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Category: genetics – Page 392

Surveillance of Bat Coronaviruses in Kenya Identifies Relatives of Human Coronaviruses NL63 and 229E and Their Recombination History

Circa 2017 Bats harbor a large diversity of coronaviruses (CoVs), several of which are related to zoonotic pathogens that cause severe disease in humans. Our screening of bat samples collected in Kenya from 2007 to 2010 not only detected RNA from several novel CoVs but, more significantly, identified sequences that were closely related to human CoVs NL63 and 229E, suggesting that these two human viruses originate from bats. We also demonstrated that human CoV NL63 is a recombinant between NL63-like viruses circulating in Triaenops bats and 229E-like viruses circulating in Hipposideros bats, with the breakpoint located near 5′ and 3′ ends of the spike (S) protein gene. In addition, two further interspecies recombination events involving the S gene were identified, suggesting that this region may represent a recombination “hot spot” in CoV genomes. Finally, using a combination of phylogenetic and distance-based approaches, we showed that the genetic diversity of bat CoVs is primarily structured by host species and subsequently by geographic distances.

bMarie Bashir Institute for Infectious Diseases and Biosecurity, Charles Perkins Centre, School of Life and Environmental Sciences and Sydney Medical School, The University of Sydney, Sydney, Australia.

Find articles by Mang Shi

aDivision of Viral Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia, USA.

Reversal of ageing- and injury-induced vision loss

If you are interested in superlongevity, then I have something that you must read. I have previously recommended a book by Dr. David Sinclair called Lifespan. Here I am recommending a research paper that discusses one of the critical experiments in epigenetic age reversal. Normally I would read a paper first before recommending it. However, I think this is a blockbuster, and it’s over 50 pages, so I can’t wait till my slow eyes finish before passing this on. Here is an excerpt:

Age reversal!

The primary research scientist is Yuancheng Lu.

Here’s a link to the research paper:

Ageing is a degenerative process leading to tissue dysfunction and death. A proposed cause of ageing is the accumulation of epigenetic noise, which disrupts youthful gene expression patterns that are required for cells to function optimally and recover from damage1 – 3. Changes to DNA methylation patterns over time form the basis of an ‘ageing clock’4, 5, but whether old individuals retain information to reset the clock and, if so, whether this would improve tissue function is not known. Of all the tissues in the body, the central nervous system (CNS) is one of the first to lose regenerative capacity6, 7. Using the eye as a model tissue, we show that expression of Oct4, Sox2, and Klf4 genes (OSK) in mice resets youthful gene expression patterns and the DNA methylation age of retinal ganglion cells, promotes axon regeneration after optic nerve crush injury, and restores vision in a mouse model of glaucoma and in normal old mice. This process, which we call recovery of information via epigenetic reprogramming or REVIVER, requires the DNA demethylases Tet1 and Tet2, indicating that DNA methylation patterns don’t just indicate age, they participate in ageing. Thus, old tissues retain a faithful record of youthful epigenetic information that can be accessed for functional age reversal.

Anticancer Activity Discovered in Dozens of Existing Noncancer Drugs

Surprising findings could springboard the development of new anticancer drugs, or potentially even directly repurpose existing drugs for cancer therapy.

Drugs that are currently used to treat a wide range of conditions such as diabetes, inflammation, alcoholism, and even canine arthritis, can also kill laboratory-grown cancer cells, according to the results of a study by scientists at the Broad Institute of MIT and Harvard and Dana-Farber Cancer Institute. Using a molecular barcoding technology called PRISM (profiling relative inhibition simultaneously in mixtures) the researchers were able to screen thousands of existing drug compounds against different types of cancer cell lines. The results identified 49 compounds with previously unrecognized anticancer activity. The researchers say their surprising findings, which highlighted novel anticancer mechanisms and targets, could feasibly be used to springboard the development of new anticancer drugs, or potentially even directly repurpose existing drugs for cancer therapy.

We thought we’d be lucky if we found even a single compound with anticancer properties, but we were surprised to find so many,” said Todd Golub, MD, CSO and director of the cancer program at the Broad, the Charles A. Dana investigator in human cancer genetics at Dana-Farber, and professor of pediatrics at Harvard Medical School. Golub and colleagues reported their findings in Nature Cancer, in a paper titled, “Discovering the anticancer potential of non-oncology drugs by systematic viability profiling.”

