Osmoregulation and ammonia removal are among key physiological processes that take place in gills and affect fish homeostasis and well-being. These processes can be disrupted by numerous environmental factors, but also by viral infections, especially those leading to severe gill disorders. The mechanisms of how viruses disrupt osmoregulation and ammonia removal in fish have not been extensively studied. We propose further exploration of the molecular and functional basis of viral induced gill disorders by studying the gene expression and enzyme activity of -ATPases (NKA) and ammonia transporters in the gills and kidney of common carp during infection with two viruses: carp edema virus (CEV) and cyprinid herpesvirus 3 (CyHV-3). In the case of NKA, the expression of subunit α of selected NKA was affected by both viruses; however, no discernible trends were observed in the gills and kidneys. The enzyme activity of NKA was significantly reduced in the gills during infection with both CEV and CyHV-3. Moreover, our immunohistochemical studies showed that during infection with CEV and CyHV-3, NKA-rich cells are transferred from the primary lamellae to the more superficial space and to the secondary lamellae of the gills. In the case of ammonia transporters, both CEV and CyHV-3 infection resulted in downregulation of the expression of major transporters gdh1, Rhag, and Rhbg, allowing us to partly explain the ammonia accumulation in blood observed during infection with these viruses. This study highlighted that virus induced gill disorders may lead to disruption of osmoregulation and ammonia removal by dysregulating the expression and activity of NKA and ammonia transporters.