Antibodies: The host’s immune system recognizes the specific VSG on the trypanosome’s surface and generates antibodies to neutralize and eliminate the parasite. However, when the trypanosome switches to a different VSG, the antibodies produced against the previous VSG are no longer effective. This rapid switching makes it extremely challenging for the host to mount an effective humoral immune response.
Failure of Immune Memory: Humoral immunity relies on the immune system’s memory of past infections. It generates antibodies tailored to the recognized antigens. However, due to the frequent and random switching of VSGs, trypanosomes can escape immune memory. This means that each time a new VSG is expressed, the immune system essentially “forgets” the previous variant, making it impossible for the host to maintain a sustained and effective immune response.
In summary, the ability of trypanosomes to undergo antigenic variation is a sophisticated strategy for evading humoral immunity. By frequently changing the VSG expressed on their surface, these parasites can “stay one step ahead” of the host’s antibody response, making it difficult for the immune system to target and eliminate the infection.
