In summary, our observations have shown that the 2D plots of intra-purine versus intra-pyrimidine differences in conserved gene sequences exhibit an apparent pattern in base distribution of the sequences that mimic the behaviour essentially of a polynomial of degree 2, and in some cases of degree 3. This is found over a wide cross section of sequences, from e.g., the members of the globin family, the histones, tubulins and heat shock proteins. Viral sequences such as the H5N1 neuraminidase, although known to mutate rapidly, also exhibit similar structure. We have seen that this may arise from the non-symmetrical mutation repair mechanism where e.g., a cytosine mutating to thymine in a GCrich sequence could lead to negating the mutation, to replacing the original paired guanine with adenine, or elongating the DNA by addition of a CG pair along with coupling the thymine with an adenine. Equivalent considerations apply to AT-rich sequences as well.