Apical membrane antigen 1 (AMA1) is one of the leading candidate antigens for inclusion in a subunit vaccine against blood-stage malaria. However, the efficacy of antibody-inducing recombinant AMA1 protein vaccines in Phase IIa/b clinical trials to date remains disappointing. Here we describe the development of recombinant human adenovirus serotype 5 (AdHu5) and modified vaccinia virus Ankara (MVA) vectors encoding AMA1 from the Plasmodium chabaudi chabaudi strain AS (PccAS). These vectors, when used in a heterologous prime-boost regime in BALB/c mice, are capable of inducing strong transgene-specific humoral as well as cellular immune responses. We show that this vaccination regime is protective against a non-lethal PccAS blood-stage challenge, resulting in reduced peak parasitemias. The role of vaccine-induced, AMA1-specific antibodies and T cells in mediating anti-parasite effect was investigated by in vivo depletion of CD4+ T cells and adoptive transfer studies into naive and immunodeficient mice. Depletion of CD4+ T cells led to a loss of vaccine-induced protection. Adoptive transfer studies confirmed that efficacy is mediated by both CD4+ T cells and antibodies functioning in the context of an intact immune system. Unlike previous studies, these results confirm that antigen-specific CD4+ T cells, induced by a clinically relevant vaccine delivery platform, can make a significant contribution to vaccine blood-stage efficacy in the P. chabaudi model. Given cell-mediated immunity may also contribute to parasite control in human malaria, these data support the clinical development of viral vectored vaccines that induce both T cell and antibodies against P. falciparum blood-stage malaria antigens like AMA1.