Some mammalian and fish double-stranded (ds)RNA viruses hijack lipid droplets (LDs) during their replication cycle, however, our understanding of how avian dsRNA viruses interact with LDs is incomplete. Here, we report data from avian reovirus (ARV) and infectious bursal disease virus (IBDV)- infected cells. Following ARV infection, there was a significant increase in the number (p < 0.0001) and size (p < 0.0001) of LDs compared to mock-infected controls, 6-24 hours post infection (hpi), in both immortalized LMH cells and primary gut cultures. Treatment with the ACCA inhibitor, TOFA, reduced ARV-mediated LD induction, indicating de novo lipogenesis was partially involved in their formation. Moreover, ARV infection decreased the expression of PGC-1α (p < 0.05) and ELOVL2 (p < 0.001). Previous reports demonstrated that inhibition of PGC-1α and ELOVL expression in mice led to cellular lipid accumulation and hepatic steatosis, suggesting ARV could upregulate LD synthesis by decreasing expression of these genes. However, it is unclear whether LD induction was pro- or anti-viral, since both TOFA treatment to inhibit LD synthesis, and oleic acid/palmitic acid treatment to overexpress LDs did not significantly alter ARV replication. In contrast, infection with IBDV did not substantially increase the size or number of LDs, or significantly reduce the expression of PGC-1α and ELOVL2. In contrast to some other dsRNA viruses like rotavirus and mammalian orthoreovirus, neither ARV nor IBDV cytoplasmic puncta colocalized with LDs. Taken together, our findings demonstrate that the two dsRNA viruses had distinct effects on cellular lipid metabolism.