Abstract
It is conceivable that an RNA virus could use a polysome, that is, a string of ribosomes covering the RNA strand, to protect the genetic material from degradation inside a host cell. This paper discusses how such a virus might operate, and how its presence might be detected by ribosome profiling. There are two possible forms for such a polysomally protected virus, depending upon whether just the forward strand or both the forward and complementary strands can be encased by ribosomes (these will be termed type 1 and type 2, respectively). It is argued that in the type 2 case the viral RNA would evolve an ambigrammatic property, whereby the viral genes are free of stop codons in a reverse reading frame (with forward and reverse codons aligned). Recent observations of ribosome profiles of ambigrammatic narnavirus sequences are consistent with our predictions for the type 2 case.
Highlights
A canonical model for the structure of a virus [1] consists of genetic material encased in a capsid composed of a protein shell
If viral RNA can be completely covered with a chain of ribosomes, it could be well protected from defence mechanisms of host organism, because the exterior of the package presents molecules which are part of the host cells
We argue that a recent observation of two ambigrammatic sequences in the C. narnavirus 1 system reported in [8, 19] is a very strong candidate to be a PolyProV2 type virus
Summary
A canonical model for the structure of a virus [1] consists of genetic material encased in a capsid composed of a protein shell. The covering structure, consisting of a chain of ribosomes attached to the viral RNA, would be analogous to a polysome [3,4,5,6], and for this reason we shall refer to these systems as ‘polysomally protected viruses’, abbreviated hereafter as PolyProV. Our results for C. narnavirus 1 and for Zheijiang mosquito virus 3 indicate that the complementary strands do not code for a functional protein These two likely candidates for polysomally protected viruses are both narnaviruses, which along with viroids and virusoids [22], are the simplest infectious agents. Our theory considers a quite different phenomenon, where the ribosomes are stationary because their release at the 3 end is blocked
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