Plasmodium gaboni | |
---|---|
Scientific classification | |
Domain: | Eukaryota |
Clade: | Diaphoretickes |
Clade: | SAR |
Clade: | Alveolata |
Phylum: | Apicomplexa |
Class: | Aconoidasida |
Order: | Haemospororida |
Family: | Plasmodiidae |
Genus: | Plasmodium |
Species: | P. gaboni |
Binomial name | |
Plasmodium gaboni Ollomo et al., 2009 | |
Plasmodium gaboni is a parasite of the genus Plasmodium subgenus Laverania .
P. gaboni was given its name in reference to Gabon, where the parasite was discovered in two wild-borne chimpanzees kept as pets in villages in that country. Plasmodium gaboni is phylogenetically very close to Plasmodium billbrayi . [1]
In 2009, Ollomo et al. published the complete mitochondrial genome of Plasmodium gaboni, which was not yet named at the time. The parasite belongs to the P falciparum/P reichenowi lineage. It has been proposed that Plasmodium gaboni diverged from the P falciparum/P reichenowi lineage about 21 million years ago, leading to the conclusion that the ancestor of this parasite clade could have been already present in hominid ancestors. [1] Plasmodium gaboni is 10-fold more diverse than human parasite Plasmodium falciparum , indicating a very recent origin of the latter. [2] Plasmodium gaboni is similar to both Plasmodium falciparum and to Plasmodium reichenowi in microscopic studies, seeming likely that all of these ape Laverania parasites represent morphologically indistinguishable species. [2]
Plasmodium gaboni can be found in western Africa. [1]
Study has confirmed the presence of Plasmodium gaboni in wild chimpanzees (subspecies Pan troglodytes troglodytes and Pan troglodytes vellerosus ). [1] Due to the close proximity between Plasmodium gaboni and the most virulent agent of malaria, Plasmodium falciparum, it has been considered the possibility of transfer risk of this species to humans. [3]
Plasmodium is a genus of unicellular eukaryotes that are obligate parasites of vertebrates and insects. The life cycles of Plasmodium species involve development in a blood-feeding insect host which then injects parasites into a vertebrate host during a blood meal. Parasites grow within a vertebrate body tissue before entering the bloodstream to infect red blood cells. The ensuing destruction of host red blood cells can result in malaria. During this infection, some parasites are picked up by a blood-feeding insect, continuing the life cycle.
Anopheles is a genus of mosquito first described by J. W. Meigen in 1818, and are known as nail mosquitoes and marsh mosquitoes. Many such mosquitoes are vectors of the parasite Plasmodium, a genus of protozoans that cause malaria in birds, reptiles, and mammals, including people. The Anopheles gambiae mosquito is the best-known species of marsh mosquito that transmits the Plasmodium falciparum, which is a malarial parasite deadly to human beings; no other mosquito genus is a vector of human malaria.
Plasmodium falciparum is a unicellular protozoan parasite of humans, and the deadliest species of Plasmodium that causes malaria in humans. The parasite is transmitted through the bite of a female Anopheles mosquito and causes the disease's most dangerous form, falciparum malaria. It is responsible for around 50% of all malaria cases. P. falciparum is therefore regarded as the deadliest parasite in humans. It is also associated with the development of blood cancer and is classified as a Group 2A (probable) carcinogen.
Microsporidia are a group of spore-forming unicellular parasites. These spores contain an extrusion apparatus that has a coiled polar tube ending in an anchoring disc at the apical part of the spore. They were once considered protozoans or protists, but are now known to be fungi, or a sister group to fungi. These fungal microbes are obligate eukaryotic parasites that use a unique mechanism to infect host cells. They have recently been discovered in a 2017 Cornell study to infect Coleoptera on a large scale. So far, about 1500 of the probably more than one million species are named. Microsporidia are restricted to animal hosts, and all major groups of animals host microsporidia. Most infect insects, but they are also responsible for common diseases of crustaceans and fish. The named species of microsporidia usually infect one host species or a group of closely related taxa. Approximately 10 percent of the species are parasites of vertebrates —several species, most of which are opportunistic, can infect humans, in whom they can cause microsporidiosis.
Plasmodium ovale is a species of parasitic protozoon that causes tertian malaria in humans. It is one of several species of Plasmodium parasites that infect humans, including Plasmodium falciparum and Plasmodium vivax which are responsible for most cases of malaria in the world. P. ovale is rare compared to these two parasites, and substantially less dangerous than P. falciparum.
