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New animal models of Zika virus (ZIKV) infection are imperative to accelerating efforts to treat or prevent disease in humans. Adams Waldorf et al. now report that ZIKV infection of a pregnant female pigtailed macaque caused brain lesions in the developing fetus, suggesting that this model may be useful for understanding ZIKV-associated congenital abnormalities in humans.
By using combined positron emission and computed tomography (PET–CT), Esmail et al. show that some patients with latent tuberculosis have signs of subclinical, active disease in the lungs and a greater likelihood of progression, suggesting a spectrum of disease rather than discrete latent and active disease states.
CRISPR–Cas9-mediated insertion of a naturally occurring benign mutation in blood cell progenitors from patients with sickle cell disease increases fetal hemoglobin expression to levels sufficient to ameliorate the pathological morphology observed in erythrocytes differentiated from these cells.
Low-dose IL-2 treatment alters the abundance of regulatory T cells, IL-17-producing T cells and follicular helper T cells, but not of T helper type 1 and 2 cells, in patients with SLE.
In mouse models of patient-derived breast cancer brain metastases, combined inhibition of PI3K and mTOR resulted in regression, and therapeutic response was correlated with a reduction in 4EBP1 phosphorylation.
An intracortical neural prosthetic system developed in animal studies is translated for clinical use in humans with paralysis. Neural control of computer cursor movements achieved with this system represent the highest performance reported to date.
Morgane Rolland and colleagues report that in HIV infection, a higher diversity of infecting founder viruses is associated with markers of poorer clinical outcome.
Lineage tracing shows that, contrary to a recent report, c-kit+ cells take on a vascular endothelial cell fate, not an epithelial one, after lung injury or during normal homeostasis.
A small clinical trial shows that short-term cold acclimation to moderately-cold temperature improves the glucose homeostasis of individuals with type 2 diabetes, without an appreciable activation of their brown adipose tissue.
The study describes the use of integrative approaches to search for candidate therapeutic targets for DIPG, and the identification of an HDAC inhibitor as a potential treatment strategy
Goel et al. report that RIFINs mediate rosetting of Plasmodium falciparum infected erythrocytes in vitro, a phenotype that is associated with severe disease in humans
Aftab Ansari and his colleagues show that antibody-mediated masking of α4β7 integrin impedes intravaginal transmission of simian immunodeficiency virus in macaques.
Hashizume et al. report a new therapeutic strategy for treating pediatric gliomas with mutations in the H3F3A gene by inhibiting histone demethylation.
Tau pathology is identified in brains of individuals with Huntington's disease (HD), and reduction of tau expression can ameliorate disease in HD model mice.
Pancreatic adenosquamous carcinomas are rare but highly aggressive tumors, and our understanding of them is limited. In a new study, Miles Wilkinson and colleagues now report that they have identified somatic mutations in an RNA helicase encoded by UPF1 in some pancreatic adenosquamous carcinomas. UPF1 is required for nonsense-mediated RNA decay, suggesting that the aberrant accumulation of altered RNA transcripts may contribute to the malignant phenotype of these tumors and could be a target of diagnostic and therapeutic approaches for this tumor type.
Mutations inactivating ARID1A, a subunit of the chromatin remodeling SWI/SNF complex, have been identified in some human cancers. This study reveals that cancer cells with mutated ARID1A are dependent on the residual activity of the complex for proliferation and that even if concomitant alterations in the ARID1A homolog ARID1B can occur, loss of ARID1B activity confers a specific vulnerability to ARID1A-mutant cells that may in the future be explored for targeting purposes.