News of Note—A virus that attacks HIV; reviving a failed antibiotic; new insight into cystic fibrosis

h.i.v. infected t cell
Dormant HIV cells may be vulnerable to attack by another virus called Maraba.

Combating HIV with a different virus

Scientists at the Ottawa Hospital and the University of Ottawa have discovered that Maraba virus, also known as MG1, can hunt down and kill the dormant HIV cells that can be difficult for standard antiretroviral treatments to target. MG1 works by targeting cells with defective interferon pathways. Those defects, which are prevalent in dormant HIV-infected cells, make cells more susceptible to viruses. By studying HIV-infected cells in the lab, the researchers discovered that MG1 eliminates the virus while leaving healthy cells alone, according to a study published in the Journal of Infectious Diseases. (Release)

How a shelved antibiotic could be repurposed

Back in the 1970s, when effective antibiotics were plentiful, a drug called pentyl pantothenamide was shelved after scientists showed that it stopped the growth of E. coli but couldn’t kill it altogether. Now, scientists at the University of Leeds are taking a second look at the antibiotic in the hopes of reviving it and using it to combat drug-resistant bugs. Published in the journal Biochemistry, the researchers explain that pentyl pantothenamide works by preventing E. coli from making vitamin B5, which it needs to metabolize energy and grow. The antibiotic binds to the bacteria via three enzymes, they discovered. They are now trying to develop a compound that mimics this mechanism, but in a more effective way, so they can eliminate E. coli and related bugs. (Release)

Restoring the lung membrane to fight cystic fibrosis

The hereditary lung disease cystic fibrosis occurs when a key chloride channel malfunctions, causing the lung’s mucus layer to dry out. Scientists at the University of Zurich are investigating whether activating an alternate chloride channel called TMEM16A could be a valuable therapy. The researchers used cryo-electron microscopy to unlock the structure of TMEM16A, and in so doing discovered that positively charged calcium ions bind to the channel, allowing negatively charged chloride ions to move through it. They believe their findings could inform efforts to develop drugs that activate the TMEM16A channel. (Release)

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