Supervirus RBHFMR
Rabies + bubonic plague + HIV + flu virus + Malaria + rotavirus
makes a MEGAVIRUS
Lab made viruses to wipe out gentile population
-- Contagious disease (Smallpox, Leprosy, Typhoid Fever, Influenza, Rotavirus, Malaria, Measles, whooping cough, mumps, Giardiasis, Dermatophytosis, flu virus, etc)
-- combine it with lethal disease such as Aids (also lab made), rabies, ebola, tb, avian flu, bubonic plague, etc
Example: Combine rabies with the ability of a flu virus to spread quickly through the air, and you might have the makings of a zombie apocalypse.
Example 2: Supervirus RBHFMR
Rabies + bubonic plague + HIV + flu virus + Malaria + rotavirus (rota also lab made)
makes a MEGAVIRUS
-- spread it
-- if feeling merciful, add diseases that cause euphoria/relaxation/pleasant feelings, to alleviate suffering
-- if feeling evil or vengeful, add diseases that causes extra suffering
Use both recombination with phenotypic. Phenotypic for entering, recombination for the ability to kill human cells, i.e. "cytolethality"
recombine non-segmented virus
reassort segmented virus
we caused the black death bubonic plague in europe back in the middle ages.
and we created aids/hiv strain.
"Zombie Virus" Possible via Rabies-Flu Hybrid?
Highly improbable genetic tweak could create mutant virus.
Recombination vs. Phenotypic mixing
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.
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Is that all right? Any important points I'm missing?
Step 1 experience (2014)
Step 2 experience (2015)
Taking Step 2CS as a DO
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.
----------------
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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Supervirus RBHFMR Rabies + bubonic plague + HIV + flu virus + Malaria + rotavirus makes a MEGAVIRUS Lab made viruses to wipe out gentile p...
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ReplyDeleteThe Great Eye controls everything.
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