As human beings, we are often obsessed with proving that we are unique or irreplaceable in some way: we crave individuality. “Be yourself!” we proclaim, “because an original is worth more than a copy”. However, in the world of viruses, copies are king. The “success” of a virus means replicating itself over and over again, creating as many copies as possible to infect more hosts and ensure the survival of the viral lineage. Dr. Jesse Bloom, professor in the Fred Hutch Divisions of Basic Sciences and Public Health Sciences, studies how natural mutations in these fast-copying viruses influence their ability to infect hosts. However, David Bacsik, a graduate student at Bloom Lab, had an even more basic question: How many copies, or offspring, are produced during single infection events? And does this have anything to do with the active transcription of a given virus during infection? The results of his study were recently published on bioRxiv.
“By looking at cells infected with the influenza virus, we wanted to understand how many viral genes each cell transcribes and how many new virions each cell generates,” Bacsik explained. “What is the relationship between these two processes? It’s a pretty basic question about how the influenza virus works, but until very recently, it couldn’t be examined empirically.” Bloom Lab specializes in harnessing highly detailed data sets to answer fundamental virology questions, and this study is no different. David analyzed data from individual cells infected with influenza, quantifying both the amount of progeny each infected cell produced and the amount of viral mRNA that was produced, and looked for a correlation between the two. Various viral gene products are crucial in putting together the packaging that allows new virus particles to leave cells and find new targets. Therefore, you may not expect viable, infectious progeny from cells that lacked the transcript of those genes (or expressed mutated forms). “The naive model that he had envisioned was one where making more viral transcripts led directly to making more viral progeny,” Bacsik explained. “But the data did not support this at all. The most exciting moment was realizing that the influenza virus transcript is No strongly correlated with the production of progeny in individual cells. In [fact], the cells that transcribe the most viral mRNA are not the cells that produce the most progeny virions. The authors proposed a partial explanation for this unexpected result: transcription of the influenza NS gene. Infected cells that do not express the NS gene produce very few offspring, and one of the proteins encoded by the NS gene regulates the switch from transcription to genome replication, another crucial step in the assembly of new viral particles. However, the authors note that “the absence of NS and other viral genetic defects only explains part of the discordance between viral transcription and the production of offspring in individual cells, as these two properties are often discordant even in cells expressing . unmutated copies of all viral genes. ”
Source: news.google.com