Quantcast
Channel: Links to the Damn Paper » Article Discussions
Viewing all articles
Browse latest Browse all 15

It turns out that the flu virus is surprisingly bad at making flu virions

0
0

In order to successfully infect a cell an influenza virus needs a small collection of proteins that are absolutely essential, and it looks like at least 90% of all individual influenza virions is lacking at least one of them, weird huh? Influenza mutates extraordinarily fast in order to outrun the immune systems of its host populations, generating new patterns that its hosts’ immune systems haven’t seen before by the time they are exposed again next flu season, and it seems like this must be just a natural consequence of how it does that.  These results do call for a re-orientation in how we see influenza infection, in addition to potentially infection by many phages, as they show that not only must new hosts be infected by a population of distinct virions but indeed also each cell.

Influenza virusInfluenza Virus with its parts, Source: http://micro.magnet.fsu.edu/cells/viruses/influenzavirus.html

Most Influenza A Virions Fail to Express At Least One Essential Viral Protein (PDF)

CB Brooke, WL Ince, et al. Published 2013 in J. Virol. doi: 10.1128/​JVI.02284-12

Segmentation of the influenza A virus (IAV) genome enables rapid gene reassortment at the cost of complicating the task of assembling the full viral genome. By simultaneously probing for the expression of multiple viral proteins in MDCK cells infected at low multiplicity with IAV, we observe that the majority of infected cells lack detectable expression of one or more essential viral proteins. Consistent with this observation, up to ninety percent of IAV-infected-cells fail to release infectious progeny, indicating that many IAV virions scored as non-infectious by traditional infectivity assays are capable of single-round infection. This fraction was not significantly affected by target or producer cell type but varied widely between different IAV strains. These data indicate that IAV exists primarily as a swarm of complementation-dependent semi-infectious virions, and thus traditional, propagation-dependent assays of infectivity may drastically misrepresent the true infectious potential of a virus population.

Here is another neat paper on the same subject if you have access,

Prisoner’s dilemma in an RNA virus.

Turner PE, Chao L. Published 1999 in Nature. doi:10.1038/18913

The evolution of competitive interactions among viruses was studied in the RNA phage phi6 at high and low multiplicities of infection (that is, at high and low ratios of infecting phage to host cells). At high multiplicities, many phage infect and reproduce in the same host cell, whereas at low multiplicities the viruses reproduce mainly as clones. An unexpected result of this study was that phage grown at high rates of co-infection increased in fitness initially, but then evolved lowered fitness. Here we show that the fitness of the high-multiplicity phage relative to their ancestors generates a pay-off matrix conforming to the prisoner’s dilemma strategy of game theory. In this strategy, defection (selfishness) evolves, despite the greater fitness pay-off that would result if all players were to cooperate. Viral cooperation and defection can be defined as, respectively, the manufacturing and sequestering of diffusible (shared) intracellular products. Because the low-multiplicity phage did not evolve lowered fitness, we attribute the evolution of selfishness to the lack of clonal structure and the mixing of unrelated genotypes at high multiplicity.



Viewing all articles
Browse latest Browse all 15

Latest Images

Trending Articles



Latest Images