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Generation of targeted Chlamydia trachomatis null mutants
TLDR
A reverse-genetic approach to create isogenic C. trachomatis mutants is described and a tryptophan synthase gene (trpB) null mutant that was otherwise isogenic to its parental clone is demonstrated by de novo genome sequencing. Expand
Frameshift Mutations in a Single Novel Virulence Factor Alter the In Vivo Pathogenicity of Chlamydia trachomatis for the Female Murine Genital Tract
TLDR
Testing innate immunity-deficient C3H/HeJ female mice intravaginally with a human serovar D urogenital isolate revealed mutations that localized to a single gene (CT135), implicating it as a critical virulence factor. Expand
A live-attenuated chlamydial vaccine protects against trachoma in nonhuman primates
In cynomolgus macaques, ocular infection with a live trachoma strain lacking the conserved 7.5-kb plasmid induced no ocular pathology but facilitated solid or partial protection from subsequentExpand
Chlamydia trachomatis Native Major Outer Membrane Protein Induces Partial Protection in Nonhuman Primates: Implication for a Trachoma Transmission-Blocking Vaccine1
TLDR
Results show that systemically administered Chlamydia trachomatis nMOMP is highly immunogenic in nonhuman primates and elicits partially protective immunity against ocular chlamydial challenge and is the first time a subunit vaccine has shown a significant reduction in ocular shedding in non human primates. Expand
Inhibition of Chlamydiae by Primary Alcohols Correlates with the Strain-Specific Complement of Plasticity Zone Phospholipase D Genes
TLDR
It is shown that the PZ PLD (pzPLD) of Chlamydia trachomatis are transcribed during both normal and persistent infection and that the corresponding PLD proteins are predominately localized in reticulate bodies on the inner leaflet of the inclusion membrane. Expand
Influence of host iron status on Plasmodium falciparum infection
TLDR
A large body of clinical and epidemiological evidence has accumulated which clearly demonstrates that host iron deficiency is protective against falciparum malaria and that hostIron supplementation may increase the risk of malaria. Expand
Anemia Offers Stronger Protection Than Sickle Cell Trait Against the Erythrocytic Stage of Falciparum Malaria and This Protection Is Reversed by Iron Supplementation
TLDR
These results confirm and quantify a plausible mechanism by which anemia protects African children against falciparum malaria, an effect that is substantially greater than the protection offered by sickle-cell trait. Expand
Biopreservation of RBCs for in vitro Plasmodium falciparum culture
TLDR
Prolonged RBC shelf-life and biopreservation could enhance malaria research by enabling standardization of the RBC source for multiple experiments, and increasing access to RBCs from individuals with unusual blood types, nutritional deficiencies, or from remote locations. Expand
Host iron status and iron supplementation mediate susceptibility to erythrocytic stage Plasmodium falciparum.
TLDR
This work demonstrates that Plasmodium falciparum infects iron-deficient erythrocytes less efficiently and reverses the protective effects of iron deficiency, and implies that in malarious regions iron supplementation should be accompanied by effective measures to prevent falcIParum malaria. Expand
The role of the red blood cell in host defence against falciparum malaria: an expanding repertoire of evolutionary alterations
TLDR
A better understanding of how changes in RBC physiology impact malaria pathogenesis may uncover new strategies to combat the disease. Expand
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