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Category: biotech/medical

A new way coronaviruses can get into human cells

CcCoV-KY43 is found in heart-nosed bats, or Cardioderma cor, an ecologically important species found mainly in eastern Africa, including eastern Sudan and northern Tanzania.

The researchers say the zoonotic (animal-to-human) and pandemic potential of alphaCoVs has remained relatively unchartered – to date, only two cellular receptors have been characterized for alphaCoVs.

They screened the CcCoV-KY43 spike against a panel of human receptors, identified direct interactions with the human CEACAM proteins CEACAM3, CEACAM5 and CEACAM6. Overexpression of human CEACAM6—a protein widely expressed in the human lung—conferred permissivity to otherwise refractory human cells.

During the study, partners provided specific expertise. They identified CcCoV-KY43’s ability to infect human cells and confirmed CEACAM6 supports human cell entry.

They measured how strongly CEACAM6 binds to the spike, and solved the spike structure and receptor binding in atomic detail. They showed that the RBD binds the amino-terminal IgV-like domain of human CEACAM6.

They also made initial CcCov detection in bats and mapped it across Kenya, and showed where CEACAM6s is expressed in the human body, testing serum from people living in CcCoV areas to see if they might have previously been infected by CcCoV-KY43.

Continue reading “A new way coronaviruses can get into human cells” | >

Efficacy and Safety of Amifampridine in Myasthenia GravisA Randomized, Double-Blind, Placebo-Controlled Crossover Trial

Class I evidence that in patients with AChRAb+ myasthenia gravis, the addition of amifampridine to pyridostigmine was not superior to treatment with pyridostigmine alone and was associated with a higher incidence of adverse events.

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Older people with HIV are especially vulnerable to influenza, yet this group remains understudied

https://doi.org/10.1172/jci.insight.199232 Here, Savita G. Pahwa & team demonstrate high-dose vaccination for influenza strengthens immunity in older adults with HIV after prior standard dosing, but not all strain-specific weaknesses were overcome.

1Department of Microbiology and Immunology.

2Division of Biostatistics, Department of Public Health Sciences; and.

3Division of Infectious Diseases, Department of Medicine, University of Miami Miller School of Medicine, Miami, Florida, USA.

How Cells Copy DNA Might Matter More Than We Ever Realized

A subtle failure during cell division can set off dramatically different outcomes, according to new research exploring whole genome duplication. A new study finds that the way a cell fails to divide after copying its DNA can shape what happens to it next. Cell division is a core process of lif

Study: Gene circuits reshape DNA folding and affect how genes are expressed

When a gene is turned on in a cell, it creates a ripple effect along the DNA strand, changing the physical structure of the strand. A new study by MIT researchers shows that these ripples can stimulate or suppress neighboring genes.

These effects, which result from the winding or unwinding of neighboring DNA, are determined by the order of genes along a strand of DNA. Genes upstream of the active gene are usually turned up, while those downstream are inhibited.

The new findings offer guidance that could make it easier to control the output of synthetic gene circuits. By altering the relative ordering and arrangement of genes, or “gene syntax,” researchers could create circuits that synergize to maximize their output, or that alternate the output of two different genes.

Zuckerberg Trying to Simulate Human Biology at the Cellular Level

Mark Zuckerberg is following a path paved by fellow billionaires Bill Gates and Warren Buffet: laundering his untold billions through a health research prestige project.

Called the Chan Zuckerberg Biohub — his wife Priscilla Chan, a pediatrician, is also involved — the foundation’s stated long-term mission is to “cure and prevent all disease through AI-powered biology, frontier research, and state-of-the-art technology.”

True to those enormous goals, the Biohub recently announced a $500 million investment into AI models of human cells, specifically, in order to “accelerate the cure and prevention of all diseases,” Euronews reported.

ALS and Huntington Disease: Unraveling the Connections between TDP-43 and Huntingtin

Amyotrophic lateral sclerosis (ALS) and Huntington disease (HD) are lethal neurodegenerative diseases affecting motor function. Though their etiology and pathology are distinct, recent evidence suggests commonalities between TAR DNA-binding protein (TDP-43), which is associated with 97% of ALS cases, and huntingtin (HTT), the causative protein of HD. ALS is a heterogeneous, lethal neurodegenerative disease characterized by the progressive loss of upper and lower motor neurons, as well as brainstem and spinal cord degeneration. The causes of ALS are complex, variable, and, in some cases, unknown, but most cases involve mislocalization of the protein TDP-43. In contrast, HD is a monogenic, autosomal dominant, lethal neurodegenerative disease caused by polyglutamine expansion in HTT protein and characterized by the progressive loss of neurons in the brain, particularly in the striatum, which results in motor, cognitive, and behavioral changes. Although HD is not typically associated with motor neuron loss, recent evidence suggests a link between HTT and TDP-43 within the context of both ALS and HD, as well as links to related neurodegenerative diseases, such as frontotemporal dementia (FTD) and spinocerebellar ataxia type 2 (SCA2). Herein, we discuss confirmed cases of concurrent ALS and HD and the overlap of underlying disease mechanisms that potentially contribute to the onset and progression of these two devastating neurodegenerative diseases, with a focus on commonalities between TDP-43 and HTT. We propose that elucidating these commonalities will aid in the identification of broad-spectrum disease risk factors and potential overlapping treatment targets.

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