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Subject to RNA‐based adaptive immune responses in their hosts, viruses have evolved a variety of genes encoding proteins capable of suppressing the immune response.
Eukaryotic viruses have evolved a variety of translational control strategies to facilitate expression of downstream open reading frames (ORFs) on polycistronic mRNAs and examples have been described at all three steps of protein synthesis - initiation, elongation and termination [1].
However, as in other pathways of innate response, viruses have evolved a variety of strategies to prevent or overcome the activation of PKR in infected cells (reviewed in [12]).
On the other hand, viruses have evolved a huge arsenal of strategies meant to either counteract or deal with this destructive process to ensure their survival.
Being obligatory intracellular parasites, viruses have evolved a variety of mechanisms to modulate specific host signal-transduction pathways to favour their own replication.
To counteract host cell RNAi-mediated immunity, viruses have evolved a variety of countermeasures, one of which is to encode RNA silencing suppressor (RSS) proteins [ 10- 14].
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Human immunodeficiency virus, herpes simplex viruses, papillomaviruses and hepatitis B and C virus have evolved a variety of strategies to persistently infect man [1] [4].
That EBV-derived plasmids have similar rates and are so much smaller in length indicates that the virus has evolved a particularly efficient mechanism to persist in proliferating cells.
In the virosphere, the conventional wisdom is that viruses have evolved from a few distinctive lineages separately.
These results suggest that RNA viruses have evolved to use a common strategy to target a critical molecule in autophagy to benefit their growth.
Many viruses have evolved to trigger an incomplete autophagy response in virus-infected cells to benefit their replications.
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