Supervirus RBHFMR

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.

        ----------------

        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)