Hi Bessie and welcome to the group,
The CD6-A mutation is classified as a mild beta thalassemia mutation and the -101 C>T mutation is classified as a silent mutation, which will show only a slight imbalance in beta and alpha globin chains. -101 C>T is found in many cases of mild intermedia. Together, they will technically be described as intermedia but would most likely behave more as a thal minor. I think the doctors are right to not be concerned. Your own mutation is barely discernible by blood tests because it is so mild. I found a nice table at
http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=gene.chapter.b-thal#b-thal.T8 and both mutations are listed in Table 5. Mild and Silent HBB Mutations Causing β-Thalassemia. I can't copy the table here but you will find both mutations there.
Silent mutations, which are characterized by normal hematologic findings and defined only by a mildly unbalanced α/β-globin chain synthesis ratio, result from mutation of the distal CACCC box, the 5' unbalanced region, the polyadenylation signal, and some splicing defects (see Table 5).
Calling this "light" intermedia is more of a characterization than a classification. It is simply a way to describe what is technically intermedia but with few symptoms. Neither of these mutations reduces the beta globin significantly, so hemoglobin levels should be fairly high for an intermedia and most likely more similar to the Hb of a minor.
Manal, although Hb Knossos is a silent mutation because of the normal HbA2 level, when combined with beta thal traits, it can lead to intermedia and even major, just as Lepore and HbE can. Knossos, in turn, can also be modified by the delta globin gene. In the case of Hb Knossos, the silent classification is because of the normal HbA2 levels. This makes it hard to detect, but like Lepore and HbE, it's outcome when combined with beta thal trait varies depending on the specific beta trait and also other genetic factors, such as presence or absence of hereditary persistence of fetal hemoglobin. In Bessie's case, both genes are known to result in a fairly asymptomatic condition and the combination of the two results in very mild intermedia. Lisa was beta thal Lepore and again, this can range from non-transfusing intermedia to transfusion dependent major. There are often other genetic factors that add or subtract severity. I think we will know much more in the coming years, as I am already seeing an increase of relevant material on the net. Progress in mapping the various genetic combinations is moving fast.