Nobody has tested any boas to see which are T-neg and which are T-pos. At least that is what Dave Barker told me a couple of years ago.
There are many mutant genes that produce T-pos albino. IMHO, the name is useless for explaining the biochemistry involved.
The results depend on whether the mutant gene for T-pos albino is or is not an allele (different form of the same gene) of T-neg albino. If independent mutants, the results also depend on whether one or both mutant genes are dominant, recessive, or codominant to the normal alleles.
In lab mice there are mutant genes that produce partially functional tyrosinase and that are alleles of the albino (T-neg albino) mutant gene. The heterozygote is approximately mid way between the two homozygotes. There is anecdotal evidence that a mutant named ultrahypomelanistic in corn snakes acts the same way with the corn's amelanistic (T-neg albino) mutant gene.
In black rat snakes, there are two independent recessive mutant genes (T-neg albino and T-pos albino). Crossing them has produced normal-looking, double heterozygous babies.
In cats dominant white x albino would produce either all dominant whites or 1/2 dominant white and 1/2 normal. These are independent mutants, but dominant white is dominant to its normal allele, while albino is recessive to its normal allele.
Clear as mud? 
In boa constrictors, the most likely scenario is like the black rat snake, but the other possibilities may show up. Salmon x albino would be analogous to the cat example. Salmon is T-pos, but whether or not it is a T-pos albino depends on how you define "albino".
Paul Hollander