Dysfunction in respiration and osmotic regulation of larval Japanese flounder affected by viral epidermal hyperplasia

Flounder herpesvirus (FHV) induces epidermal hyperplasia in larval Japanese flounder Paralichthys olivaceus. We examined the influence of ambient oxygen and salinity concentrations on mortality of flounder larvae by FHV infection. FHV-infected fish showed markedly higher mortality than uninfected fish under normoxia (partial oxygen pressure; PO2 = ca. 160 Torr), but survived at high rates under hyperoxia (PO2 = ca. 280 Torr or higher) as in uninfected fish. In the PO2 range from 100 to 400 Torr, infected fish always displayed lower levels of oxygen consumption (MO2) compared to the uninfected fish. Under PO2 of 260 Torr, the 48 h-survival rate of infected fish in diluted seawater (salinity 8 or 16 ppt) was much higher than that in full-strength seawater (salinity 32 ppt). Whole-mount immunocytochemistry to detect Nasup(+)/Ksup(+)-ATPase and Nasup(+)/Ksup(+)/2Clsup(-) cotransporter of the skin of both infected and uninfected larvae revealed that the infected larvae had a significantly lower number of chloride cells. These results suggest that flounder larvae infected with FHV die of dysfunction in respiration and osmotic regulation.