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Title:   Author  item
                                            SU, CHUNLEI - WA. UNIV. SCH. MED.item
                                            HOWE, DANIEL - WA. UNIV. SCH. MED.item
                                            Dubey, Jitenderitem
                                            AJIOKA, JIM - CAMBRIDGE UNIV.item
                                            SIBLEY, L. - WA. UNIV. SCHO. MED.
  Submitted to: Proceedings of the National Academy of Sciences (PNAS)
                                    Publication Type: Abstract Only
                                    Publication Acceptance Date: 8/10/2002
                                    Publication  Date: N/A
                                    Citation: N/AInterpretive Summary: Toxoplasma gondii is a single celled parasite that can infect virtually all warm-blooded hosts.  It causes mental retardation in congenitally infected children and abortion in livestock.  Why some individuals become sick with this parasite whereas others show no symptoms is not known.  Toxoplasma gondii strains vary in virulence and have been genetically divided into 3 types, I to III.  Scientists at the Beltsville Agricultural Research Center and the Washington School of Medicine, St. Louis, Missouri performed crosses (inter-breeding) between Type I (which are virulent) and type III (which are not virulent) strains and found that half of the progeny shared virulence with the parenteral strains.  These results will be of interest to biologists, parasitologists, and geneticists.
                                Technical Abstract: Strains of T. gondii can be grouped into three predominant clonal lineages with members of the type I group being uniformly lethal in mice.  To elucidate the basis of this extreme virulence, a genetic cross was performed between a highly virulent type I strain (GT-1) and a less-virulent type III strain (CTG) and the phenotype of resulting progeny was analyzed by genetic linkage mapping.  Analysis of independent recombinant progeny identified several quantitative trait loci (QTL) that contributed to acute virulence.  A major QTL located on chromosome VII accounted for approximately 50% of the virulence phenotype, while a minor locus on chromosome IV, linked to the ROP1 gene, accounted for approximately 10%.  These loci are conserved in other type I strains indicating that virulence is controlled by discrete genes common to the type I lineage.


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