Candida albicansandStreptococcus mutansare known to synergistically interact with each other in the oral cavity. For example, glucosyltransferase B (GtfB), secreted byS. mutans, can bind to theC. albicanscell surface, promoting dual-species biofilm formation. However, the fungal factors mediating interactions withS. mutansare unknown. TheC. albicansadhesins Als1, Als3, and Hwp1 are key players inC. albicanssingle-species biofilm formation, but their roles, if any, in interacting withS. mutanshave not been assessed. Here, we investigated the roles of theC. albicanscell wall adhesins Als1, Als3, and Hwp1 on forming dual-species biofilms withS. mutans. We assessed the abilities of theC. albicanswild-typeals1Δ/Δ,als3Δ/Δ,als1Δ/Δ/als3Δ/Δ, andhwp1Δ/Δ strains to form dual-species biofilms withS. mutansby measuring optical density, metabolic activity, cell enumeration, biomass, thickness, and architecture of the biofilms. We observed that theC. albicanswild-type strain formed enhanced dual-species biofilms in the presence ofS. mutansin these different biofilm assays, confirming thatC. albicansandS. mutanssynergistically interact in the context of biofilms. Our results reveal thatC. albicansAls1 and Hwp1 are major players in interacting withS. mutans, since dual-species biofilm formation was not enhanced when theals1Δ/Δ orhwp1Δ/Δ strains were cultured withS. mutansin dual-species biofilms. Als3, however, does not seem to play a clear role in interacting withS. mutansin dual-species biofilm formation. Overall, our data suggest that theC. albicansadhesins Als1 and Hwp1 function to modulate interactions withS. mutansand could be potential targets for future therapeutics.