J Paramyxovirus (JPV) was first isolated from moribund mice with hemorrhagic lung lesions in Australia in 1972. JPV is a paramyxovirus with a non-segmented, negative-strand RNA-genome. JPV is currently included in a proposed jeilongvirus genus within the paramyxoviridae family. Small hydrophobic (SH) protein is an integral membrane protein present in jeilongviruses, rubulaviruses, and pneumoviruses. SH has a role in blocking apoptosis by inhibiting the tumor necrosis factor-alpha (TNF-α)-mediated extrinsic apoptotic pathway. JPV caused severe disease in mice. We used JPV to study the role of SH in pathogenicity using laboratory mouse model. Deletion of SH resulted in the attenuation of JPV. We found that the SH of JPV can be replaced with SH of mumps virus (MuV) or respiratory syncytial virus (RSV) to restore the virulence of JPV-ΔSH. Similar functions of these SH proteins despite the lack of sequence similarity of JPV, MuV, and RSV SH genes, suggests the structural resemblance of the SH of paramyxoviruses. JPV genome is large when compared to other paramyxoviruses. The reverse genetics system of JPV allows us to incorporate foreign nucleic acid sequences into its genome to develop JPV-based vectored vaccines. We have replaced the SH gene of JPV with the hemagglutinin (HA) of a highly pathogenic avian influenza H5N1. Recombinant JPV expressing HA protected mice from a lethal challenge with H5N1. Together, these results show that the deletion of genes or gene segments responsible for virulence is a safe and efficient way to develop JPV based vaccines.