Severe fever with thrombocytopenia syndrome virus (SFTSV) is an emerging bandavirus (order Bunyavirales) that causes high case fatality ratios in humans and cats. Since its discovery in 2009 in China, annual case counts have steadily risen across its endemic range. In addition, one prominent SFTSV tick vector, Haemaphysalis longicornis, has become an invasive species throughout the world. Though SFTSV infections have thus far been limited to Southeast Asia, the genetically similar heartland bandavirus (HRTV) was discovered in the United States in 2011. Despite the significant public health threat posed by these viruses, no vaccines currently exist. To address this need, we evaluated the safety and efficacy of a recombinant vesicular stomatitis virus (rVSV) vaccine encoding the SFTSV glycoproteins (rVSV-SFTSV) in an interferon-incompetent mouse model of lethal SFTSV infection. A single dose rVSV-SFTSV was well-tolerated and cross-protected mice from lethal SFTSV and mouse-adapted HRTV challenge. However, rVSV-SFTSV was highly attenuated in cell culture, likely due to a mismatch between the intracellular retention of SFTSV glycoproteins GN/GC and the cell surface assembly sites of VSV. Sequence homology identified a putative coatomer complex I (COPI) binding motif in the cytosolic tail of GC. Genetic disruption of this motif redistributed chimeric fluorescent reporter proteins and full-length GN/GC to the cell surface and correlated with more rapid recovery of infectious VSV pseudotypes. The same change in HRTV GN/GC similarly increased yields of infectious VSV pseudotypes. This work demonstrates rVSV-SFTSV is a safe vaccine candidate whose immunogenicity may be enhanced by genetic alteration of retention signals encoded within the SFTSV glycoproteins. Future rVSVs encoding bandavirus glycoproteins may also be improved by genetic ablation of the putative COPI binding site in the GC.