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This question is aimed mainly towards viruses with ssRNA, is transcription required, for the +ve strand RNA? If so, why?

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    $\begingroup$ I thought I had commented on this, but apparently not. Please clarify what you mean by "is transcription required, for them?" What is "them"? The word "them" would seem to refer to viruses, but this alone makes no sense. Your title suggests you mean "the translation of their +ve-strand RNA". Please ammend, and I would suggest you delete the second part of your question because its premise would appear to be incorrect. "If so why?" would do. $\endgroup$ – David Feb 28 '17 at 17:19
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I am assuming that the question is whether, in single-standed +ve RNA viruses, translation of plus-strand RNA can occur before transcription.

First, there are many different families of viruses, and there are bound to be counter-examples to whatever I say here. However, with that rider:

  1. We generally refer to replication of RNA viruses by RNA-dependent RNA polymerase, rather than transcription. I am not aware of any RNA virus that has an RNA polymerase recognizing promotors and transcribing specific genes. These viruses tend to replicate in the cytoplasm and therefore do not have access to host RNA polymerase.

  2. There has to be replication, and this tends to be conservative, rather than semi-conservative. By this I mean that when minus-strands are generated they act as templates for many plus-strands, which are needed for the virus particles.

  3. In the case of picornaviruses, such as polio, translation can occur before replication. As is common with small RNA viruses, there is a single initiation site for translation — in the case of polio, a polyprotein is produced, which is subsequently cleaved into individual polypeptides. The diagram below is from the Wikipedia entry for poliovirus and is reproduced here under the Creative Commons license. poliovirus life cycle

[Nidia H De Jesus (image and caption) - De Jesus NH (2007). "Epidemics to eradication: the modern history of poliomyelitis". Virol. J. 4: 70. DOI:10.1186/1743-422X-4-70. PMID 17623069. The cellular life cycle of poliovirus. It is initiated by binding of a poliovirion to the cell surface macromolecule CD155, which functions as the receptor (1). Uncoating of the viral RNA is mediated by receptor-dependent destabilization of the virus capsid (2). Cleavage of the viral protein VPg is performed by a cellular phosphodiesterase, and translation of the viral RNA occurs by a cap-independent (IRES-mediated) mechanism (3). Proteolytic processing of the viral polyprotein yields mature structural and non-structural proteins (4). The positive-sense RNA serves as template for complementary negative-strand synthesis, thereby producing a double-stranded RNA (replicative form, RF) (5). Initiation of many positive strands from a single negative strand produces the partially single-stranded replicative intermediate (RI) (6). The newly synthesized positive-sense RNA molecules can serve as templates for translation (7) or associate with capsid precursors to undergo encapsidation and induce the maturation cleavage of VP0 (8), which ultimately generates progeny virions. Lysis of the infected cell results in release of infectious progeny virions (9).]

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