Absence of Erythrocyte Sequestration and Lack of Multicopy Gene Family Expression in Plasmodium falciparum from a Splenectomized Malaria Patient

BACKGROUND:To avoid spleen-dependent killing mechanisms parasite-infected erythrocytes (IE) of Plasmodium falciparum malaria patients have the capacity to bind to endothelial receptors. This binding also known as sequestration, is mediated by parasite proteins, which are targeted to the erythrocyte surface. Candidate proteins are those encoded by P. falciparum multicopy gene families, such as var, rif, stevor or PfMC-2TM. However, a direct in vivo proof of IE sequestration and expression of multicopy gene families is still lacking. Here, we report on the analysis of IE from a black African immigrant, who received the diagnosis of a malignant lymphoproliferative disorder and subsequently underwent splenectomy. Three weeks after surgery, the patient experienced clinical falciparum malaria with high parasitemia and circulating developmental parasite stages usually sequestered to the vascular endothelium such as late trophozoites, schizonts or immature gametocytes. METHODOLOGY/PRINCIPAL FINDINGS:Initially, when isolated from the patient, the infected erythrocytes were incapable to bind to various endothelial receptors in vitro. Moreover, the parasites failed to express the multicopy gene families var, A-type rif and stevor but expression of B-type rif and PfMC-2TM genes were detected. In the course of in vitro cultivation, the parasites started to express all investigated multicopy gene families and concomitantly developed the ability to adhere to endothelial receptors such as CD36 and ICAM-1, respectively. CONCLUSION/SIGNIFICANCE:This case strongly supports the hypothesis that parasite surface proteins such as PfEMP1, A-type RIFIN or STEVOR are involved in interactions of infected erythrocytes with endothelial receptors mediating sequestration of mature asexual and immature sexual stages of P. falciparum. In contrast, multicopy gene families coding for B-type RIFIN and PfMC-2TM proteins may not be involved in sequestration, as these genes were transcribed in infected but not sequestered erythrocytes

The eROSITA Final Equatorial Depth Survey (eFEDS)

Aims. The circumgalactic medium (CGM) plays an important role in galaxy evolution as the main interface between the star-forming body of galaxies and the surrounding cosmic network of in- and out-flowing matter. In this work, we aim to characterize the hot phase of the CGM in a large sample of galaxies using recent soft-X-ray observations made by SRG/eROSITA. Methods. We stack X-ray events from the ‘eROSITA Final Equatorial Depth Survey’ (eFEDS) around central galaxies in the 9hr field of the ‘GAlaxy and Mass Assembly’ (GAMA) survey to construct radially projected X-ray luminosity profiles in the 0.5–2 keV rest frame energy band as a function of their stellar mass and specific star formation rate. We consider samples of quiescent (star-forming) galaxies in the stellar mass range 2 × 1010–1012 M⊙ (3 × 109–6 × 1011 M⊙). Results. For quiescent galaxies, the X-ray profiles are clearly extended throughout the available mass range; however, the measured profile is likely biased high because of projection effects, as these galaxies tend to live in dense and hot environments. For the most massive star-forming samples (≥1011 M⊙), there is a hint of detection of extended emission. On the other hand, for star-forming galaxies with 80 kpc) scales at masses ≥1011 M⊙, but disagreement on the small scales, where brighter-than-observed compact cores are predicted. The simulations also do not predict the clear differentiation that we observe between quiescent and star-forming galaxies in our samples. Conclusions. This is a stepping stone towards a more profound understanding of the hot phase of the CGM, which holds a key role in the regulation of star formation. Future analysis using eROSITA all-sky survey data, combined with future generation galaxy evolution surveys, shall provide much enhanced quantitative measurements and mapping of the CGM and its hot phase(s)