  Over the past 60 years, the Mycobacterium bovis bacille Calmette-Gu\'erin
(BCG) has been used worldwide to prevent tuberculosis (TB). However, BCG has
shown a very variable efficacy in different trials, showing a wide range of
protection in adults against pulmonary TB. Previous studies indicate that this
failure is related to pre-existing immune response to antigens that are common
to environmental sources of mycobacterial antigens and Mycobacterium
tuberculosis. Specifically, two different mechanisms have been hypothesized:
the masking, (previous sensitization confers some level of protection against
TB), and the blocking (previous immune response prevent vaccine taking of a new
TB vaccine), effects. In this work we introduce a series of models to
discriminate between masking and blocking mechanisms and address their relative
likelihood. The application of our models to interpret the results coming from
the BCG-REVAC clinical trials, specifically designed for the study of sources
of efficacy variability yields estimates that are consistent with high levels
of blocking (41% in Manaus -95% C.I. [14%-68%]- and 96% in Salvador -95% C.I.
[52%-100%]-), and no support for masking to play any relevant role in modifying
vaccine efficacy either alone or aside blocking. The quantification of these
effects around a plausible model constitutes a relevant step towards impact
evaluation of novel anti-tuberculosis vaccines, which are susceptible of being
affected by similar effects if applied on individuals previously exposed to
mycobacterial antigens.
