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The Parasite's Way of life
Published in Eric S. Loker, Bruce V. Hofkin, Parasitology, 2015
Eric S. Loker, Bruce V. Hofkin
We have already mentioned some of the strategies used by various parasites to overcome this obstacle. Gut parasites may invade the intestinal epithelium, as we saw in the case of Toxoplasma gondii, or like Giardia lamblia, they may adhere with adhesive disks (see Figure 3.9). Acanthocephalans and tapeworms rely on their proboscis or scolex, respectively, whereas many intestinal nematodes utilize powerful longitudinal muscles to maintain their location via vigorous sinusoidal motion. Trematodes generally come equipped with powerful ventral suckers or acetabula that assist in adherence. Male and female schistosomes form pairs with the female lying within the gynecophoral canal of the male. A male with it’s more powerful musculature and with the aid of it’s oral sucker and acetabulum moves the pair upstream into smaller venules where the pair becomes lodged. Some Plasmodium species, on the other hand, once they have adhered to and entered erythrocytes, enjoy a moveable feast of sorts, circulating through the host in the safety of their cellular shuttle. P. falciparum, on the other hand, the most pathogenic of the human malaria parasites, takes a different tack. Once inside erythrocytes, this species encodes a protein called Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1) that protrudes from the surface of infected cells. This protein is involved in the formation of knobs, which bind the infected cells to capillary walls and consequently interfere with blood flow. Such interference is an important factor in the severe pathology caused by P. falciparum.
The Parasite's Way of Life
Published in Eric S. Loker, Bruce V. Hofkin, Parasitology, 2023
Eric S. Loker, Bruce V. Hofkin
We have already mentioned some of the strategies used by various parasites to overcome this obstacle. Gut parasites such as Toxoplasma gondii may invade the intestinal epithelium, or like Giardia lamblia, they may adhere with adhesive disks (see Figure 3.9). Acanthocephalans and tapeworms rely on their proboscis or scolex, respectively, whereas many intestinal nematodes utilize powerful longitudinal muscles to maintain their location via vigorous sinusoidal motion. Trematodes generally come equipped with powerful ventral suckers or acetabula that assist in adherence. Male and female schistosomes form pairs with the female lying within the gynecophoral canal of the male. A male with its more powerful musculature and with the aid of its oral sucker and acetabulum moves the pair upstream into smaller venules where the pair becomes lodged. Some Plasmodium species, alternatively, having adhered to and entered erythrocytes, enjoy a moveable feast of sorts, circulating through the host in the safety of their cellular shuttle. P. falciparum, on the other hand, the most pathogenic of the human malaria parasites, takes a different tack. Once inside erythrocytes, this species encodes a protein called Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1) that protrudes from the surface of infected cells (Figure 3.23). This protein is involved in the formation of knobs, which bind the infected cells to capillary walls and consequently interferes with blood flow. Such interference, to be discussed more fully in Chapter 5, figures prominently in the severe pathology caused by P. falciparum.
Progress and new horizons toward a VAR2CSA-based placental malaria vaccine
Published in Expert Review of Vaccines, 2021
Justin Yai Alamou Doritchamou, Jennifer Suurbaar, Nicaise Tuikue Ndam
Among the variant surface antigens mediating IE cytoadhesion to host receptors, the best-studied and clinically most important family of adhesins is P. falciparum erythrocyte membrane protein 1 (PfEMP1), encoded by the var gene family [17–20]. A key finding, now widely accepted, is that antibodies with specificity for PfEMP1 are crucial for clinical immunity to malaria. In placental malaria, antibodies against VAR2CSA (the PfEMP1 member specifically expressed by parasites in this context) are acquired in a parity-dependent manner; these antibodies block adhesion of IEs to the placenta and mediate their clearance by engaging innate immune cells and activating the complement system [9,21–25]. Placental malaria studies have provided the best proof-of-concept that clinical immunity is correlated with neutralizing antibodies targeting a VAR2CSA, paving the way for the first PfEMP1-based vaccine which is currently undergoing clinical trials in Africa [26–30].
Platelet interactions with viruses and parasites
Published in Platelets, 2015
GPIV (CD36) is a glycosylated protein [88] present in platelets and other cells such as macrophages, dendritic cells, adipocytes, muscle and some types of endothelial cells, and is a cell receptor for P. falciparum-infected erythrocytes [89, 90] although other receptors may be involved [80, 91]. Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1) is the protein that binds to CD36 [92]. While PfEMP1 can directly bind to CD36 and a number of CD36 ligands can induce platelet aggregation, there is no evidence that PfEMP1 triggers platelet activation. However, P. falciparum does trigger clumping of infected erythrocytes that is mediated by platelets in a CD36-dependent manner [80], and thus it is possible that this may be due to PfEMP1-CD36 mediated platelet activation.
A vaccine targeted specifically to prevent cerebral malaria – is there hope?
Published in Expert Review of Vaccines, 2018
Lars Hviid, Thomas Lavstsen, Anja TR Jensen
Until recently, it was unclear which PfEMP1 variants mediate the adhesion of infected erythrocytes in cerebral malaria patients, and to which receptors they bind. However, several lines of evidence are converging to indicate that specific PfEMP1 proteins and host receptors are involved, and that neither is restricted to the brain or to cerebral malaria [8]. This is quite unlike the situation with placental malaria, which as mentioned appears to be precipitated by a single PfEMP1 antigen (VAR2CSA) binding to a single receptor (onchofetal chondroitin sulfate), mediating infected erythrocyte sequestration in just one tissue (the placenta), and therefore completely restricted in time (pregnancy). With that in mind, let us consider the question posed in the title of this editorial.