HIV and sulfonamide allergy:
Aromatic sulfonamides are an important group of antibiotics. Up to 3% of patients treated with sulfonamides present with exanthema and sometimes with fever and mild elevation of liver enzymes [45, 46]. In patients, these reactions give rise to numerous T cell clones, many of which have been investigated in great detail [47, 48]. One of the sulfamethoxazole reactive T cell clones (“H13”) was analyzed for reactivity to 11 other sulfanilamides and patients were found to react to half of these. Molecular docking and computational analysis revealed that the reactive sulfanilamides were bound to TCR Vβ20.1, while the non-reactive sulfanilamides failed to bind [48][50]. Interestingly, the binding site was a common site on this TCRVβ chain, which is present in all individuals (in 1-3% of all T cells).
These data may explain two questions concerning DH to sulfonamides:
a) The incidence of DHR to sulfonamides rises from 3 to 33 % in HIV+ patients receiving sulfamethoxazole/trimethoprim, either as prophylaxis [4, 49], or as a treatment for pneumocystis pneumonia [50]. One possible explanation could be that such HIV+ patients are undergoing a massive immune stimulation and that under these conditions the binding of sulfamethoxazole to TCR Vβ20.1 becomes more functionally and clinically relevant. b) “Sulfa-allergy” is a term mostly used in the USA and may describe a rash appearing after exposure to various sulfonamide-containing drugs [5]. This ominous “sulfa-allergy” may be the result of sulfamethoxazole binding to the common site on TCRVβ20-1, which, in those people where this T cell subset is already activated may result in symptoms [9].