Gene/Protein Disease Symptom Drug Enzyme Compound
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Multiple skin nodules, with histological features of adnexal tumours consistent with trichoepithelioma, were observed on the head and trunk of Syrian hamsters. Skin biopsies from 20 hamsters from five different colonies were affected, and two of the affected hamsters also had lymphoma. Two owners reported that 16 of 70 hamsters and 50 of 100 hamsters in their colonies had similar skin lesions. These tumours have previously been associated in laboratory colonies with hamster polyomavirus (HaPV) infection. Examination of skin tissues by electron microscopy failed to reveal intranuclear virus particles. Using recombinant major capsid protein VP1 of HaPV, VP1-specific antibodies were detected in sera from 12 of 12 affected hamsters and in four of four unaffected in-contact hamsters, by ELISA. The ELISA data were verified by immunoblot analysis. Eleven of 13 serum samples contained antibodies which reacted with at least one recombinant structural HaPV protein (VP2), including samples from three in-contact unaffected hamsters. Nine of the 11 anti-VP2-positive samples also reacted with recombinant VP3 of HaPV, and six reacted with VP1. Amplification by PCR and sequencing detected VP1 -encoding sequences showing a high degree of homology with HaPV. The findings suggest a possible infection by HaPV or a HaPV-like virus and it is likely that such an infection was enzootic within the affected colonies.
Vet Rec 2002 Jul 06
PMID:Polyomavirus infection in hamsters and trichoepitheliomas/cutaneous adnexal tumours. 1213 18

Following the first ever case of bluetongue in Denmark during late 2007, further outbreaks were observed in Denmark during 2008, despite vaccination against bluetongue virus (BTV) serotype 8 (BTV-8) in the southern part of the country. In total, 15 separate outbreaks of infection were identified, mostly as a result of clinical suspicions but also because of surveillance of bulk milk samples. These outbreaks led to extensions of the original vaccination zone planned for 2008. Blood samples from clinical suspects were analysed using ELISA and real-time RT-PCR assays for the presence of anti-BTV antibodies and viral RNA, respectively. A newly infected calf from the primary outbreak in 2008 was studied for a period of three months, during which time it seroconverted to BTV, but the presence of viral RNA in its blood was maintained throughout this time. Each outbreak was caused by BTV-8, as determined by a serotype-specific real-time RT-PCR assay. Furthermore, the nucleotide sequence of a portion of segment 2 of the viral RNA (encoding the outer capsid protein VP2) from the samples analysed was identical to the BTV-8 segment 2 that circulated in the Netherlands during 2006.
Vet Rec 2010 Jun 05
PMID:Bluetongue in Denmark during 2008. 2052 47

Rodent parvoviruses (PV) such as rat H-1PV and MVM, are small icosahedral, single stranded, DNA viruses. Their genome includes two promoters P4 and P38 which regulate the expression of non-structural (NS1 and NS2) and capsid proteins (VP1 and VP2) respectively(1). They attract high interest as anticancer agents for their oncolytic and oncosuppressive abilities while being non-pathogenic for humans(2). NS1 is the major effector of viral cytotoxicity(3). In order to further enhance their natural antineoplastic activities, derivatives from these vectors have been generated by replacing the gene encoding for the capsid proteins with a therapeutic transgene (e.g. a cytotoxic polypeptide, cytokine, chemokine, tumour suppressor gene etc.)(4). The recombinant parvoviruses (recPVs) vector retains the NS1/2 coding sequences and the PV genome telomeres which are necessary for viral DNA amplification and packaging. Production of recPVs occurs only in the producer cells (generally HEK293T), by co-transfecting the cells with a second vector (pCMV-VP) expressing the gene encoding for the VP proteins (Fig. 1)(4). The recPV vectors generated in this way are replication defective. Although recPVs proved to possess enhanced oncotoxic activities with respect to the parental viruses from which they have been generated, their production remains a major challenge and strongly hampers the use of these agents in anti-cancer clinical applications. We found that introduction of an Ad-5 derived vector containing the E2a, E4(orf6) and the VA RNA genes (e.g. pXX6 plasmid) into HEK293T improved the production of recPVs by more than 10 fold in comparison to other protocols in use. Based on this finding, we have constructed a novel Ad-VP-helper that contains the genomic adenoviral elements necessary to enhance recPVs production as well as the parvovirus VP gene unit(5). The use of Ad-VP-helper, allows production of rec-PVs using a protocol that relies entirely on viral infection steps (as opposed to plasmid transfection), making possible the use of cell lines that are difficult to transfect (e.g. NB324K) (Fig. 2). We present a method that greatly improves the amount of recombinant virus produced, reducing both the production time and costs, without affecting the quality of the final product(5). In addition, large scale production of recPV (in suspension cells and bioreactors) is now conceivable.
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PMID:Efficient recombinant parvovirus production with the help of adenovirus-derived systems. 2254 7

Canine parvovirus type 2 (CPV-2) is a highly contagious viral disease with three variants (CPV-2a, CPV-2b and CPV-2c) currently circulating in dogs worldwide. The main aim of this study was to determine the prevalent CPV-2 variant in faecal samples from 53 dogs presenting with acute gastroenteritis suspected to be and consistent with CPV-2 to Nigerian Veterinary Clinics in 2013-2014. Seventy-five per cent of these dogs tested positive for CPV-2 in a commercial antigen test and/or by PCR. Partial sequencing of the VP2 gene of six of these demonstrated them to be CPV-2a. Most of the dogs (60 per cent) were vaccinated, with 74 per cent of them puppies less than six months old.
Vet Rec Open 2016
PMID:Canine parvovirus (CPV-2) variants circulating in Nigerian dogs. 2793 90

Positive canine parvovirus (CPV) faecal test results have been reported in dogs after modified live virus (MLV) vaccination. Thus, the aim was to investigate feline panleucopenia virus (FPV) shedding in recently vaccinated, adult, clinically healthy cats and to assess related factors. Forty cats were vaccinated with an FPV MLV vaccine. Faeces of cats were tested for presence of parvovirus DNA on days 7, 14, 21 and 28 by quantitative real-time PCR; DNA-positive samples were subjected to partial VP2 gene sequencing. Virus isolation was performed whenever sufficient amounts of faeces were available. Serum antibody titres were measured by haemagglutination inhibition on days 0, 7 and 28. Overall, 30.0 per cent (12/40; 95% CI 18.0 to 45.6) of cats shed parvovirus DNA. Sequencing revealed FPV vaccine virus DNA in three cats, FPV field virus DNA in four cats and CPV field virus DNA in one cat. Shedding was significantly associated with lack of prevaccination antibody titres (40) (P=0.016; OR: 6.44; 95% CI 1.44 to 28.89) and with postvaccination titre increases (fourfold) (P=0.029; OR: 5.00; 95% CI 1.17 to 21.39). Shedding of field or vaccine virus DNA seems to be common in healthy cats which can be a concern in shelters and catteries. Diagnostic tools should be developed to facilitate differentiation of vaccine and field virus shedding.
Vet Rec 2019 07 20
PMID:Faecal shedding of parvovirus deoxyribonucleic acid following modified live feline panleucopenia virus vaccination in healthy cats. 3104 Feb 16