Dynamics of Virus Shedding and In Situ Confirmation of Chelonid Herpesvirus 5 in Hawaiian Green Turtles With Fibropapillomatosis

• Published in: Veterinary pathology Vol. 52; no. 6; pp. 1195 - 1201
• Main Authors: Work, T. M., Dagenais, J., Balazs, G. H., Schettle, N., Ackermann, M.
• Format: Journal Article
• Language: English
• Published: Los Angeles, CA SAGE Publications 01-11-2015
• Subjects: Animals; Cercopithecus aethiops; Fibroma - virology; Genes, Reporter; Herpesviridae - genetics; Herpesviridae - isolation & purification; Herpesviridae - physiology; Herpesviridae Infections - virology; Inclusion Bodies, Viral; Intranuclear Inclusion Bodies; Papilloma - virology; Skin Neoplasms - virology; Turtles; Vero Cells; Virus Shedding; histopathology; fibropapillomatosis; green turtle; shedding; herpesvirus
• ISSN: 0300-9858; 1544-2217
• DOI: 10.1177/0300985814560236

Cancers in humans and animals can be caused by viruses, but virus-induced tumors are considered to be poor sites for replication of intact virions (lytic replication). Fibropapillomatosis (FP) is a neoplastic disease associated with a herpesvirus, chelonid herpesvirus 5 (ChHV5), that affects green turtles globally. ChHV5 probably replicates in epidermal cells of tumors, because epidermal intranuclear inclusions (EIIs) contain herpesvirus-like particles. However, although EIIs are a sign of herpesvirus replication, they have not yet been firmly linked to ChHV5. Moreover, the dynamics of viral shedding in turtles are unknown, and there are no serological reagents to confirm actual presence of the specific ChHV5 virus in tissues. The investigators analyzed 381 FP tumors for the presence of EIIs and found that overall, about 35% of green turtles had lytic replication in skin tumors with 7% of tumors showing lytic replication. A few (11%) turtles accounted for more than 30% cases having lytic viral replication, and lytic replication was more likely in smaller tumors. To confirm that turtles were actively replicating ChHV5, a prerequisite for shedding, the investigators used antiserum raised against F-VP26, a predicted capsid protein of ChHV5 that localizes to the host cell nucleus during viral replication. This antiserum revealed F-VP26 in EIIs of tumors, thus confirming the presence of replicating ChHV5. In this light, it is proposed that unlike other virus-induced neoplastic diseases, FP is a disease that may depend on superspreaders, a few highly infectious individuals growing numerous small tumors permissive to viral production, for transmission of ChHV5.