Hiv-3
Combine Contagious flu & contagious common cough with HIV-1/HIV-2
HIV-4
Add malaria and/or smallpox to HIV-3
HIV-5
Add rabies to HIV-4
HIV-6
combine yersinia pestis with a lentivirus to create a HIV-bubonic plague supervirus
Create more variants end humanity.
Or create viruses for specific races based on their DNA.
If eliminate africa create virus taht kills africans only based on their dna. attacks a specific dna haplo
If eliminate asians, indians, chinese, different specified viri for each
Niche viruses
Why? humans wiped out ocean life also animal life on planet earth
many animals extinct
Make earth desolate project
---------------------------
Make earth like mars, mercury, venus, jupiter, uranus..
devoid of any life
HIV 1-10 to eliminate human race
Viruses that target animal life
Viruses that target plant life
Make Earth desolate
Monday, February 18, 2019
Thursday, February 14, 2019
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)
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)
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