[2][1][7] As a perforin, PV2s are able to disrupt intestinal cells altering the plasma membrane conductance and to form large pores in artificial lipid bilayers.
In PV2 toxins, the lectin would bind to target membranes through the recognition of specific glycans, acting as a delivery “B” subunit, and then the pore-forming “A” subunit would disrupt lipid bilayers forming large pores and leading to cell death, therefore constituting a true pore-forming toxin.
and those receiving sublethal doses displayed neurological signs including weakness and lethargy, low head and bent down position (ortopneic), half-closed eyes, taquipnea, hirsute hair, extreme abduction of the rear limbs, paresia and were not able to support their body weight (tetraplegic), among others.
At the system level, oral administration of PV2 induces large morphological changes on mice intestine mucosa, reducing its absorptive surface.
[9][10] According to the fossil record, some 3 MYA, when Pomacea diverged from Marisa and began laying eggs above the water, these two genes were subjected to extensive duplication and these unrelated proteins were combined by a covalent bond resulting in the dimerization into PV2 AB toxin that co-opted to new roles.