Genomics and BioPharma Pioneer!! — Dr. William Haseltine — Biologist, entrepreneur and philanthropist, now focusing on the issues of healthcare costs, dementia care, and aging — ideaXme — Ira Pastor

From Blood to Bone (and Back)! — Dr. Rhonda Prisby — University of Texas, Arlington — Fascinating ossification research in the Bone Vascular and Micro-Circulation Laboratory — ideaXme — Ira Pastor

CAR T treatments could have fewer side effects than other cancer immunotherapies

New cancer immunotherapies involve extracting a patient’s T cells and genetically engineering them so they will recognize and attack tumors. This technique is a true medical breakthrough, with an increasing number of leukemia and lymphoma patients experiencing complete remissions since CAR T therapy was FDA approved in 2017.

This type of therapy is not without challenges, however. Engineering a patient’s T is laborious and expensive. And when successful, the alterations to the immune system immediately make patients very sick for a short period of time, with symptoms including fever, nausea and neurological effects.

Now, University of Pennsylvania researchers have demonstrated a new engineering technique that, because it is less toxic to the T cells, could enable a different mechanism for altering the way they recognize cancer.

CRISPR gene-editing corrects muscular dystrophy in pigs

Duchenne muscular dystrophy (DMD) is one of the most common and most devastating muscular diseases, greatly reducing patients’ quality of life and life expectancy. Now, researchers in Germany have managed to use the CRISPR gene-editing tool to correct the condition in pigs, bringing the treatment ever closer to human trials.

A protein called dystrophin is necessary for muscles to regenerate themselves, but people with DMD have a genetic mutation that removes the gene that produces dystrophin. That means that affected children usually begin to show symptoms of muscle weakness by age five, lose the ability to walk by about age 12, and rarely live through their 30s as their heart muscles give out.

Because it’s a genetic condition, DMD is a prime target for treatment with the gene-editing tool CRISPR. This system is prized for its ability to cut out problematic genes and replace them with more beneficial ones, and has been put to work treating cancer, HIV and forms of blindness.

Brian Kennedy Joins the LEAF Scientific Advisory Board

We are delighted to announce that Dr. Brian Kennedy, a Distinguished Professor in the Department of Biochemistry and Physiology at the National University of Singapore (NUS) will be joining the LEAF scientific advisory board.

Professor Kennedy is an important figure in the research community, as he is internationally recognized for his research and efforts to translate those findings into therapies that could potentially slow, delay, or even prevent age-related diseases. He previously served as the President of the Buck Institute, where he still remains as a Professor.

At the NUS, he is developing therapeutic interventions that directly target human aging along with biomarkers that can validate if a therapy has worked or not. Professor Kennedy and his team have been exploring the epigenetic clock, a biomarker that measures methylation of the human genome to determine biological age. They are also investigating inflammatory biomarkers of aging using metabolomics, the study of chemical processes involving metabolites, the intermediates and products of metabolism.

Mutations in donors’ stem cells may cause problems for cancer patients

A new study from Washington University School of Medicine in St. Louis suggests that bone marrow — or blood stem cells — from healthy donors can harbor extremely rare mutations that can cause health problems for the cancer patients who receive them.

A stem cell transplant — also called a bone marrow transplant — is a common treatment for blood cancers, such as acute myeloid leukemia (AML). Such treatment can cure blood cancers but also can lead to life-threatening complications, including heart problems and graft-versus-host disease, in which new immune cells from the donor attack a patient’s healthy tissues.

A new study from Washington University School of Medicine in St. Louis suggests that extremely rare, harmful genetic mutations present in healthy donors’ stem cells — though not causing health problems in the donors — may be passed on to cancer patients receiving stem cell transplants. The intense chemo- and radiation therapy prior to transplant and the immunosuppression given after allow cells with these rare mutations the opportunity to quickly replicate, potentially creating health problems for the patients who receive them, suggests the research, published Jan. 15 in the journal Science Translational Medicine.

Among the concerns are heart damage, graft-versus-host disease and possible new leukemias.

DNA sleuths read the coronavirus genome, tracing its origins

Analyses of the viral genome are already providing clues to the origins of the outbreak and even possible ways to treat the infection, a need that is becoming more urgent by the day: Early on Saturday in China, health officials reported 15 new fatalities in a single day, bringing the death toll to 41. There are now nearly 1,100 confirmed cases there.

Reading the genome (which is made of RNA, not DNA) also allows researchers to monitor how 2019-nCoV is changing and provides a roadmap for developing a diagnostic test and a vaccine.

“The genetics can tell us the true timing of the first cases” and whether they occurred earlier than officials realized, said molecular biologist Kristian Andersen of Scripps Research, an expert on viral genomes. “It can also tell us how the outbreak started — from a single event of a virus jumping from an infected animal to a person or from a lot of animals being infected. And the genetics can tell us what’s sustaining the outbreak — new introductions from animals or human-to-human transmission.”