A recent study in Cell suggests that the transition from HIV infection to AIDS may involve a marked expansion of viral communities in the gut. Through experiments involving monkey models infected with simian immunodeficiency virus, or SIV, researchers from Washington University, Beth Israel Deaconess Medical Center, and elsewhere looked at the gut virome during AIDS development. Through deep sequencing analyses of fecal samples from SIV-infected monkeys that were or were not vulnerable to AIDS development, the investigators saw that animals with the pathogenic SIV infections had more viral sequences in their samples, including undescribed viruses. Moreover, study authors say, results of experiments in monkey models suggest that "enteric viral infections may contribute to AIDS enteropathy and disease progression." For more on the study, check out our sister publication GenomeWeb Daily News.
A team led by investigators at Harvard Medical School and Boston Children's Hospital describes the single-neuron sequencing strategy it used to assess genomic variability in human brain cells. The group used single-neuron sequencing to assess genome-wide LINE-1, or L1, retrotransposon insertion patterns in hundreds of neurons apiece from three different individuals, focusing on samples collected in brain regions called the cerebral cortex and the caudate nucleus. In the samples tested, somatic L1 insertion events turned up now and then, they report. But these somatic mutations occurred less than once per neuron, on average, prompting the team to conclude that the L1 insertions are not a major source of neuronal diversity in the brain regions considered. Still, the team says, "single-neuron sequencing allows systematic assessment of genomic diversity in the human brain."
A group of antibiotics known as macrolide antibiotics deter the synthesis of some, but not all, bacterial proteins, according to another Cell study by University of Illinois at Chicago researchers. In experiments done using an Escherichia coli strain that's susceptible to macrolide antibiotics, the group found that these compounds partly block the so-called polypeptide exit tunnel of protein-producing ribosomes. In so doing, the drugs allow certain polypeptides through, researchers report, while halting the translation of others. "The structure of a protein defines its ability to thread through the antibiotic-obstructed tunnel," Alexander Mankin and his colleagues write.
"Our findings reveal that small-molecule effectors can accentuate the discriminatory properties of the ribosomal exit tunnel," they add, "and that macrolide antibiotics reshape the cellular proteome rather than block global protein synthesis."