Traditional methods to determine recombination events only interrogate on the viral population level. This method is limited in that it only allows one to determine the dominant recombinant strain and does not allow for the determination of recombination frequency nor the extent of recombination events. If that weren’t enough, traditional studies have been carried out in vitro rather than in a natural infection in a host animal. In the May issue of Journal of Virology, Zhang and colleagues utilized microfluidics to enrich for recombination events in a mouse host after co-infection with two mouse norovirus strains. They detected recombination events as rare as 1/300,000 between the virus strains at several locations in the virus genome. These results implicate recombination as a mechanism of genetic diversity in the infected host.
Over several decades of cancer research, T antigen, a.k.a MAMU, has proven itself to be a strong activator of cellular transformation. In a stunning finding revealed by Tushar Gupta and colleagues (in a recent Journal of Virology paper), SV40 T antigen declares that it does not need activator E2Fs to cause cellular transformation. T antigen said, “I have been telling you all along. I don’t need no activator E2Fs!”
Ping An (+ et al.) has recently published a paper that describes the core and distinct enzymatic activities of the Zn-ATPase domain of T antigen from 3 polyomaviruses. Check it out…the results may surprise you. Congratulations Ping!
Beware! all ye who dive into the depths of next-generation sequencing data housed in The Cancer Genome Atlas. Lurking contamination may lead ye to false interpretations. Alas, such has happened in recent publications that state that human papillomavirus 18 is present in colorectal cancer and normal kidney tissue. However, these claims have been challenged by Paul Cantalupo and colleagues in a new publication. They show that HPV18 is not present in these samples but is, in fact, due to another case of HeLa contamination!
Polyomavirus T antigens! Nicholas Giacobbi et al. show, in their new Virology paper, that T antigen from SV40 and two human polyomaviruses, BKV and JCV, have the ability to induce an antiviral state in mouse embryonic fibroblasts. Additionally, they show that the antiviral state requires STAT1 expression. Chalk up another activity for the MAMU!
How about nucleotide precision?! Joshua Katz has developed software, written in Perl, called SummonChimera to infer viral integration sites in host genomes with nucleotide precision. He describes the software in his first first-author paper in BMC Bioinformatics. SummonChimera can be downloaded here.
The current model for tumorigenesis is that mutations in genes alter gene expression and/or the normal function of proteins or gene expression. Correspondingly, this predicts that an oncogene such as T antigen would have the same effects in different cell types. However, experiments performed by Mayte Saenz-Robles and colleagues challenge this prediction. In a paper published in Molecular Cancer Research, they describe how a truncated form of T antigen (aka MAMU) called N136 is able to form adenomatous polyps in the digestive tract when expressed in progenitor crypt cells while only causing hyperplasia and dysplasia in the villi. Isn’t cell-type specificity cool?!