Viral Encephalopathy and Retinopathy (VER), otherwise known as Viral Nervous Necrosis (VNN), is responsible for frequent outbreaks with high mortality in a wide variety of marine fish species all over the world. The disease mainly affects the larval and juvenile stages which show neurological symptoms due to the typical vacuolating lesions in the brain, spinal cord and retina. The disease is caused by a virus of the Betanodavirus genus; seven viral species have been classified in this genus. This classification is based on the fish species from which the virus was isolated, but recently the isolation of the same virus from different host species has become very frequent. Cross-infection tests highlighted that the capacity of the virus to infect different species is mainly due to the environmental temperature at which the fish are farmed, thus at which the infection occurs, more than the host species itself. Using capsid protein gene analysis it was possible to classify four genotypes of Betanodavirus: Striped Jack Nervous Necrosis Virus (SJNNV), Tigger Puffer Nervous Necrosis Virus (TPNNV), Barfin Flounder Nervous Necrosis Virus (BFNNV) and Redspotted Grouper Nervous Necrosis Virus. Iwamoto et al. (1999) demonstrated the different infection temperature ranges for the four genotypes. Both the infection and disease seem to be very temperature-dependent, in fact most of the outbreaks happen in the summer season. This preliminary study elucidates the in vitro effects of temperature on Betanodavirus infection in the SSN-1 cell line. NNV-infected SSN-1 cells incubated at 10–30°C after viral adsorption were observed for cytopathic effect and viral growth in the culture media supernatant and cell pellets were evaluated by titration.
CIULLI S., OSTANELLO F., BATTILANI M., PROSPERI S., HEDRICK R.P. (2004). Effect of temperature on betanodavirus infection in SSN-1 cell line. VETERINARY RESEARCH COMMUNICATIONS, 28, 283-286 [10.1023/B:VERC.0000045427.96443.fd].
Effect of temperature on betanodavirus infection in SSN-1 cell line
CIULLI, SARA;OSTANELLO, FABIO;BATTILANI, MARA;PROSPERI, SANTINO;
2004
Abstract
Viral Encephalopathy and Retinopathy (VER), otherwise known as Viral Nervous Necrosis (VNN), is responsible for frequent outbreaks with high mortality in a wide variety of marine fish species all over the world. The disease mainly affects the larval and juvenile stages which show neurological symptoms due to the typical vacuolating lesions in the brain, spinal cord and retina. The disease is caused by a virus of the Betanodavirus genus; seven viral species have been classified in this genus. This classification is based on the fish species from which the virus was isolated, but recently the isolation of the same virus from different host species has become very frequent. Cross-infection tests highlighted that the capacity of the virus to infect different species is mainly due to the environmental temperature at which the fish are farmed, thus at which the infection occurs, more than the host species itself. Using capsid protein gene analysis it was possible to classify four genotypes of Betanodavirus: Striped Jack Nervous Necrosis Virus (SJNNV), Tigger Puffer Nervous Necrosis Virus (TPNNV), Barfin Flounder Nervous Necrosis Virus (BFNNV) and Redspotted Grouper Nervous Necrosis Virus. Iwamoto et al. (1999) demonstrated the different infection temperature ranges for the four genotypes. Both the infection and disease seem to be very temperature-dependent, in fact most of the outbreaks happen in the summer season. This preliminary study elucidates the in vitro effects of temperature on Betanodavirus infection in the SSN-1 cell line. NNV-infected SSN-1 cells incubated at 10–30°C after viral adsorption were observed for cytopathic effect and viral growth in the culture media supernatant and cell pellets were evaluated by titration.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
