Journal articles: 'Virology, Rinderpest virus (RPV), Cattle Diseases'

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Heaney, J., S. L. Cosby, and T. Barrett. "Inhibition of host peripheral blood mononuclear cell proliferation ex vivo by Rinderpest virus." Journal of General Virology 86, no. 12 (2005): 3349–55. http://dx.doi.org/10.1099/vir.0.81370-0.

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Rinderpest, or cattle plague, is caused by Rinderpest virus (RPV), which is related most closely to human Measles virus (MV), both being members of the genus Morbillivirus, a group of viruses known to have strong immunosuppressive effects in vitro and in vivo. Here, it was shown that peripheral blood mononuclear cells (PBMCs) isolated from cattle experimentally infected with either wild-type or vaccine strains of RPV impaired the proliferation of PBMCs derived from uninfected animals; however, in contrast to either mild or virulent strains of wild-type virus, the inhibition induced by the vaccine was both weak and transient. Flow-cytometric analysis of PBMCs obtained from cattle infected with different strains of RPV showed that the proportion of infected cells was virus dose-dependent and correlated with lymphoproliferative suppression.

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Baron, Michael D., Mildred Foster-Cuevas, Jana Baron, and Thomas Barrett. "Expression in cattle of epitopes of a heterologous virus using a recombinant rinderpest virus." Journal of General Virology 80, no. 8 (1999): 2031–39. http://dx.doi.org/10.1099/0022-1317-80-8-2031.

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We have investigated the bovine immune response to heterologous proteins expressed using a recombinant rinderpest virus (RPV). A new gene unit was created in a cDNA copy of the genome of the vaccine strain of RPV, and an open reading frame inserted that encodes the polymerase (3Dpol) and parts of the capsid protein VP1 from foot-and-mouth disease virus (FMDV). Infectious recombinant RPV was rescued and shown to express the FMDV-derived protein at good levels in infected cells. The rescued virus was only slightly more attenuated in tissue culture than the original virus. Cattle infected with this recombinant generated a normal immune response to RPV, and were protected from lethal challenge by that virus. Experimental animals showed a specific delayed-type hypersensitivity response to FMDV 3Dpol, similar to that seen in FMDV infection; however, no antibodies were detected recognizing either of the components of the FMDV-derived protein, nor was any proliferative response to these epitopes found in isolated peripheral blood lymphocytes from infected animals. No protection was seen against FMDV infection.

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Parida, Satya, Madhuchhanda Mahapatra, Sai Kumar, et al. "Rescue of a chimeric rinderpest virus with the nucleocapsid protein derived from peste-des-petits-ruminants virus: use as a marker vaccine." Journal of General Virology 88, no. 7 (2007): 2019–27. http://dx.doi.org/10.1099/vir.0.82913-0.

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The nucleocapsid (N) protein of all morbilliviruses has a highly conserved central region that is thought to interact with and encapsidate the viral RNA. The C-terminal third of the N protein is highly variable among morbilliviruses and is thought to be located on the outer surface and to be available to interact with other viral proteins such as the phosphoprotein, the polymerase protein and the matrix protein. Using reverse genetics, a chimeric rinderpest virus (RPV)/peste-des-petits-ruminants virus (PPRV) was rescued in which the RPV N gene open reading frame had been replaced with that of PPRV (RPV–PPRN). The chimeric virus maintained efficient replication in cell culture. Cattle vaccinated with this chimeric vaccine showed no adverse reaction and were protected from subsequent challenge with wild-type RPV, indicating it to be a safe and efficacious vaccine. The carboxyl-terminal variable region of the rinderpest N protein was cloned and expressed in Escherichia coli. The expressed protein was used to develop an indirect ELISA that could clearly differentiate between RPV- and PPRV-infected animals. The possibility of using this virus as a marker vaccine in association with a new diagnostic ELISA in the rinderpest eradication programme is discussed.

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Yoneda, M., S. K. Bandyopadhyay, M. Shiotani, et al. "Rinderpest virus H protein: role in determining host range in rabbits." Journal of General Virology 83, no. 6 (2002): 1457–63. http://dx.doi.org/10.1099/0022-1317-83-6-1457.

