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Simple Summary: The cause of Chinese mitten crab Eriocheir sinensis hepatopancreas necrosis disease (HPND) remains a mystery. In this study, metatranscriptomics sequencing was conducted to characterize the changes in the structure and gene expression of hepatopancreatic flora of crabs with and without typical symptoms of HPND; an imbalance of hepatopancreatic flora can be found in the crab with HPND, and the detected microbial taxa decreased, whereas the prevalence of Spiroplasma eriocheiris significantly increased in the hepatopancreatic flora of crabs with typical symptoms of HPND, and the relative abundances of the virus and microsporidia in crabs with HPND were very low and did not increase with disease progression. The differentially-expressed genes (DEGs) in hepatopancreatic flora between crabs with and without HPND were enriched ribosome, retinol metabolism, and biosynthesis of unsaturated fatty acid KEGG pathways. These results suggested that an imbalance of hepatopancreatic flora was associated with crab HPND, and the enriched pathways of DEGs were associated with the pathological mechanism of HPND. Hepatopancreas necrosis disease (HPND) of the Chinese mitten crab Eriocheir sinensis causes huge economic loss in China. However, the pathogenic factors and pathogenesis are still a matter of dissension. To search for potential pathogens, the hepatopancreatic flora of diseased crabs with mild symptoms, diseased crabs with severe symptoms, and crabs without visible symptoms were investigated using metatranscriptomics sequencing. The prevalence of Absidia glauca and Candidatus Synechococcus spongiarum decreased, whereas the prevalence of Spiroplasma eriocheiris increased in the hepatopancreatic flora of crabs with HPND. Homologous sequences of 34 viral species and 4 Microsporidian species were found in the crab hepatopancreas without any significant differences between crabs with and without HPND. Moreover, DEGs in the hepatopancreatic flora between crabs with severe symptoms and without visible symptoms were enriched in the ribosome, retinol metabolism, metabolism of xenobiotics by cytochrome P450, drug metabolism—cytochrome P450, biosynthesis of unsaturated fatty acids, and other glycan degradation. Moreover, the relative abundance of functions of DEDs in the hepatopancreatic flora changed with the pathogenesis process. These results suggested that imbalance of hepatopancreatic flora was associated with crab HPND. The identified DEGs were perhaps involved in the pathological mechanism of HPND; nonetheless, HPND did not occur due to virus or microsporidia infection. [ABSTRACT FROM AUTHOR]