Lickity-split

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SARS-CoV-2, the virus that causes covid, can only infect cells expressing a certain protein called ACE2

ACE2 is expressed widely in nasal cavity epithelial cells but not in olfactory sensory neurons. 

Seo et al. (2021) studied potential nasal targets for SARS-CoV-2 using golden hamsters as a model organism (commonly used as a proxy for humans in virology studies)

They found ACE2 expression in the main olfactory bulb epithelium (MOE, your “normal” nose organ) as well as the vomeronasal organ (VNO)

Several cell types in the VNO were able to be infected and they also found significant inflammatory activity (macrophage activation, apoptotic cells, etc) 

The specifics of how covid actually causes dysosmia are not known for sure but epithelial damage by local inflammatory immune responses likely plays a role, especially because sensory neurons themselves are not affected (Bilinska, & Butowt, 2020). Therefore I would suggest a potential similar effect of VNO dysfunction as we see in the main olfactory bulb

From Seo et al.: “Considering the function of the VNO, infection and subsequent pathologic changes may affect the behavior of Syrian hamsters”

If it stands to reason that omegaverse individuals have functioning VNOs similar to members of the animal kingdom, then it is more than reasonable to conclude that covid may cause them to lose not only their main olfactory function, but also their VNO function as well

 References: (1) (2)