Singapore grouper iridovirus protein VP088 is essential for viral infectivity

Abstract

Viral infection is a great challenge in healthcare and agriculture. The Singapore grouper iridovirus (SGIV) is highly infectious to numerous marine fishes and increasingly threatens mariculture and wildlife conservation. SGIV intervention is not available because little is known about key players and their precise roles in SGVI infection. Here we report the precise role of VP088 as a key player in SGIV infection. VP088 was verified as an envelope protein encoded by late gene orf088. We show that SGIV could be neutralized with an antibody against VP088. Depletion or deletion of VP088 significantly suppresses SGIV infection without altering viral gene expression and host responses. By precisely quantifying the genome copy numbers of host cells and virions, we reveal that VP088 deletion dramatically reduces SGIV infectivity through inhibiting virus entry without altering viral pathogenicity, genome stability and replication and progeny virus release. These results pinpoint that VP088 is a key player in SGIV entry and represents an ideal target for SGIV intervention.

Development of a gene-deleted live attenuated candidate vaccine against fish virus (ISKNV) with low pathogenicity and high protection

“…For example, the knockout of non-virion gene in Snakehead rhabdovirus did not influence viral replication in cultured fish cells, and it had a similar lethality with the parental virus in zebrafish (Alonso et al, 2004). On the contrary, deletion of some genes, such as ORF057R of Ambystoma tigrinum virus (Jancovich and Jacobs, 2011), and VP51 (Yu et al, 2017) and VP88 (Yuan et al, 2016) of Singapore grouper iridovirus, resulted in the attenuation of virulence. However, the protective effects of these mutant strains were not mentioned in the articles.…”

A comparative review of viral entry and attachment during large and giant dsDNA virus infections

“…A56-K2 complex interacts with A16 and G9 subunits and prevents the superinfection [ 158 ]. Iridoviruses Tiger frog virus, Ranavirus genus HepG2 cells pH, cholesterol, dynamin, actin and caveolin-mediated endocytosis [ 159 ] Frog virus 3, Ranavirus genus BHK-21 cells Low pH and clathrin-mediated endocytosis [ 160 ] ISKNV, Megalocytivirus Mandarin fish fry cells Major capsid protein ∞ caveolin-1 and induces caveolin-endocytosis [ 161 , 162 ] SGIV Grouper spleen cell line pH-dependent clathrin-endocytosis and macropinocytosis [ 163 ]; the deletion of VP088 envelope protein inhibits viral entry [ 164 ]. Large yellow croaker iridovirus Bluegill fry (BF-2) cells 037L (RGD motif) ∞ integrins inducing fusion [ 165 , 166 ] …”

“…Frog virus 3, tiger frog virus, and infectious spleen and kidney necrosis virus enter BHK-21, HepG2 and Mandarin fish fry cells, respectively, by endocytosis [ 159 – 162 ]. The VP088 protein encoded by SGIV facilitates both endocytosis and macropinocytosis into a grouper spleen cell line [ 163 , 164 ].…”