Equivalent residueswithin the same predicted VP2 region disrupt VLS formation across non-RVA.We also observed interspecies VLS formation, most notably between theclosely related pairs RVA–RVC, RVH–RVJ, and RVD–RVF.Interestingly, substituting the N-terminal region of VP2 from RVB with thatof VP2 from RVG supported VLS formation with NSP5 from RVB in avian cells.Elucidating the formation of viroplasms is essential for developingstrategies to halt infection across RV species A to J. This evidence concerns the gene SPECC1 and infection.