The role of resetting in the multiplication of Plasmodium falciparum:: Rosette formation neither enhances nor targets parasite invasion into uninfected red cells
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Clough, B
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Northwick Pk & St Marks Hosp, Lister Unit, Imperial Coll Sch Med, Dept Infect & Trop Med, Harrow, Middx, EnglandNorthwick Pk & St Marks Hosp, Lister Unit, Imperial Coll Sch Med, Dept Infect & Trop Med, Harrow, Middx, England
Clough, B
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Atilola, FA
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Northwick Pk & St Marks Hosp, Lister Unit, Imperial Coll Sch Med, Dept Infect & Trop Med, Harrow, Middx, EnglandNorthwick Pk & St Marks Hosp, Lister Unit, Imperial Coll Sch Med, Dept Infect & Trop Med, Harrow, Middx, England
Atilola, FA
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Pasvol, G
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Northwick Pk & St Marks Hosp, Lister Unit, Imperial Coll Sch Med, Dept Infect & Trop Med, Harrow, Middx, EnglandNorthwick Pk & St Marks Hosp, Lister Unit, Imperial Coll Sch Med, Dept Infect & Trop Med, Harrow, Middx, England
Pasvol, G
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[1] Northwick Pk & St Marks Hosp, Lister Unit, Imperial Coll Sch Med, Dept Infect & Trop Med, Harrow, Middx, England
The effect of rosette formation on the multiplication in vitro of Plasmodium falciparum was studied in order to establish whether resetting acts as a major virulence factor in the pathogenesis of severe malaria by facilitating invasion of uninfected red cells, Invasion rates for resetting (R+) and non-resetting (R-) parasites selected from the same clone, PA1, of P. falciparum were similar over a range of starting parasite concentrations when assayed in both static cultures and conditions of shear stress comparable with microvascular flow However, incubation of both R+ and R- parasites under simulated conditions of flow led to decreased invasion and fewer multiply-infected red cells as we have previously observed. Studies using fluorescently labelled red cells or reticulocytes demonstrated that resetting did not alter the rates of invasion or target merozoites into the uninfected cells comprising a rosette. Preferential invasion of reticulocytes occurred regardless of resetting or conditions of now Although the role of resetting in the pathogenesis of malaria might relate to microvascular obstruction or perhaps the restriction of phagocytosis, our data suggest that resetting does not play a role in the invasion or targeting of parasites into uninfected cells, eliminating this mechanism to explain the association of virulence with the resetting parasite phenotype.