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A major molecular determinant of virus host-range is thought to be the viral protein required for cell attachment. We used a recombinant strain of Rinderpest virus (RPV) to examine the role of this protein in determining the ability of RPV to replicate in rabbits. The recombinant was based on the RBOK vaccine strain, which is avirulent in rabbits, carrying the haemagglutinin (H) protein gene from the lapinized RPV (RPV-L) strain, which is pathogenic in rabbits. The recombinant virus (rRPV-lapH) was rescued from a cDNA of the RBOK strain in which the H gene was replaced with that from the RPV-L strain. The recombinant grew at a rate equivalent to the RPV-RBOK parental virus in B95a cells but at a lower rate than RPV-L. The H gene swap did not affect the ability of the RBOK virus to act as a vaccine to protect cattle against virulent RPV challenge. Rabbits inoculated with RPV-L became feverish, showed a decrease in body weight gain and leukopenia. High virus titres and histopathological lesions in the lymphoid tissues were also observed. Clinical signs of infection were never observed in rabbits inoculated with either RPV-RBOK or with rRPV-lapH; however, unlike RPV-RBOK, both RPV-L and rRPV-lapH induced a marked antibody response in rabbits. Therefore, the H protein plays an important role in allowing infection to occur in rabbits but other viral proteins are clearly required for full RPV pathogenicity to be manifest in this species.

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Lund, Brett T., Ashok Tiwari, Sareen Galbraith, Michael D. Baron, W. Ivan Morrison, and Tom Barrett. "Vaccination of cattle with attenuated rinderpest virus stimulates CD4+ T cell responses with broad viral antigen specificity." Journal of General Virology 81, no. 9 (2000): 2137–46. http://dx.doi.org/10.1099/0022-1317-81-9-2137.

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The immune responses of cattle inoculated with either a virulent or an attenuated vaccine strain of rinderpest virus (RPV) were examined by measuring the proliferation of peripheral blood mononuclear cells (PBMC) to whole RPV antigen preparations and to individual RPV major structural proteins expressed using recombinant adenoviruses. Responses to the T cell mitogen concanavalin A (ConA) were also measured as a control to monitor non-specific effects of infection with RPV on T cell responses. Infection with the vaccine strain of RPV was found to induce a strong CD4+ T cell response. A specific response was detected to all RPV proteins tested, namely the haemagglutinin (H), fusion (F), nucleocapsid (N) and matrix (M) proteins, in animals vaccinated with the attenuated strain of the virus. No one protein was found to be dominant with respect to the induction of T cell proliferative responses. As expected, vaccination of cattle with an unrelated virus vaccine, a capripox vaccine, failed to produce a response to RPV antigens. While profound suppression of T cell responses was observed following infection with the virulent strain of RPV, no evidence of impairment of T cell responsiveness was observed following RPV vaccination, or on subsequent challenge of vaccinated animals with virulent virus.

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Banyard, Ashley C., Michael D. Baron, and Thomas Barrett. "A role for virus promoters in determining the pathogenesis of Rinderpest virus in cattle." Journal of General Virology 86, no. 4 (2005): 1083–92. http://dx.doi.org/10.1099/vir.0.80752-0.

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Rinderpest virus (RPV) is a morbillivirus that causes cattle plague, a disease of large ruminants. The viral genome is flanked at the 3′ and 5′ genome termini by the genome promoter (GP) and antigenome promoter (AGP), respectively. These promoters play essential roles in directing replication and transcription as well as RNA encapsidation and packaging. It has previously been shown that individual changes to the GP of RPV greatly affect promoter activity in a minigenome assay and it was therefore proposed that individual nucleotide changes in the GP and AGP might also have significant effects on the ability of the virus to replicate and cause disease in cattle. The Plowright vaccine strain of RPV has been derived by tissue-culture passage from the virulent Kabete ‘O’ isolate (KO) and is highly attenuated for all ruminant species in which it has been used. Here, it was shown that swapping the GP and the first 76 nt of the AGP between virulent and avirulent strains affected disease progression. In particular, it was shown that flanking the virulent strain with the vaccine GP and AGP sequences, while not appreciably affecting virus growth in vitro, led to attenuation in vivo. The reverse was not true, since the KO promoters did not alter the vaccine's attenuated nature. The GP/AGP therefore play a role in attenuation, but are not the only determinants of attenuation in this vaccine.

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Verardi, Paulo H., Fatema H. Aziz, Shabbir Ahmad, et al. "Long-Term Sterilizing Immunity to Rinderpest in Cattle Vaccinated with a Recombinant Vaccinia Virus Expressing High Levels of the Fusion and Hemagglutinin Glycoproteins." Journal of Virology 76, no. 2 (2002): 484–91. http://dx.doi.org/10.1128/jvi.76.2.484-491.2002.

