hi! just wanna say i love ur meta posts about the abo desire universe, its exactly my type of shit and im so thrilled someone is as interested in understanding the mechanisms of this crazy world building from a health pov as i am!!! me and my friend (who ive talked abt desire to At Length and lowkey hates me for it now) spent a good 40 minutes discussing genetics after seeing ur post over the weekend trying to understand how betas would pass down their genes since its very difficult for them to become pregnant (and im not sure they can impregnate someone else?)(and also the population dynamics over the years becoming increasingly more alpha/omega and betas slowly disappearing since their reproduction rates are way lower but thats another conversation lmao) and im actually more interested in understanding how physically that reproduction happens, since any omega regardless of primary gender can carry children and any alpha impregnate someone in the same logic. where do betas stand in that? is their ability to impregnate/become pregnant then solely dependant on their primary gender since they are considered "normal humans"? also how likely is it for little huasheng to be an enigma? if we are to assume enigmas are an entirely new mutation on blood types and say its E allele as opposed to A or i, hua yong must be Ei right? so little huasheng would have a very high likelihood of becoming an alpha/enigma but also a very low chance of being ii from shaoyou's Ai and hua yong's Ei, if thats the case...
anyways! this already got all too long i apologize! and please correct me if im wrong on anything because despite being a biologist, i am neither a geneticist (my field is marine bio) nor a omegaverse aficionado like many who watched this show, i truly stumbled on it by accident and fell in love with the characters
i hope you're well and thank you again for your posts! from user shaoyou
The thing with show's genetics is that...they didn't think it through.
I'm not a geneticist either, I'm a clinician...but my base training was in molecular biology.
Betas' population won't diminish, because they demonstrated through Gao Tu that an alpha and omega CAN believably have a beta child. Other than the first generation of betas that resulted from the Y46 infection, all subsequent betas have to be from alpha and omega parents... since betas themselves are sterile.
In order for this to be true... ABO Blood Group and A/B/O secondary gendar CANNOT be the same gene.
It took me like... a week of thinking about it on and off, but I think I figured it out.
The idea that B type blood = beta -> ONLY applies to the first generation of people that was infected with Y46. After the first generation of people died, B antigen ceases to exist.
Y46 virus carries different exons that encode for both Alpha AND Omega expression. Through respiratory infection the viral gene is spliced via viral transposons into each infected human.
The target cells which are susceptible to the splicing of Y46 and subsequent creation of secondary genders are probably the vestigial tissues from the mullerian or wolfian ducts...which may through viral signaling become pluripotent.
How the Y46 viral genome gets EXPRESSED inside each individual, is dependent on its interaction with existing human gene/proteins.
I've named viral exon 1 = alpha exon, exon 2 = omega exon, exon 3 = death exon aka the resp infection.
A antigen (found in Type A blood), INHIBITS the expression of exon 2 (the omega exon).
Exon 2 (omega) normally INHIBITS the expression of exon 1 (alpha). Therefore in the PRESENCE of Antigen A, exon 2 is inhibited, RELEASING the expression of exon 1 (think: inhibiting the inhibitor). TLDR Antigen A activates exon 1 -> the individual is an alpha.
In the absence of any blood type antigens (no A, no B,), an O type blood individual allows for the expression of exon 2, inhibiting exon 1, and they become an omega.
HOWEVER, heterozygous A type blood (aka one allele of A, and one nil allele) has VARIABLE PENETRANCE of Y46 viral expression. They may have incomplete inhibition of exon 2, and therefore incomplete expression of exon 1. A non-functional enzyme Beta is often created in this circumstance, which can be detected on immuno assays or ELISA -> leading to the sterile gender Beta.
All Betas are therefore heterozygous A type blood, but not all heterozygous A type blood are betas. Some heterozygous A individuals through good enough gene penetrance will become full fledged alphas.
As a matter of fact, after the first generation of infected humans, there can only 2 types of ABO blood typing in the world: heterozygous A, and homozygous O. Because if alphas can only procreated with omegas...and omegas is obligatory homozygous ii, then there will never be another homozygous AA.
This explains why there are Tiers of Alphas -> variable penetrance of exon 1 expression.
WITH REGARDS TO generation one survival: Antigen B also had partial inhibition of exon 2, similar to heterozygous A blood, except Antigen B's effect on exon 2 did not have too wide a range of penetrance, hence all Bs became Betas.
Mortality from Y46 had to do with the host's susceptibility to exon 3, the gene that was thought to be responsibility for the respiratory infection resulting from Y46.
Now ENIGMAS... .that I haven't figured out... likely a single nucleotide polymorphism leading to a gain of function mutation of exon 1... something something something.
