Ranid herpesvirus 1  Ranid herpesvirus 1 (RaHV-1), also known as the Lucké tumor herpesvirus (LTHV), is a double-stranded DNA virus within the order "Herpesvirales". The virus was initially observed within renal tumors in 1934 by Baldwin Lucké, and more recently has become identifiable through the use of PCR in samples isolated from frog tumors. RaHV-1 causes renal tumors within the northern leopard frog, "Rana pipiens". The virus has not yet been isolated "in vitro" within cell lines, meaning that while its existence and symptoms are fairly evident, its methods of transmission, cell infection, and reproduction are largely unknown. Since it has not been cultured "in vitro," temporal studies regarding the kinetics of virus growth and biological and molecular events in the replication cycle have not been undergone extensively. "Ranid herpesvirus 1", along with "Ranid herpesvirus 2" and "3", are the only herpes viruses known to infect amphibians. With its lipid envelope, the virus is approximately 170 nm in diameter. The capsid itself has been measured to be approximately 90-110 nm in diameter and expresses T=16 icosahedral symmetry. The complete virion includes a capsid with triangular facets. The facets contain five shared capsomeres per edge. The facet edges enclose three central capsomeres. The entire capsid contains 162 capsomeres. Other viruses within the family "Alloherpesviridae" have been shown to have spherical lipid envelopes with capsids expressing T=16 icosahedral symmetry, fitting with these measurements. "Ranid herpesvirus 1" is a double-stranded DNA virus approximately 217kbp in size. The genome is highly linear in structure and has a GC content of 45-47%. RaHV-1 and similar amphibian herpesviruses have been placed in the family "Alloherpesviridae" instead of being associated with mammalian herpesviruses. This is due to the fact that it shares many of its genomic and pathogenic characteristics with Ictalurid herpesvirus 1, another virus within the family Alloherpesviridae. During the cooler winter months, the virus replicates rapidly without the host exhibiting many symptoms. Once the warmer months roll around, viral replication rates dramatically lower to the point of little to no replication, and tumor growth begins. This is not due to the lack of an immune response in the frogs during hibernation, but the temperature of the months themselves.