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ABSTRACT Rinderpest is an acute and highly contagious viral disease of ruminants, often resulting in greater than 90% mortality. We have constructed a recombinant vaccinia virus vaccine (v2RVFH) that expresses both the fusion (F) and hemagglutinin (H) genes of rinderpest virus (RPV) under strong synthetic vaccinia virus promoters. v2RVFH-infected cells express high levels of the F and H glycoproteins and show extensive syncytium formation. Cattle vaccinated intramuscularly with as little as 103 PFU of v2RVFH and challenged 1 month later with a lethal dose of RPV were completely protected from clinical disease; the 50% protective dose was determined to be 102 PFU. Animals vaccinated with v2RVFH did not develop pock lesions and did not transmit the recombinant vaccinia virus to contact animals. Intramuscular vaccination of cattle with 108 PFU of v2RVFH provided long-term sterilizing immunity against rinderpest. In addition to being highly safe and efficacious, v2RVFH is a heat-stable, inexpensive, and easily administered vaccine that allows the serological differentiation between vaccinated and naturally infected animals. Consequently, mass vaccination of cattle with v2RVFH could eradicate rinderpest.

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Yoneda, Misako, Ryuichi Miura, Thomas Barrett, Kyoko Tsukiyama-Kohara, and Chieko Kai. "Rinderpest Virus Phosphoprotein Gene Is a Major Determinant of Species-Specific Pathogenicity." Journal of Virology 78, no. 12 (2004): 6676–81. http://dx.doi.org/10.1128/jvi.78.12.6676-6681.2004.

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ABSTRACT We previously demonstrated that the rinderpest virus (RPV) hemagglutinin (H) protein plays an important role in determining host range but that other viral proteins are clearly required for full RPV pathogenicity to be manifest in different species. To examine the effects of the RPV nucleocapsid (N) protein and phosphoprotein (P) genes on RPV cross-species pathogenicity, we constructed two new recombinant viruses in which the H and P or the H, N, and P genes of the cattle-derived RPV RBOK vaccine were replaced with those from the rabbit-adapted RPV-Lv strain, which is highly pathogenic in rabbits. The viruses rescued were designated recombinant RPV-lapPH (rRPV-lapPH) and rRPV-lapNPH, respectively. Rabbits inoculated with RPV-Lv become feverish and show leukopenia and a decrease in body weight gain, while clinical signs of infection are never observed in rabbits inoculated with RPV-RBOK or with rRPV-lapH. However, rabbits inoculated with either rRPV-lapPH or rRPV-lapNPH became pyrexic and showed leukopenia. Further, histopathological lesions and high virus titers were clearly observed in the lymphoid tissues from animals infected with rRPV-lapPH or rRPV-lapNPH, although they were not observed in rabbits infected with RPV-RBOK or rRPV-lapH. The clinical, virological, and histopathological signs in rabbits infected with the two new recombinant viruses did not differ significantly; therefore, the RPV P gene was considered to be a key determinant of cross-species pathogenicity.

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Walsh, Edmund P., Michael D. Baron, Louise F. Rennie, Paul Monaghan, John Anderson, and Thomas Barrett. "Recombinant Rinderpest Vaccines Expressing Membrane-Anchored Proteins as Genetic Markers: Evidence of Exclusion of Marker Protein from the Virus Envelope." Journal of Virology 74, no. 21 (2000): 10165–75. http://dx.doi.org/10.1128/jvi.74.21.10165-10175.2000.

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ABSTRACT Rinderpest virus (RPV) causes a severe disease of cattle resulting in serious economic losses in parts of the developing world. Effective control and elimination of this disease require a genetically marked rinderpest vaccine that allows serological differentiation between animals that have been vaccinated against rinderpest and those which have recovered from natural infection. We have constructed two modified cDNA clones of the vaccine strain RNA genome of the virus, with the coding sequence of either a receptor site mutant form of the influenza virus hemagglutinin (HA) gene or a membrane-anchored form of the green fluorescent protein (GFP) gene (ANC-GFP), inserted as a potential genetic marker. Infectious recombinant virus was rescued in cell culture from both constructs. The RPVINS-HA and RPVANC-GFP viruses were designed to express either the HA or ANC-GFP protein on the surface of virus-infected cells with the aim of stimulating a strong humoral antibody response to the marker protein. In vitro studies showed that the marker proteins were expressed on the surface of virus-infected cells, although to different extents, but neither was incorporated into the envelope of the virus particles. RPVINS-HA- or RPVANC-GFP-vaccinated cattle produced normal levels of humoral anti-RPV antibodies and significant levels of anti-HA or anti-GFP antibodies, respectively. Both viruses were effective in stimulating protective immunity against RPV and antibody responses to the marker protein in all animals when tested in a cattle vaccination trial.

