[3] Lymphocystiviruses infect more than 140 freshwater and marine species,[4] spanning at least 42 host families worldwide,[5] causing the chronic, self-limiting clinical disease, lymphocystis.

The LCDV-1 genome is approximately 102.7 kilobase pairs (kbp) in length, with 195 potential open reading frames (ORF), and codes for two DNA-dependent RNA polymerase subunits, a DNA methyltransferase, a DNA polymerase, a guanosine triphosphate phosphohydrolase (GTPase), a helicase, protein kinases, a ribonucleoside diphosphate reductase, and zinc-finger proteins, among others.

As lymphocystis viruses are not easily grown in cell culture,[4] diagnosis is based on clinical signs, gross pathology, histopathology, serology, and/or polymerase chain reaction (PCR)-based molecular assays.

[16] In a recent comparison of lymphocystis histopathology of four unrelated marine species, lesions consistently associated with lymphocystis included hypertrophied cells displaying irregular nuclei, basophilic cytoplasmic inclusion bodies that stained positively via Feulgen and Mann's reaction and Periodic acid-Shiff (PAS)-positive hyaline capsules.

[5] Hyaline capsules arise from the extracellular matrix that is produced by the infected cells,[14] and are composed of sulphated and carboxylated glycoproteins (acid mucopolysaccharides).

[14] In contrast, the inclusion body shape, distribution of viral particles within the cytoplasm and overall appearance of lymphocystis nodules varied by species.

[5] The species examined in this study included the white-spotted puffer (Arothron hispidus), the Japanese sea bass (Lateolabrax japonicus), olive flounder (Paralichthys olivaceus) and the "sting fish" or Schlegel's black rockfish (Sebastes schegeli) [5] Several serologic assays have been developed to identify LCDV infections, including flow cytometry,[17] immunoblot,[17][18] and immunofluorescence.