Recombination vs. Phenotypic mixing

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Apoplexy__

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Alright, viral genetics question: How can you tell from the stem of the question that the mechanism of increased viral virulence is Recombination vs. Phenotypic mixing? My understanding is this:

Phenotypic mixing: Emphasis on entering cell:
Virus A: Can enter human cells
Virus B: Can't enter human cells, but can enter non-human experimental cells

Non-human cells infected with Viruses A + B -->
Progeny can enter human cells -->
Progeny of progeny can't enter human cells

Seen in any type of virus - Due to post-translational mixing of proteins.

----------------

Recombination: Emphasis on cytotoxicity:
Viruses A and B both can enter human cells but can't kill them

Human cells infected with Viruses A + B -->
Progeny kill human cells

Seen in dsDNA viruses only - Due to pre-transcriptional crossing over of DNA.

----------------

Is that all right? Any important points I'm missing?
 
Alright, viral genetics question: How can you tell from the stem of the question that the mechanism of increased viral virulence is Recombination vs. Phenotypic mixing? My understanding is this:

Phenotypic mixing: Emphasis on entering cell:
Virus A: Can enter human cells
Virus B: Can't enter human cells, but can enter non-human experimental cells

Non-human cells infected with Viruses A + B -->
Progeny can enter human cells -->
Progeny of progeny can't enter human cells

Seen in any type of virus - Due to post-translational mixing of proteins.

----------------

Recombination: Emphasis on cytotoxicity:
Viruses A and B both can enter human cells but can't kill them

Human cells infected with Viruses A + B -->
Progeny kill human cells

Seen in dsDNA viruses only - Due to pre-transcriptional crossing over of DNA.

----------------

Is that all right? Any important points I'm missing?

That sounds about right. I am not sure how much increasing phenotypic mixing can confer virulence however--the progeny (F1) can infect the cells, but then the road ends there. I would imagine for any clinical symptoms to arise, it would require a few more generations. I have never thought about it with respect to entry vs cytotoxicity, but that it is a good way to look at it. The only thing is I wonder if dsRNA could recombine? In a theoretical example of course--I cant think of any dsRNA except for reoviridae and they wouldn't recombine, they would reassort (segmented virus)
 
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