Avulavirus Infections
Complete nucleotide sequence of avian paramyxovirus type 6 isolated from ducks. (1/30)
There are nine serotypes of avian paramyxovirus (APMV). Only the genome of APMV type 1 (APMV-1), also called Newcastle disease virus (NDV), has been completely sequenced. In this study, the complete nucleotide sequence of an APMV-6 serotype isolated from ducks is reported. The 16236 nt genome encodes eight proteins, nucleocapsid protein (NP), phosphoprotein (P), V protein, matrix protein (M), fusion protein (F), small hydrophobic (SH) protein, haemagglutinin-neuraminidase (HN) protein and large (L) protein, which are flanked by a 55 nt leader sequence and a 54 nt trailer sequence. Sequence comparison reveals that the protein sequences of APMV-6 are most closely related to those of APMV-1 (NDV) and -2, with sequence identities ranging from 22 to 44%. However, APMV-6 contains a gene that might encode the SH protein, which is absent in APMV-1, but present in the rubulaviruses simian virus type 5 and mumps virus. The presence of an SH gene in APMV-6 might provide a link between the evolution of APMV and rubulaviruses. Phylogenetic analysis demonstrates that APMV-6, -1, -2 (only the F and HN sequences were available for analysis) and -4 (only the HN sequences were available for analysis) all cluster into a single lineage that is distinct from other paramyxoviruses. This result suggests that APMV should constitute a new genus within the subfamily Paramyxovirinae. (+info)Inhibition of replication of goose paramyxovirus SF02 by hammerhead ribozyme targeting to the SF02 F mRNA in chicken embryo fibroblasts. (2/30)
Hammerhead ribozyme RzF598 and its dysfunctional mutant dRzF598 targeting to the (F) gene of goose paramyxovirus SF02 have been designed. The transgenic plasmids pcDNA-RzF598 and pcDNA-dRzF598 were constructed by inserting ribozyme genes into eukaryotic expression vector pcDNA3. The plasmid pcDNA3 that lacks full ribozyme gene was used as a control. Plasmids pcDNA-RzF598, pcDNA-dRzF598 and pcDNA3 were transfected into chicken embryo fibroblasts (CEFs). The concentration of virus released by infected CEFs and the survival percentages of CEFs were identified. The results indicated that RzF598 successfully suppressed the replication of SF02 in CEFs. Survival percentage of CEFs being transfected with pcDNA-RzF598 and infected SF02 was up to 78.8%, while the survival percentages of untransfected CEFs and CEFs transfected with pcDNA3 after infection with SF02 were only about 5%. (+info)Antitumor vaccination of patients with glioblastoma multiforme: a pilot study to assess feasibility, safety, and clinical benefit. (3/30)
PURPOSE: Prognosis of patients with glioblastoma is poor. Therefore, in glioblastoma patients, we analyzed whether antitumor vaccination with a virus-modified autologous tumor cell vaccine is feasible and safe. Also, we determined the influence on progression-free survival and overall survival and on vaccination-induced antitumor reactivity. PATIENTS AND METHODS: In a nonrandomized study, 23 patients were vaccinated and compared with nonvaccinated controls (n = 87). Vaccine was prepared from patient's tumor cell cultures by infection of the cells with Newcastle Disease Virus, followed by gamma-irradiation, and applied up to eight times. Antitumor immune reactivity was determined in skin, blood, and relapsed tumor by delayed-type hypersensitivity skin reaction, ELISPOT assay, and immunohistochemistry, respectively. RESULTS: Establishment of tumor cell cultures was successful in approximately 90% of patients. After vaccination, we observed no severe side effects. The median progression-free survival of vaccinated patients was 40 weeks (v 26 weeks in controls; log-rank test, P = .024), and the median overall survival of vaccinated patients was 100 weeks (v 49 weeks in controls; log-rank test, P < .001). Forty-five percent of the controls survived 1 year, 11% survived 2 years, and there were no long-term survivors (> or = 3 years). Ninety-one percent of vaccinated patients survived 1 year, 39% survived 2 years, and 4% were long-term survivors. In the vaccinated group, immune monitoring revealed significant increases of delayed-type hypersensitivity reactivity, numbers of tumor-reactive memory T cells, and numbers of CD8(+) tumor-infiltrating T-lymphocytes in secondary tumors. CONCLUSION: Postoperative vaccination with virus-modified autologous tumor cells seems to be feasible and safe and to improve the prognosis of patients with glioblastomas. This could be substantiated by the observed antitumor immune response. (+info)Screening of feral pigeon (Colomba livia), mallard (Anas platyrhynchos) and graylag goose (Anser anser) populations for Campylobacter spp., Salmonella spp., avian influenza virus and avian paramyxovirus. (4/30)
