April 05, 2019

Even viruses get viruses...

April 05, 2019/ Robert P. Ruggiero, phd

Even Viruses Can Get Infected With Other Viruses

Three tiny, newly described viruses—named Larry, Curly, and Moe—target bigger viruses.

SARAH ZHANG, The Atlantic

In a single drop of water from Lake Ontario, you can find an abundance of algae. In these algae, scientists in 2015 found a new virus belonging to an enigmatic group called giant viruses. And nested inside these giant viruses, scientists have now found yet more novel viruses—three tiny ones that they have named CpV-PLV Larry, Curly, and Moe.

“I originally named them to see if I can get away with it,” says Joshua Stough, now a postdoctoral research fellow at the University of Michigan. He’s a co-author of a new paper describing and naming the Three Stooges, so, in fact, he has gotten away with it.

The origins of an important cancer causing virus

March 14, 2019/ Robert P. Ruggiero, phd

Origin and evolution of papillomavirus (onco)genes and genomes

Anouk Willemsen and Ignacio G. Bravo

biorxiv (Research Article)

Abstract—Papillomaviruses (PVs) are ancient viruses infecting vertebrates, from fish to mammals. Although the genomes of PVs are small and show conserved synteny, PVs display large genotypic diversity and ample variation in the phenotypic presentation of the infection. Most PVs genomes contain two small early genes E6 and E7. In a bunch of closely related human PVs, the E6 and E7 proteins provide the viruses with oncogenic potential. The recent discoveries of PVs without E6 and E7 in different fish species place a new root on the PV tree, and suggest that the ancestral PV consisted of the minimal PV backbone E1-E2-L2-L1. Bayesian phylogenetic analyses date the most recent common ancestor of the PV backbone to 424 million years ago (Ma). Common ancestry tests on extant E6 and E7 genes indicate that they share respectively a common ancestor dating back to at least 184 Ma. In AlphaPVs infecting primates, the appearance of the E5 oncogene 53-58 Ma concurred with i) a significant increase in substitution rate, ii) a basal radiation, and iii) key gain of functions in E6 and E7. This series of events was instrumental to build the extant phenotype of oncogenic human PVs. Our results assemble the current knowledge on PV diversity and present an ancient evolutionary timeline punctuated by evolutionary innovations in the history of this successful viral family.

Viral coinfection increases variation, fitness

March 14, 2019/ Robert P. Ruggiero, phd

Beneficial coinfection can promote within-host viral diversity

Asher Leeks, Ernesto A. Segredo-Otero, Rafael Sanjuán, and Stuart A. West

Virus Evolution (Research Article)

Abstract—In many viral infections, a large number of different genetic variants can coexist within a host, leading to more virulent infections that are better able to evolve antiviral resistance and adapt to new hosts. But how is this diversity maintained? Why do faster-growing variants not outcompete slower-growing variants, and erode this diversity? One hypothesis is if there are mutually beneficial interactions between variants, with host cells infected by multiple different viral genomes producing more, or more effective, virions. We modelled this hypothesis with both mathematical models and simulations, and found that moderate levels of beneficial coinfection can maintain high levels of coexistence, even when coinfection is relatively rare, and when there are significant fitness differences between competing variants. Rare variants are more likely to be coinfecting with a different variant, and hence beneficial coinfection increases the relative fitness of rare variants through negative frequency dependence, and maintains diversity. We further find that coexisting variants sometimes reach unequal frequencies, depending on the extent to which different variants benefit from coinfection, and the ratio of variants which leads to the most productive infected cells. These factors could help drive the evolution of defective interfering particles, and help to explain why the different segments of multipartite viruses persist at different equilibrium frequencies.

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