Final answer:
Individuals with the h allele cannot produce fucosyltransferase, which is needed for H antigen formation, leading to the 'hh' or Bombay phenotype. This issue is different from sickle cell carriers and those unable to produce MHC I molecules, both of which have significant health implications.
Step-by-step explanation:
Persons who inherit the h allele do not produce fucosyltransferase necessary for the formation of the H antigen structure on red blood cells. The presence of the fucosyltransferase enzyme allows for the attachment of a fucose sugar to the precursor substance on the red blood cell surface, which is a critical step in the creation of the H antigen. Without the enzyme due to inheriting the h allele, individuals cannot synthesize the H antigen, which serves as a foundation for ABO blood group antigens. Carriers of the mutant recessive allele, such as in conditions like sickle cell anemia, may not express the associated disorder if they have only one copy of the allele. However, in the case of the H antigen, the lack of production of the fucosyltransferase enzyme leads directly to the 'hh' or Bombay phenotype.
Moreover, the inability to synthesize MHC I molecules, which is not related to the initial H antigen issue, would lead to severe immunodeficiency since these molecules are crucial for the immune system to recognize infected or aberrant cells.