Isolation of salmon pancreas disease virus (SPDV) in cell culture and its ability to protect against infection by the ‘wild-type’ agent

ABSTRACT Cell culture isolates of salmon pancreas disease virus (SPDV) of farmed Atlantic salmon and sleeping disease virus (SDV) of rainbow trout were compared. Excluding the poly(A) tracts, the genomic nucleotide sequences of SPDV and SDV RNAs include 11,919 and 11,900 nucleotides, respectively. Phylogenetic analysis places SPDV and SDV between the New World viruses of Venezuelan equine encephalitis virus and Eastern equine encephalitis virus and the Old World viruses of Aura virus and Sindbis virus. When compared to each other, SPDV and SDV show 91.1% nucleotide sequence identity over their complete genomes, with 95 and 93.6% amino acid identities over their nonstructural and structural proteins, respectively. Notable differences between the two viruses include a 24-nucleotide insertion in the C terminus of nsP3 protein of SPDV and amino acid sequence variation at the C termini of the capsid and E1 proteins. Experimental infections of Atlantic salmon and rainbow trout with SPDV and SDV confirmed that the disease lesions induced by SPDV and SDV were similar in nature. Although infections with SPDV and SDV produced similar levels of histopathology in rainbow trout, SDV induced significantly less severe lesions in salmon than did SPDV. Virus neutralization tests performed with sera from experimentally infected salmon indicated that SPDV and SDV belonged to the same serotype; however, antigenic variation was detected among SDV and geographically different SPDV isolates by using monoclonal antibodies. Although SPDV and SDV exhibit minor biological differences, we conclude on the basis of the close genetic similarity that SPDV and SDV are closely related isolates of the same virus species for which the name Salmonid alphavirus is proposed.

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A serological survey of salmon pancreas disease virus (SPDV) antibodies in farmed Atlantic salmon, Salmo salar L.

Journal of Fish Diseases ◽

10.1046/j.1365-2761.1998.00109.x ◽

1998 ◽

Vol 21 (4) ◽

pp. 305-307 ◽

Cited By ~ 24

Author(s):

McLoughlin ◽

Rowley ◽

Doherty

Keyword(s):

Atlantic Salmon ◽

Disease Virus ◽

Salmo Salar ◽

Serological Survey ◽

Pancreas Disease ◽

Atlantic Salmon Salmo Salar ◽

Farmed Atlantic Salmon ◽

Salmon Pancreas Disease Virus

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Estimation of the reproduction number of salmon pancreas disease virus subtype 3 in homogeneously mixed populations of Norwegian farmed Atlantic salmon

Preventive Veterinary Medicine ◽

10.1016/j.prevetmed.2013.05.012 ◽

2013 ◽

Vol 111 (3-4) ◽

pp. 329-332 ◽

Cited By ~ 7

Author(s):

Saraya Tavornpanich ◽

Hildegunn Viljugrein ◽

Anne Stene ◽

Edgar Brun

Keyword(s):

Atlantic Salmon ◽

Disease Virus ◽

Reproduction Number ◽

Pancreas Disease ◽

Mixed Populations ◽

Farmed Atlantic Salmon ◽

Salmon Pancreas Disease Virus ◽

Virus Subtype ◽

Subtype 3

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Expansion of a Unique Region in the Marek's Disease Virus Genome Occurs Concomitantly with Attenuation but Is Not Sufficient To Cause Attenuation

Journal of Virology ◽

10.1128/jvi.78.2.733-740.2004 ◽

2004 ◽

Vol 78 (2) ◽

pp. 733-740 ◽

Cited By ~ 38

Author(s):

R. F. Silva ◽

S. M. Reddy ◽

B. Lupiani

Keyword(s):

Cell Culture ◽

Disease Virus ◽

Infectious Virus ◽

Virus Genome ◽

Marek's Disease ◽

Marek’S Disease ◽

Repeat Region ◽

Wild Type ◽

Unique Region

ABSTRACT Pathogenic Marek's disease viruses (MDVs) have two head-to-tail copies of a 132-bp repeat. As MDV is serially passaged in cell culture, the virus becomes attenuated and the number of copies of the 132-bp repeat increases from 2 to often more than 20 copies. To determine the role of the repeats in attenuation, we used five overlapping cosmid clones that spanned the MDV genome to reconstitute infectious virus (rMd5). By mutating the appropriate cosmids, we generated clones of infectious MDVs that contained zero copies of the 132-bp repeats, rMd5(Δ132); nine copies of the 132-bp repeats, rMd5(9-132); and nine copies of the 132-bp repeats inserted in the reverse orientation, rMd5(rev9-132). After two passages in cell culture, wild-type Md5, rMd5, and rMd5(Δ132) were stable. However, rMd5(9-132) and rMd5(rev9-132) contained a population of viruses that contained from 3 to over 20 copies of the repeats. A major 1.8-kb mRNA, containing two copies of the 132-bp repeat, was present in wild-type Md5 and rMd5 but was not present in rMd5(Δ132), rMd5(9-132), rMd5(rev9-132), or an attenuated MDV. Instead, the RNAs transcribed from the 132-bp repeat region in rMd5(9-132) and rMd5(rev9-132) closely resembled the pattern of RNAs transcribed in attenuated MDVs. When inoculated into susceptible day-old chicks, all viruses produced various lesions. Thus, expansion of the number of copies of 132-bp repeats, which accompanies attenuation, is not sufficient in itself to attenuate pathogenic MDVs.

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