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Holzer, Barbara, Sophia Hodgson, Nicola Logan, Brian Willett, and Michael D. Baron. "Protection of Cattle against Rinderpest by Vaccination with Wild-Type but Not Attenuated Strains of Peste des Petits Ruminants Virus." Journal of Virology 90, no. 10 (2016): 5152–62. http://dx.doi.org/10.1128/jvi.00040-16.

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ABSTRACTAlthough rinderpest virus (RPV) has been eradicated in the wild, efforts are still continuing to restrict the extent to which live virus is distributed in facilities around the world and to prepare for any reappearance of the disease, whether through deliberate or accidental release. In an effort to find an alternative vaccine which could be used in place of the traditional live attenuated RPV strains, we have determined whether cattle can be protected from rinderpest by inoculation with vaccine strains of the related morbillivirus, peste des petits ruminants virus (PPRV). Cattle were vaccinated with wild-type PPRV or either of two established PPRV vaccine strains, Nigeria/75/1 or Sungri/96. All animals developed antibody and T cell immune responses to the inoculated PPRV. However, only the animals given wild-type PPRV were protected from RPV challenge. Animals given PPRV/Sungri/96 were only partially protected, and animals given PPRV/Nigeria/75/1 showed no protection against RPV challenge. While sera from animals vaccinated with the vaccine strain of RPV showed cross-neutralizing ability against PPRV, none of the sera from animals vaccinated with any strain of PPRV was able to neutralize RPV although sera from animals inoculated with wild-type PPRV were able to neutralize RPV-pseudotyped vesicular stomatitis virus.IMPORTANCERinderpest virus has been eradicated, and it is only the second virus for which this is so. Significant efforts are still required to ensure preparedness for a possible escape of RPV from a laboratory or its deliberate release. Since RPV vaccine protects sheep and goats from PPRV, it is important to determine if the reverse is true as this would provide a non-RPV vaccine for dealing with suspected RPV outbreaks. This is probably the lastin vivostudy with live RPV that will be approved.

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Kamata, Hiroshi, Kazue Ohishi, Ellena Hulskotte, et al. "Rinderpest virus (RPV) ISCOM vaccine induces protection in cattle against virulent RPV challenge." Vaccine 19, no. 25-26 (2001): 3355–59. http://dx.doi.org/10.1016/s0264-410x(01)00069-x.

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Servan de Almeida, Renata, Djénéba Keita, Geneviève Libeau, and Emmanuel Albina. "Control of ruminant morbillivirus replication by small interfering RNA." Journal of General Virology 88, no. 8 (2007): 2307–11. http://dx.doi.org/10.1099/vir.0.82981-0.

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Peste-des-petits-ruminants virus (PPRV) and rinderpest virus (RPV) are two morbilliviruses of economic relevance in African and Asian countries. Although efficient vaccines are available for both diseases, they cannot protect the animals before 14 days post-vaccination. In emergencies, it would be desirable to have efficient therapeutics for virus control. Here, two regions are described in the nucleocapsid genes of PPRV and RPV that can be targeted efficiently by synthetic short interfering RNAs (siRNAs), resulting in a >80 % reduction in virus replication. The effects of siRNAs on the production of viral RNA by real-time quantitative PCR, of viral proteins by flow cytometry and of virus particles by appreciation of the cytopathic effect and virus titration were monitored. The findings of this work highlight the potential for siRNA molecules to be developed as therapeutic agents for the treatment of PPRV and RPV infections.

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Nanda, Sambit K., and Michael D. Baron. "Rinderpest Virus Blocks Type I and Type II Interferon Action: Role of Structural and Nonstructural Proteins." Journal of Virology 80, no. 15 (2006): 7555–68. http://dx.doi.org/10.1128/jvi.02720-05.

