Variable and Variant Protein Multigene Families in Babesia bovis Persistence

Allred, David R.

doi:10.3390/pathogens8020076

Cited by 18 publications

(11 citation statements)

References 88 publications

(164 reference statements)

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“…Excessive Babesiainduced erythrocyte adherence may contribute to babesiosis complications. Babesia-induced red cell cytoadherence has been associated with B. bovis and B. duncani induced pathology (Clark et al, 2006a;Usmani-Brown et al, 2013;Allred, 2019). B. bovis strains with increased cytoadherence activity in vitro have increased virulence in cattle (O'Connor et al, 1999).…”

Section: Erythrocyte Cytoadherencementioning

confidence: 99%

“…In contrast, recrudescence is more common in highly immunocompromised patients, especially those with defective antibody production (Krause et al, 2008). Prolonged Babesia disease has been described in immunocompromised hosts, with relapsing symptoms lasting up to 9 months and parasitemia continuing for more than 2 years (Krause et al, 2008;Raffalli and Wormser, 2016;Allred, 2019;Bloch et al, 2019). These patients are markedly immunocompromised with underlying diagnoses that include HIV/AIDS, malignancy, and asplenia.…”

Section: Persistent Infectionmentioning

confidence: 99%

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Babesia microti: Pathogen Genomics, Genetic Variability, Immunodominant Antigens, and Pathogenesis

et al. 2021

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More than 100 Babesia spp. tick-borne parasites are known to infect mammalian and avian hosts. Babesia belong to Order Piroplasmid ranked in the Phylum Apicomplexa. Recent phylogenetic studies have revealed that of the three genera that constitute Piroplasmida, Babesia and Theileria are polyphyletic while Cytauxzoon is nested within a clade of Theileria. Several Babesia spp. and sub-types have been found to cause human disease. Babesia microti, the most common species that infects humans, is endemic in the Northeastern and upper Midwestern United States and is sporadically reported elsewhere in the world. Most infections are transmitted by Ixodid (hard-bodied) ticks, although they occasionally can be spread through blood transfusion and rarely via perinatal transmission and organ transplantation. Babesiosis most often presents as a mild to moderate disease, however infection severity ranges from asymptomatic to lethal. Diagnosis is usually confirmed by blood smear or polymerase chain reaction (PCR). Treatment consists of atovaquone and azithromycin or clindamycin and quinine and usually is effective but may be problematic in immunocompromised hosts. There is no human Babesia vaccine. B. microti genomics studies have only recently been initiated, however they already have yielded important new insights regarding the pathogen, population structure, and pathogenesis. Continued genomic research holds great promise for improving the diagnosis, management, and prevention of human babesiosis, and in particular, the identification of lineage-specific families of cell-surface proteins with potential roles in cytoadherence, immune evasion and pathogenesis.

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Section: Erythrocyte Cytoadherencementioning

confidence: 99%

Section: Persistent Infectionmentioning

confidence: 99%

Babesia microti: Pathogen Genomics, Genetic Variability, Immunodominant Antigens, and Pathogenesis

et al. 2021

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“…Thus, alterations in the adhesive properties of IEs due to antigenic modifications of their membrane (Cooke et al, 2005;Hutchings et al, 2007), caused by the expression of a variant of the parasite-derived erythrocyte surface antigen protein (VESA), can be observed (Jackson et al, 2014). VESAs are proteins encoded by various families of ves1α and ves1β genes and secreted by the parasite (Allred et al, 2000;Allred, 2019). In addition, VESAs appear to play essential roles in pathogenicity (Pedroni et al, 2013), immune evasion (Jackson et al, 2014), persistence, and survival of the parasites (Allred, 2019).…”

Section: Adhesion Of Babesia To the Placentamentioning

confidence: 99%

Congenital Transmission of Apicomplexan Parasites: A Review

et al. 2021

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Apicomplexans are a group of pathogenic protists that cause various diseases in humans and animals that cause economic losses worldwide. These unicellular eukaryotes are characterized by having a complex life cycle and the ability to evade the immune system of their host organism. Infections caused by some of these parasites affect millions of pregnant women worldwide, leading to various adverse maternal and fetal/placental effects. Unfortunately, the exact pathogenesis of congenital apicomplexan diseases is far from being understood, including the mechanisms of how they cross the placental barrier. In this review, we highlight important aspects of the diseases caused by species of Plasmodium, Babesia, Toxoplasma, and Neospora, their infection during pregnancy, emphasizing the possible role played by the placenta in the host-pathogen interaction.

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“…The mechanisms involved in sequestration of B. bovis remain poorly defined, but it is known that B. bovis express proteins that can produce important modifications in the architecture of the infected erythrocyte [25,26,27,28,29]. In addition to cytoadhesion and sequestration, the parasite is also able to generate antigenic diversity in the molecules exposed on the erythrocyte surface, such the members of the VESA family, to escape the antibody responses of the host [30,31]. In summary, cytoadhesion and rapid antigenic variation acting together are widely considered as the main mechanisms used by B. bovis to allow persistent infections.…”

Section: Acute and Persistent Babesia Infectionsmentioning

confidence: 99%

Interplay between Attenuation- and Virulence-Factors of Babesia bovis and Their Contribution to the Establishment of Persistent Infections in Cattle

2019

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Bovine babesiosis is an acute and persistent tick-borne global disease caused mainly by the intraerythrocytic apicomplexan parasites Babesia bovis and B. bigemina. B. bovis infected erythrocytes sequester in blood capillaries of the host (cytoadhesion), causing malaria-like neurological signs. Cytoadhesion and antigenic variation in B. bovis are linked to the expression of members of the Variant Erythrocyte Surface Antigen (VESA) gene family. Animals that survive acute B. bovis infection and those vaccinated with attenuated strains remain persistently infected, suggesting that B. bovis parasites use immune escape mechanisms. However, attenuated B. bovis parasites do not cause neurological signs in vaccinated animals, indicating that virulence or attenuation factors play roles in modulating parasite virulence phenotypes. Artificial overexpression of the SBP2t11 protein, a defined attenuation factor, was associated with reduced cytoadhesion, suggesting a role for this protein as a key modulator of virulence in the parasite. Hereby, we propose a model that might be functional in the modulation of B. bovis virulence and persistence that relies on the interplay among SBP2t, VESA proteins, cytoadhesion, and the immune responses of the host. Elucidation of mechanisms used by the parasite to establish persistent infection will likely contribute to the design of new methods for the control of bovine babesiosis.

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Variable and Variant Protein Multigene Families in Babesia bovis Persistence

Cited by 18 publications

References 88 publications

Babesia microti: Pathogen Genomics, Genetic Variability, Immunodominant Antigens, and Pathogenesis

Babesia microti: Pathogen Genomics, Genetic Variability, Immunodominant Antigens, and Pathogenesis

Congenital Transmission of Apicomplexan Parasites: A Review

Interplay between Attenuation- and Virulence-Factors of Babesia bovis and Their Contribution to the Establishment of Persistent Infections in Cattle

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