Plasmodium knowlesi is a parasite that causes malaria in humans and other primates. It is found throughout Southeast Asia, and is the most common cause of human malaria in Malaysia. Like other Plasmodium species, P. knowlesi has a life cycle that requires infection of both a mosquito and a warm-blooded host. While the natural warm-blooded hosts of P. knowlesi are likely various Old World monkeys, humans can be infected by P. knowlesi if they are fed upon by infected mosquitoes. P. knowlesi is a eukaryote in the phylum Apicomplexa, genus Plasmodium, and subgenus Plasmodium. It is most closely related to the human parasite Plasmodium vivax as well as other Plasmodium species that infect non-human primates.
The Chimpanzee Genome Project was an effort to determine the DNA sequence of the chimpanzee genome. Sequencing began in 2005 and by 2013 twenty-four individual chimpanzees had been sequenced. This project was folded into the Great Ape Genome Project.
Plasmodium berghei is a single-celled parasite causing rodent malaria. It is in the Plasmodium subgenus Vinckeia.
Antigenic variation or antigenic alteration refers to the mechanism by which an infectious agent such as a protozoan, bacterium or virus alters the proteins or carbohydrates on its surface and thus avoids a host immune response, making it one of the mechanisms of antigenic escape. It is related to phase variation. Antigenic variation not only enables the pathogen to avoid the immune response in its current host, but also allows re-infection of previously infected hosts. Immunity to re-infection is based on recognition of the antigens carried by the pathogen, which are "remembered" by the acquired immune response. If the pathogen's dominant antigen can be altered, the pathogen can then evade the host's acquired immune system. Antigenic variation can occur by altering a variety of surface molecules including proteins and carbohydrates. Antigenic variation can result from gene conversion, site-specific DNA inversions, hypermutation, or recombination of sequence cassettes. The result is that even a clonal population of pathogens expresses a heterogeneous phenotype. Many of the proteins known to show antigenic or phase variation are related to virulence.
Laverania is a subgenus of the parasite genus Plasmodium. Infection with these species results in malaria. The subgenus was first described in 1958.
Pregnancy-associated malaria (PAM) or placental malaria is a presentation of the common illness that is particularly life-threatening to both mother and developing fetus. PAM is caused primarily by infection with Plasmodium falciparum, the most dangerous of the four species of malaria-causing parasites that infect humans. During pregnancy, a woman faces a much higher risk of contracting malaria and of associated complications. Prevention and treatment of malaria are essential components of prenatal care in areas where the parasite is endemic – tropical and subtropical geographic areas. Placental malaria has also been demonstrated to occur in animal models, including in rodent and non-human primate models.
The parasitophorous vacuole (PV) is a structure produced by apicomplexan parasites in the cells of its host. The PV allows the parasite to develop while protected from the phagolysosomes of the host cell.
Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1) is a family of proteins present on the membrane surface of red blood cells that are infected by the malarial parasite Plasmodium falciparum. PfEMP1 is synthesized during the parasite's blood stage inside the RBC, during which the clinical symptoms of falciparum malaria are manifested. Acting as both an antigen and adhesion protein, it is thought to play a key role in the high level of virulence associated with P. falciparum. It was discovered in 1984 when it was reported that infected RBCs had unusually large-sized cell membrane proteins, and these proteins had antibody-binding (antigenic) properties. An elusive protein, its chemical structure and molecular properties were revealed only after a decade, in 1995. It is now established that there is not one but a large family of PfEMP1 proteins, genetically regulated (encoded) by a group of about 60 genes called var. Each P. falciparum is able to switch on and off specific var genes to produce a functionally different protein, thereby evading the host's immune system. RBCs carrying PfEMP1 on their surface stick to endothelial cells, which facilitates further binding with uninfected RBCs, ultimately helping the parasite to both spread to other RBCs as well as bringing about the fatal symptoms of P. falciparum malaria.
Plasmodium billbrayi is a parasite of the genus Plasmodium subgenus Laverania.
Plasmodium billcollinsi is a species of the genus Plasmodium subgenus Laverania.
Dominic Kwiatkowski was an English medical researcher and geneticist who was head of the parasites and microbes programme at the Wellcome Sanger Institute in Cambridge and a Professor of Genomics at the University of Oxford. Kwiatkowski applied genomics and computational analysis to problems in infectious disease, with the aim of finding ways to reduce the burden of disease in the developing world.
The Plasmodium helical interspersed subtelomeric proteins (PHIST) or ring-infected erythrocyte surface antigens (RESA) are a family of protein domains found in the malaria-causing Plasmodium species. It was initially identified as a short four-helical conserved region in the single-domain export proteins, but the identification of this part associated with a DnaJ domain in P. falciparum RESA has led to its reclassification as the RESA N-terminal domain. This domain has been classified into three subfamilies, PHISTa, PHISTb, and PHISTc.
David A. Fidock, is the CS Hamish Young Professor of Microbiology and Immunology and Professor of Medical Sciences at Columbia University Irving Medical Center in Manhattan.