Multi-targeted gene silencing strategies inhibit replication of Canine morbillivirus.

Background: Canine morbilivirus (canine distemper virus, CDV) is a highly contagious pathogen associated with high morbidity and mortality in susceptible carnivores. Although there are CDV vaccines available, the disease poses a huge threat to dogs and wildlife hosts due to vaccine failures and lack of effective treatment. Thus, the development of therapeutics is an urgent need to achieve rapid outbreak control and reduce mortality in target species.

Increased efficacy of an adenovirus-vectored foot-and-mouth disease capsid subunit vaccine expressing nonstructural protein 2B is associated with a specific T cell response.

We previously demonstrated that an adenovirus-based foot-and-mouth disease virus (FMDV) serotype A24 capsid subunit vaccine, Ad5-A24, expressed under the control of a cytomegalovirus promoter (CMV) can protect swine and bovines against homologous challenge, but in a similar approach using swine vaccinated with an Ad5-vectored FMDV O1 Campos vaccine, Ad5-O1C, the animals were only partially protected when challenged at 21 days post-vaccination (dpv). Recently, we demonstrated that inclusion of the complete coding region of nonstructural protein 2B in the Ad5-A24 vector resulted in improved immune responses in pigs. We also found that inclusion of a modified CMV promoter (pCI), Ad5-CI-A24-2B, enhanced the efficacy of the vector.

Sequencing and phylogenetic analysis of the infectious bursal disease virus isolates from outbreak in layer flocks in the state of Minas Gerais.

Sequencing and phylogenetic analysis based on the nucleotide sequence of the gene encoding VP2 protein was carried out in order to characterize the agent of two outbreaks of infectious bursal disease in layer flocks in the state of Minas Gerais in 2004. The results indicate the outbreaks could be related to the vaccinal virus.

Delivery of a foot-and-mouth disease virus empty capsid subunit antigen with nonstructural protein 2B improves protection of swine.

To develop a more efficacious human adenovirus (Ad5)-vectored foot-and-mouth disease virus (FMDV) subunit vaccine (Ad5-A24) we have included coding regions for FMDV nonstructural proteins 2B and 2C. These proteins are involved in membrane re-arrangements resulting in the proliferation of cytoplasmic vesicles which serve as the sites of virus replication. Cells infected with a vector containing full-length 2B (Ad5-CI-A24-2B) had a significant increase in the number of cytoplasmic vesicles as compared to cells infected with the original vector or a vector containing full-length 2BC.

Evading the host immune response: how foot-and-mouth disease virus has become an effective pathogen.

Foot-and-mouth disease virus (FMDV) causes an economically devastating disease of cloven-hoofed animals. In this review, we discuss the mechanisms FMDV has evolved to counteract the host innate and adaptive immune responses and the role of viral proteins in this process. The viral leader proteinase, L pro, limits the host innate response by inhibiting the induction of interferon beta (IFN beta) mRNA and blocking host cell translation.

Enhanced antiviral activity against foot-and-mouth disease virus by a combination of type I and II porcine interferons.

Previously, we showed that type I interferon (alpha/beta interferon [IFN-alpha/beta]) can inhibit foot-and-mouth disease virus (FMDV) replication in cell culture, and swine inoculated with 10(9) PFU of human adenovirus type 5 expressing porcine IFN-alpha (Ad5-pIFN-alpha) were protected when challenged 1 day later. In this study, we found that type II pIFN (pIFN-gamma) also has antiviral activity against FMDV in cell culture and that, in combination with pIFN-alpha, it has a synergistic antiviral effect. We also observed that while each IFN alone induced a number of IFN-stimulated genes (ISGs), the combination resulted in a synergistic induction of some ISGs.