A total of 119 fresh faecal samples were collected from graylag geese migrating northwards in April. Also, cloacal swabs were taken from 100 carcasses of graylag geese shot during the hunting season in August. In addition, samples were taken from 200 feral pigeons and five mallards. The cultivation of bacteria detected Campylobacter jejuni jejuni in six of the pigeons, and in one of the mallards. Salmonella diarizona 14: k: z53 was detected in one graylag goose, while all pigeons and mallards were negative for salmonellae. No avian paramyxovirus was found in any of the samples tested. One mallard, from an Oslo river, was influenza A virus positive, confirmed by RT-PCR and by inoculation of embryonated eggs. The isolate termed A/Duck/Norway/ 1/03 was found to be of H3N8 type based on sequence analyses of the hemagglutinin and neuraminidase segments, and serological tests. This is the first time an avian influenza virus has been isolated in Norway. The study demonstrates that the wild bird species examined may constitute a reservoir for important bird pathogens and zoonotic agents in Norway. (+info)Antiviral activity and RNA polymerase degradation following Hsp90 inhibition in a range of negative strand viruses. (5/30)
We have analyzed the effectiveness of Hsp90 inhibitors in blocking the replication of negative-strand RNA viruses. In cells infected with the prototype negative strand virus vesicular stomatitis virus (VSV), inhibiting Hsp90 activity reduced viral replication in cells infected at both high and low multiplicities of infection. This inhibition was observed using two Hsp90 inhibitors geldanamycin and radicicol. Silencing of Hsp90 expression using siRNA also reduced viral replication. Hsp90 inhibition changed the half-life of newly synthesized L protein (the large subunit of the VSV polymerase) from >1 h to less than 20 min without affecting the stability of other VSV proteins. Both the inhibition of viral replication and the destabilization of the viral L protein were seen when either geldanamycin or radicicol was added to cells infected with paramyxoviruses SV5, HPIV-2, HPIV-3, or SV41, or to cells infected with the La Crosse bunyavirus. Based on these results, we propose that Hsp90 is a host factor that is important for the replication of many negative strand viruses. (+info)Complete sequence of the genome of avian paramyxovirus type 2 (strain Yucaipa) and comparison with other paramyxoviruses. (6/30)
(+info)Complete genome sequence of avian paramyxovirus type 3 reveals an unusually long trailer region. (7/30)
(+info)Molecular characterization and complete genome sequence of avian paramyxovirus type 4 prototype strain duck/Hong Kong/D3/75. (8/30)
(+info)Avulavirus infections are veterinary medical conditions caused by Avulaviruses, a genus of viruses in the family Paramyxoviridae. These viruses are responsible for causing a variety of important diseases in birds and mammals, including Newcastle disease in birds and several different illnesses in humans, such as:
1. Madagascar pneumonia or meningopneumonitis (caused by Avulavirus serotype 12, also known as MAPV-12)
2. Tubular lung disease (caused by Avulavirus serotype 4, also known as A/turkey/England/50-92/91)
Avulavirus infections can lead to respiratory, gastrointestinal, and neurological symptoms in both birds and mammals. The severity of the disease depends on various factors, including the specific Avulavirus serotype involved, the host's age and immune status, and the route of infection.
In birds, Newcastle disease is a highly contagious and often fatal illness affecting domestic poultry and wild birds worldwide. It can cause severe economic losses in the poultry industry due to high mortality rates and trade restrictions.
In humans, Avulavirus infections are rare but have been associated with contact with infected birds or their droppings. The majority of human cases have been reported in Australia, although sporadic cases have also been documented in other countries. Human illnesses caused by Avulaviruses typically present as respiratory or neurological symptoms and can range from mild to severe, depending on the individual's age and overall health status.
Preventive measures for Avulavirus infections include maintaining good biosecurity practices, such as proper hand hygiene, wearing protective clothing, and limiting contact with potentially infected birds or their droppings. Vaccination is available for some Avulavirus serotypes and is widely used in the poultry industry to control Newcastle disease.
Avulavirus is a genus of viruses in the family Paramyxoviridae, order Mononegavirales. Avulaviruses are enveloped, negative-sense, single-stranded RNA viruses that primarily infect birds, causing various clinical manifestations such as respiratory, digestive, and reproductive diseases. Some avulaviruses have been associated with sporadic human infections, usually resulting in mild or asymptomatic illnesses. The most well-known avulavirus is the Newcastle disease virus (NDV), which can cause severe disease in birds and poses a significant threat to the poultry industry worldwide.