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Sotrastaurin may also explain the killing of the ΔentF strain that constantly utilizes ATP to charge erythritol, but could not further metabolize it to obtain energy. Further, complementation of the ΔentF strain successfully overcame the growth restriction in IMM supplemented with erythritol (Fig. 6) and argues against any possible polar effects relative to entF. In contrast to the in vitro results, using the wild-type strain 2308 as a comparator, the ΔentF strain was not affected with respect to survival and growth inside murine macrophages (data not shown). This suggests either a lesser requirement or an alternate pathway for iron acquisition inside macrophages by Brucella spp. In addition, cell culture medium with 10% FBS

contains many iron-containing proteins that may not be chelated by 30 μM DFA. Increasing the concentration of DFA to 60 μM inhibited the growth of macrophages (data not shown), and further DFA studies on the survival and growth of bacterial strains inside the macrophages was not pursued. In conclusion, these results suggest a role of the entF gene in iron acquisition by B. abortus 2308 under iron-limiting conditions. Deletion of the entF ABT-263 chemical structure gene also had a major effect on erythritol metabolism by the pathogen under iron-limiting conditions. However the exact role of EntF and its relation to erythritol metabolism is still open for further analysis. Fig. S1. Intracellular survival and growth Protein kinase N1 of Brucella abortus 2308 and BAN1 in J774.A1 murine macrophages growth as a function of DFA. Please note: Wiley-Blackwell is not responsible for the content or functionality of any supporting materials supplied by the authors. Any queries (other than missing material) should be directed to the corresponding author for the article. “
“We read with interest the recent article from Waters et al. comparing response to antiretroviral therapy (ART) in late presenters (individuals diagnosed and starting ART

with a CD4 count <200 cells/μL) and late starters (individuals diagnosed with a CD4 count >350 cells/μL but starting ART at <200 cells/μL) [1]. The article revealed that 3688 individuals commenced ART with a CD4 count <200 cells/μL; of these, 2741 (74%) were deemed late presenters. In their analysis, the majority of clinical events (AIDS-defining illness or death) occurred in late presenters. In contrast, we had noticed that an increasing number of new opportunistic infections (OIs) and AIDS events were occurring in patients with established HIV infection in our cohort. To test the validity of this observation, we performed a review of our cohort to assess whether those presenting for the first time with a serious OI had previously undergone an HIV test.

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