In the early, online edition of the Proceedings of the National Academy of Sciences, an international team led by investigators at the University of Massachusetts used genome sequencing to delve into the diversity, genome structure, mutational patterns, and recombination rates found in cytomegalovirus isolates from 47 infants with congenital CMV infections and one infected adult with glioblastoma multiforme. The researchers' analyses uncovered parts of the CMV genome that tend to be highly conserved, including regions coding for DNA processing enzymes, capsid proteins, and so on. But they also detected parts of the genome that are prone to variation, along with compartments in the human host where diversity is enhanced or constrained. GenomeWeb has more on the study, here.
For another PNAS study, researchers from Brookhaven National Laboratory took a look at homologous recombination patterns in Escherichia coli genomes using a multiple sequence alignment involving 32 E. coli genome sequences. After removing mobile elements, the team scrutinized SNP profiles in the remaining sequences to group clusters of related strains and tease apart recombination events. "We find that the entire basic genome is continually exchanged by homologous recombination with genome fragments acquired from other genomes in the population," the study's authors write, noting that "[c]o-evolving populations of phages that package genome fragments and deliver them to cell that have appropriate receptors are likely mediators of most DNA transfers, distributing variability throughout the species."
Finally, a group from China and the US describes a long non-coding RNA called lncRNA-CD244 that helps regulate the effects of T-cell immune responses following tuberculosis infection. Based on gene expression profiles in cells from individuals with active TB infections and healthy controls, the researchers found that a T cell inhibiting molecule called CD244 is uprelated in CD8+ T-cells in those with TB infection. This appears to produce a chromatin state that sets loose expression of lncRNA-CD244, allowing it to interact with a chromatin modifying enzyme involved in regulating repressive histone trimethylation marks that interfere with CD8+ T-cell function.