Erythrocyte invasion

Blackman, M. J. (2000). Proteases involved in erythrocyte invasion by the malaria parasite Function and potential as chemotherapeutic targets. Curr. Drug Targets 1,59-83. 

Chitnis, C. E. (2001). Molecular insights into receptors used by malaria parasites for erythrocyte invasion. Chit. Opin. Hematol. 8, 85-91. 

Chitnis, C. E., and Miller, L. H. (1994). Identification of the erythrocyte binding domains of Plasmodium vivax and Plasmodium knowlesi proteins involved in erythrocyte invasion. J. Exp. Med. 180, 497-506. 

Kaneko, O. (2007). Erythrocyte invasion Vocabulary and grammar of the Plasmodium rhoptry. Parasitol. Int. 56, 255-262. 

Miller, L. H. (1977). Hypothesis on the mechanism of erythrocyte invasion by malaria merozoites. Bull. World Health Organ. 55,157-162. 

O Donnell, R. A., Hackett, F., Howell, S. A., Treeck, M., Struck, N., Krnajski, Z., Withers-Martinez, C., Gilberger, T. W., and Blackman, M. J. (2006). Intramembrane proteolysis mediates shedding of a key adhesin during erythrocyte invasion by the malaria parasite. J. Cell Biol. 174,1023-1033. 

Rayner, J. C., Vargas-Serrato, E., Huber, C. S., Galinski, M. R., and Barnwell, J. W. (2001). A Plasmodium falciparum homologue of Plasmodium vivax reticulocyte binding protein (PvRBPl) defines a trypsin-resistant erythrocyte invasion pathway. ]. Exp. Med. 194, 1571-1581. 

Singh, A. P., Puri, S. K., and Chitnis, C. E. (2002). Antibodies raised against receptor-binding domain of Plasmodium knowlesi Duffy binding protein inhibit erythrocyte invasion. Mol. Biochem. Parasitol. 121, 21-31. 

A parasite phospholipase (most likely PLA2) may participate in host cell invasion by T. gondii (21). The presumptive PLAj enhanced host cell invasion. Phospholipase has been shown to solubilize rhoptry proteins of P. falciparum presumably involved in erythrocyte invasion (22). Solubilization of internal, latent, membrane-bound rhoptry proteins by lipid degradation may be a general method in the Apicomplexa for initiating active host cell penetration and parasitophorous vacuole membrane formation after attachment. 

Fleck SL, Birdsall B, Babon J, Dluzewski AR, Martin SR, Morgan WD, Angov E, Kettleborough CA, Feeney J, Blackman MJ, Holder AA, Suramin and suramin analogues inhibit merozoite surface protein-1 secondary processing and erythrocyte invasion by the malaria parasite Plasmodium falciparum, J. Biol. Chem. 2003 278 47670-47677. 

Hesselgesser, J., Chitnis, C. E., Miller, L. H., Yansura, D. G., Simmons, L. C., Fairbrother, W. J., Kotts, C., Wirth, C., Gillece-Castro, B. L., and Homk, R. (1995) A mutant of melanoma growth stimulating activity does not activate neutrophils but blocks erythrocyte invasion by malaria. J. Biol. Chem. 270,11,472-11,476. 

Because cholinesterase inhibition is a very sensitive biomarker for other chemicals, it is not always conclusive evidence of disulfoton exposure. However, depression of cholinesterase activity can alert a physician to the possibility of more serious neurological effects. Erythrocyte acetylcholinesterase activity more accurately reflects the degree of synaptic cholinesterase inhibition in nervous tissue, while serum cholinesterase activity may be associated with other sites (Goldfrank et al. 1990). In addition, a recent study showed that after rats received oral doses of disulfoton for 14 days, acetylcholinesterase levels in circulating lymphocytes correlated better with brain acetylcholinesterase activity than did erythrocyte cell cholinesterase activities during exposure (Fitzgerald and Costa 1993). However, recovery of the activity in lymphocytes was faster than the recovery of activity in the brain, which correlated better with the activity in erythrocytes. Animal studies have also demonstrated that brain acetylcholinesterase depression is a sensitive indicator of neurological effects (Carpy et al. 1975 Costa et al. 1984 Schwab and Murphy 1981 Schwab et al. 1981, 1983) however, the measurement of brain acetylcholinesterase in humans is too invasive to be practical. 

In P falciparum and P malariae infection, only one cycle of liver cell invasion and multiplication occurs, and liver infection ceases spontaneously in less than 4 weeks. Thus, treatment that eliminates erythrocytic parasites will cure these infections. In P vivax and P ovale infections, a dormant hepatic stage, the hypnozoite, is not eradicated by most drugs, and subsequent relapses can therefore occur after therapy directed against erythrocytic parasites. Eradication of both erythrocytic and hepatic parasites is... 

Dvorak JA, Miller LH, Whitehouse WC, Shiroishi T (1975) Invasion of erythrocytes by malaria merozoites. Science 187(4178) 748-750... 

Hossain ME, Dhawan S, Mohmmed A (2012) The cysteine-rich regions of Plasmodium falciparum RON2 bind with host erythrocyte and AMA1 during merozoite invasion. Parasitol Res 110(5) 1711- 1721... 

Endocytosis may not be required for the entry of an invasive adenylate cyclase from Bordello pertussis (Hanski and Ferfel, 1985 Donovan and Storm, 1990). This is a single chain protein (mol. wt. approx. 200 kDa) which resembles the edema factor from anthrax toxin in that it must interact with calmodulin to become active. In contrast to anthrax toxin, it consists of only one polypeptide which is, however, easily cleaved by proteases and thereby activated. An enzymatically active 45 kDa fragment is not active on whole cells, but it could in conjunction with the rest of the molecule enter the cytosol. The facts that this toxin acts much more rapidly than anthrax toxin, and that it is active even at 4 °C and on erythrocytes that have little, if any, endocytosis, suggest that the toxin is able to penetrate directly through the cell surface membrane. 

Mechanisms to control parasitic protozoa are similar to those utilized for other infectious agents they can be divided into non-specific mechanism(s) and specific mechanism(s) involving the immune system. The best studied non-specific mechanisms include those that affect the entry of parasites into the red blood cell. The sickle cell haemoglobin trait and lack of the Duffy factor on the erythrocyte surface make the red cell more resistant to invasion by Plasmodium. These traits are commonly found in populations from malaria-endemic regions. A second example of a non-specific factor is the presence of trypanolytic factors in the serum of humans which confer resistance to T. brucei, Although nonspecific factors can play a key role in resistance, usually they work in conjunction with the host s immune system. 

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