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The vaccine consists of an auxotroph<jats:named-content content-type=\"genus-species\">Mycobacterium tuberculosis<\/jats:named-content>strain that coexpresses HIV antigens. Utilizing an infant rhesus macaque model, we have previously shown that this attenuated<jats:named-content content-type=\"genus-species\">M. tuberculosis<\/jats:named-content>(A<jats:italic>Mtb<\/jats:italic>)-simian immunodeficiency virus (SIV) vaccine is immunogenic, and although the vaccine did not prevent oral SIV infection, a subset of vaccinated animals was able to partially control virus replication. However, unexpectedly, vaccinated infants required fewer SIV exposures to become infected compared to naive controls. Considering that the current TB vaccine,<jats:named-content content-type=\"genus-species\">Mycobacterium bovis<\/jats:named-content>bacillus Calmette-Gu\u00e9rin (BCG), can induce potent innate immune responses and confer pathogen-unspecific trained immunity, we hypothesized that an imbalance between enhanced myeloid cell function and immune activation might have influenced the outcome of oral SIV challenge in A<jats:italic>Mtb<\/jats:italic>-SIV-vaccinated infants. To address this question, we used archived samples from unchallenged animals from our previous A<jats:italic>Mtb<\/jats:italic>-SIV vaccine studies and vaccinated additional infant macaques with BCG or A<jats:italic>Mtb<\/jats:italic>only. Our results show that vaccinated infants, regardless of vaccine strain or regimen, had enhanced myeloid cell responses. However, CD4<jats:sup>+<\/jats:sup>T cells were concurrently activated, and the persistence of these activated target cells in oral and\/or gastrointestinal tissues may have facilitated oral SIV infection. Immune activation was more pronounced in BCG-vaccinated infant macaques than in A<jats:italic>Mtb<\/jats:italic>-vaccinated infant macaques, indicating a role for vaccine attenuation. 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