Experimental first-in-class heart drug may also help heal kidneys

Ebola infections may persist in the brain and other organs for months, and a troubling spread of drug-resistant bacteria outside of the hospital setting. An experimental drug for healing heart tissue has been green-lighted for pilot trials in humans.

EXPERIMENTAL HEART DRUG ​SHOWS PROMISE IN KIDNEYS

An experimental drug for healing heart tissue recently green-lighted for pilot trials in humans may have promise for healing kidney tissues as well, lab experiments suggest.

The ‌drug, AD-NP1, which is under development at UCLA, is designed to help avoid heart failure after a heart attack by blocking the protein ENPP1 that disrupts healing and prevents full recovery.

When UCLA researchers examined kidney biopsies from people with chronic kidney disease, they found this same protein at higher levels than in healthy tissues.

When they induced kidney injuries in normal mice and mice with ENPP1 blocked by genetic engineering, all of the animals initially showed some damage. But weeks later, the mice without ​ENPP1 had enhanced kidney repair, reduced scarring, and improved kidney function, the researchers reported in Cell Stem Cell.

The researchers then induced kidney damage in normal mice and administered AD-NP1. One week later, the ​mice showed improved kidney function and healing.

The ENPP1 protein interferes with critical pathways that are needed for a cell to derive energy, study leader Arjun Deb of ⁠UCLA said in a statement.

“We found that the same mechanisms we observed in the heart were also applicable in the kidney,” Deb said.

Development of the first-in-class drug has been supported by grants from the U.S. ​National Institutes of Health, the Department of Defense, and the California Institute for Regenerative Medicine.

SCIENTISTS LEARN HOW EBOLA SURVIVES IN THE BRAIN FOR MONTHS

New lab experiments are shedding light on how the Ebola virus can survive ​unnoticed in the body for months or even years after initial infection, with the potential to trigger a relapse.

Infectious Ebola virus has been detected in semen for months or even a year after infection, and it can also persist in the central nervous system, particularly the brain, researchers explain in discussing their study published in Nature Microbiology.

That’s because testicles – the source of semen – and the central nervous system are considered to be “immune-privileged,” meaning the immune system reacts in a weakened and controlled manner ​in these areas in order to protect sensitive tissue. As a result, it cannot always eliminate the virus completely.

To learn more, researchers programmed human stem cells to grow into so-called cerebral organoids, spherical brain-like structures consisting ​of central nervous system cells.

The Ebola virus infected multiple cell types in the cerebral organoids and could replicate for up to 120 days, they found.

The virus was able to spread in the cerebral organoids in two ways: directly from ‌an infected cell ⁠to a neighboring cell, and by budding from the host cell, which is the classical way the virus spreads.

“These cerebral organoids enable us to investigate in detail the mechanisms that Ebola virus and other filoviruses use to persist in the human central nervous system,” study leader Lina Widerspick of the Bundeswehr Institute of Microbiology in Munich said in a statement.

“Through experiments in this model system, we can gain insights that help us improve our understanding of the long-term effects of persistence, like the severe and sometimes fatal inflammation seen in Ebola virus disease survivors with meningoencephalitis.”

Studying the infected organoids, the researchers discovered genome mutations that may be helping the ​virus to lurk undetected, including some mutations that had ​not previously been described in Ebola survivors.

They called ⁠for further studies, particularly into less well understood strains, such as the Bundibugyo virus causing the current outbreak in Africa.

DRUG-RESISTANT BACTERIA SPREADING OUTSIDE OF HOSPITALS

A hard-to-kill species of pneumonia-causing bacteria that has traditionally been found mainly in hospitals is now spreading in U.S. community settings, according to research that could help lead to new ​treatments.

To learn more about its patterns of spread, researchers analyzed multidrug-resistant Klebsiella pneumoniae detected in urine and blood samples from more than 2,000 people in ​42 states at local offices ⁠of Quest Diagnostics , a leading provider of outpatient laboratory testing.

Of the 267 different strains they identified, nearly 70% were resistant to the three most common oral antibiotics.

Geographical trends showed regional and statewide spread, and multi-state dissemination, “indicating widespread, underrecognized community reservoirs,” according to a report of the study in Nature Communications.

“For a long time, highly resistant superbugs were primarily considered a problem for hospitals, but this study reveals a dangerous shift,” Meghan Starolis of Quest said in a ⁠statement.

“These bacteria are ​spreading, and causing common infections that are resistant to the recommended antibiotics used to treat them.”

The main culprit is a gene ​known as CTX-M-15, which confers not only antibiotic-resistance traits but also tolerance for stress and metal exposure, the researchers said.

“This research provides… the genetic blueprint needed to start developing vaccines or other treatments for vulnerable patients,” Starolis said.

pneumoniae kills about 600,000 annually worldwide, according ​to the World Health Organization. In the United States, it is the most common cause of hospital-acquired pneumonia.