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ABSTRACT Rinderpest virus (RPV) is a paramyxovirus closely related to the human pathogen Measles virus. It causes severe disease in cattle, buffalo, and some wild animals; although it can infect humans, it does not cause disease. Here, we demonstrate that RPV blocks the action of both type I (α) and type II (γ) interferons (IFNs) by blocking the phosphorylation and nuclear translocation of STAT1 and STAT2 and that this block is not related to species specificity. In addition, both wild-type virulent and vaccine strains of the virus blocked IFN action. Unlike the case with some other paramyxoviruses, neither STAT1 nor STAT2 is degraded upon virus infection. STAT1 is bound by both the viral structural protein P, and thereby recruited to concentrations of viral protein in the cell, and the nonstructural protein V. Although both P and V proteins bind to STAT1 and can block IFN action when expressed in transfected cells, the IFN antagonist activity of the P protein is weaker than that of the V protein. The viral C protein also seems to weakly block IFN-induced activation of STAT1 in transfection experiments. However, studies with knockout viruses showed that the viral V protein appears to be the dominant inhibitor of IFN signaling in the context of virus infection, since prevention of viral V expression restored the IFN sensitivity of infected cells. Although a change in the distribution pattern of STAT2 was observed in virus-infected cells, STAT2 was not bound by any viral protein.

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Ohishi, Kazue, Hiroshi Kamata, Kazuya Yamanouchi, and Thomas Barrett. "Identification of T-helper cell epitopes in the hypervariable region of the nucleocapsid (N) protein of rinderpest virus (RPV) in cattle." Vaccine 18, no. 27 (2000): 3077–81. http://dx.doi.org/10.1016/s0264-410x(99)00538-1.

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Brown, David D., Bertus K. Rima, Ingrid V. Allen, et al. "Rational Attenuation of a Morbillivirus by Modulating the Activity of the RNA-Dependent RNA Polymerase." Journal of Virology 79, no. 22 (2005): 14330–38. http://dx.doi.org/10.1128/jvi.79.22.14330-14338.2005.

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ABSTRACT Negative-strand RNA viruses encode a single RNA-dependent RNA polymerase (RdRp) which transcribes and replicates the genome. The open reading frame encoding the RdRp from a virulent wild-type strain of rinderpest virus (RPV) was inserted into an expression plasmid. Sequences encoding enhanced green fluorescent protein (EGFP) were inserted into a variable hinge of the RdRp. The resulting polymerase was autofluorescent, and its activity in the replication/transcription of a synthetic minigenome was reduced. We investigated the potential of using this approach to rationally attenuate a virus by inserting the DNA sequences encoding the modified RdRp into a full-length anti-genome plasmid from which a virulent virus (rRPVKO) can be rescued. A recombinant virus, rRPVKOL-RRegfpR, which grew at an indistinguishable rate and to an identical titer as rRPVKO in vitro, was rescued. Fluorescently tagged polymerase was visible in large cytoplasmic inclusions and beneath the cell membrane. Subcutaneous injection of 104 TCID50 of the rRPVKO parental recombinant virus into cattle leads to severe disease symptoms (leukopenia/diarrhea and pyrexia) and death by 9 days postinfection. Animals infected with rRPVKOL-RRegfpR exhibited transient leukopenia and mild pyrexia, and the only noticeable clinical signs were moderate reddening of one eye and a slight ocular-nasal discharge. Viruses that expressed the modified polymerase were isolated from peripheral blood lymphocytes and eye swabs. This demonstrates that a virulent morbillivirus can be attenuated in a single step solely by modulating RdRp activity and that there is not necessarily a correlation between virus growth in vitro and in vivo.

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Njeumi, Felix, Dalan Bailey, Jean Jacques Soula, Bouna Diop, and Berhe G. Tekola. "Eradicating the Scourge of Peste Des Petits Ruminants from the World." Viruses 12, no. 3 (2020): 313. http://dx.doi.org/10.3390/v12030313.

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Peste des Petits Ruminants (PPR) is a highly contagious viral disease of both domestic (goats and sheep) and wild ruminants. Caused by a morbillivirus, that belongs to the family Paramyxoviridae. The disease is clinically and pathologically similar to rinderpest of cattle and human measles. PPR is one of the most economically devastating viral diseases of small ruminants. In April 2015, the Food and Agriculture Organization of the United Nations (FAO) and the World Organisation for Animal Health (OIE) launched the PPR Global Control and Eradication Strategy (PPR GCES) with the vision for global eradication by 2030. There is a strong and lasting international consensus to eradicate the disease in order to protect the livelihoods of the world’s poorest populations. As with any disease, eradication is feasible when, policy, scientific and technical challenges are addressed. Ten majors challenges are described in this paper namely: understanding small ruminant production, facilitating research to support eradication, refining laboratory testing, improving epidemiological understanding of the virus, defining infection of wildlife and other species, optimizing vaccine delivery and novel vaccines, developing better control of animal movement, heightening serological monitoring, understanding socio-economic impact, and garnering funding and political will.

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Journal articles on the topic 'Virology, Rinderpest virus (RPV), Cattle Diseases'

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