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Phone: 208-885-6079 Fax: 208-885-6518 Email:gustavo@uidaho.edu Ph.D. Massachusetts Institute of Technology Biology,
1999 RESEARCH INTERESTS: Toxoplasma gondii egress and invasion.
RESEARCH SUMMARY: Toxoplasma gondii is an obligate intracellular parasite
capable of infecting virtually any nucleated cell from a wide
range of mammalian and avian species. Toxoplasma is one of the
most widespread and successful protozoan pathogens and is a common
parasite in humans where it has become one of the main opportunistic
pathogens in AIDS patients. Moreover, in congenital infections,
the disease can lead to severe neurological problems or even
death of the developing fetus. Toxoplasmosis affects approximately
one in every10,000 births in the United States. Because of its
host broad range, Toxoplasma is also an important pathogen of
animals. Toxoplasmosis is one of the principle causes of abortions
in sheep and goats. In some sheep flocks it can be responsible
for the deaths of half the newborns and thus it has devastating
effects on this industry. Some of the most devastating effects
of infections by intracellular parasites are a direct consequence
of their lytic cycle, which consists of attachment to the host
cell, invasion, intracellular replication and egress. Both invasion
and egress by the human pathogen Toxoplasma gondii are
essential for infection and survival, involve fluctuation in
intracellular [Ca+2], morphological changes and secretion from
various organelles. The goals of our lab are to answer the specific
questions: "what are the molecular and genetic elements
involved in egress?"; "what are the cues telling the
parasite to exit its host cell?"; and "what are the
molecular mechanisms involved in invasion?". To answer these
questions, our lab utilizes a combination of molecular genetics,
cell biology, and biochemistry. Infection of the fetus by Toxoplasma
requires crossing of the placental barrier and thus, invasion
and egress from various cell types. Consequently, inhibiting
invasion or egress would stop the progress of congenital infection.
A better understanding of the genes and events involved in the
way the parasite invades and comes out of the host cell will
shed light into its pathogenesis as well as reveal potential
targets for drug and vaccine development.
REPRESENTATIVE PUBLICATIONS: Karasov AO, Boothroyd JC, Arrizabalaga G. (2005) Identification and disruption of a rhoptry-localized homologue of sodium hydrogen exchangers in Toxoplasma gondii. Int J Parasitol. 35(3):285-91. Saeij JP, Boyle JP, Grigg ME, Arrizabalaga G, Boothroyd JC. (2005) Bioluminescence imaging of Toxoplasma gondii infection in living mice reveals dramatic differences between strains. Infect Immun. 73(2):695-702. Arrizabalaga G, Ruiz F, Moreno S, Boothroyd JC. (2004) Ionophore-resistant mutant of Toxoplasma gondii reveals involvement of a sodium/hydrogen exchanger in calcium regulation. J Cell Biol. 165(5):653-62. Arrizabalaga G, Boothroyd JC. (2004) Role of calcium during Toxoplasma gondii invasion and egress. Int J Parasitol. 34(3):361-8. Review. Camps M, Arrizabalaga G, Boothroyd J. (2002) An rRNA mutation identifies the apicoplast as the target for clindamycin in Toxoplasma gondii. Mol Microbiol. 43(5):1309-18. Black MW, Arrizabalaga G, Boothroyd JC. (2000) Ionophore-resistant
mutants of Toxoplasma gondii reveal host cell permeabilization
as an early event in egress. Arrizabalaga G, Lehmann R. (1999) A selective screen
reveals discrete functional domains in Drosophila Nanos. Genetics.
153(4):1825-38.
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