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Recent Advances on the Bovine Viral Diarrhea Virus Molecular Pathogenesis, Immune Response, and Vaccines Development.

ABSTRACT: The bovine viral diarrhea virus (BVDV) consists of two species and various subspecies of closely related viruses of varying antigenicity, cytopathology, and virulence-induced pathogenesis. Despite the great ongoing efforts to control and prevent BVDV outbreaks and the emergence of new variants, outbreaks still reported throughout the world. In this review, we are focusing on the molecular biology of BVDV, its molecular pathogenesis, and the immune response of the host against the viral infection. Special attention was paid to discuss some immune evasion strategies adopted by the BVDV to hijack the host immune system to ensure the success of virus replication. Vaccination is one of the main strategies for prophylaxis and contributes to the control and eradication of many viral diseases including BVDV. We discussed the recent advances of various types of currently available classical and modern BVDV vaccines. However, with the emergence of new strains and variants of the virus, it is urgent to find some other novel targets for BVDV vaccines that may overcome the drawbacks of some of the currently used vaccines. Effective vaccination strategy mainly based on the preparation of vaccines from the homologous circulating strains. The BVDV-E2 protein plays important role in viral infection and pathogenesis. We mapped some important potential neutralizing epitopes among some BVDV genomes especially the E2 protein. These novel epitopes could be promising targets against the currently circulating strains of BVDV. More research is needed to further explore the actual roles of these epitopes as novel targets for the development of novel vaccines against BVDV. These potential vaccines may contribute to the global eradication campaign of the BVDV.

SUBMITTER: Al-Kubati AAG

PROVIDER: S-EPMC8160231 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Bovine viral diarrhea virus (BVDV) is a (+) ssRNA virus that belongs to the family Flaviviridae. BVDV is a significant animal pathogen causing substantial economic losses to the cattle industry worldwide through respiratory and gastrointestinal infections and abortion or birth of persistently infected calves. While the immunogenic profile of some of the BVDV proteins (i.e., Erns, E2 and NS3) is well established during viral pathogenesis, very little information is available about most of BVDV's non-structural proteins in this regard. In recent times, the NS4B protein has emerged as an interesting target of diagnostic, vaccination and therapeutic value in viral infections of other members of the family Flaviviridae due to its key scaffold-like contribution in the viral replication complex. Although, BVDV-NS4B has a membrane topology alongside its role in induction of autophagosomes in vitro. However, information on its immunogenicity during BVDV pathogenesis and vaccination is scarce. To characterize the immunogenic profile of the NS4B, five cows were vaccinated with the live attenuated BVDV vaccine Bovela® and blood samples were taken pre- and post-immunization for serum isolation. Virus neutralization assay (VNA) confirmed the presence of anti-BVDV antibodies in the sera of vaccinated cows. VNA also revealed pre-existing antibodies against BVDV in the pre-immunization sera of two cows. To identify BVDV-NS4B specific antibodies, the NS4B protein was expressed in mammalian cells by using the pCI-neo vector system. The sera from BVDV vaccinated cows were evaluated for the presence of BVDV-NS4B specific antibodies through western blot and indirect ELISA. Interestingly, t sera from cows with pre-existing immunity against BVDV were able to detect NS4B in western blot and ELISA, suggesting the presence of NS4B-specific antibodies. The obtained results provide the first indication of the immunogenic nature of BVDV-NS4B protein in sero-converted animals. These findings are consistent with the observation made for NS4B in other Flaviviridae members and confirm this protein as an interesting target with diagnostic, vaccination and therapeutic value.

Project description:Bovine viral diarrhea virus (BVDV) is an important pathogen of cattle that plays a complex role in disease. There are two biotypes of BVDV: non-cytopathic (NCP) and cytopathic (CP). One strategy that has been used to treat or prevent virus-associated diseases is the modulation of autophagy, which is used by the innate immune system to defend against viral infection; however, at present, the interplay between autophagy and BVDV remains unclear. Madin-Darby bovine kidney cells stably expressing microtubule-associated protein 1 light chain 3B (LC3B) with green fluorescent protein (GFP) (GFP-LC3-MDBK cells) and autophagy-deficient MDBKs (shBCN1-MDBK cells) were constructed. Then MDBK, GFP-LC3-MDBK and shBCN1-MDBK cells were infected with CP or NCP BVDV strains. The LC3-II turnover rate was estimated by western blot, autophagosomes were visualized by confocal microscopy, and ultrastructural analysis was performed using electron microscopy. Autophagy flux was observed using chloroquine as an inhibitor of the autophagic process. The influence of autophagy on BVDV replication and release was investigated using virus titration, and its effect on cell viability was also studied. The effect of BVDV-induced autophagy on the survival of BVDV-infected host cell, cell apoptosis, and interferon (IFN) signalling was studied by flow cytometric analysis and quantitative RT-(q)PCR using shBCN1-MDBK cells. we found that infection with either CP or NCP BVDV strains induced steady-state autophagy in MDBK cells, as evident by the increased number of double- or single-membrane vesicles, the accumulation of GFP- microtubule-associated protein 1 light chain 3 (LC3) dots, and the conversion of LC3-I (cytosolic) to LC3-II (membrane-bound) forms. The complete autophagic process was verified by monitoring the LC3-II turnover ratio, lysosomal delivery, and proteolysis. In addition, we found that CP and NCP BVDV growth was inhibited in MDBK cells treated with high levels of an autophagy inducer or inhibitor, or in autophagy deficient-MDBK cells. Furthermore, our studies also suggested that CP and NCP BVDV infection in autophagy-knockdown MDBK cells increased apoptotic cell death and enhanced the expression of the mRNAs for IFN-?, Mx1, IFN-?, and OAS-1 as compared with control MDBK cells. Our study provides strong evidence that BVDV infection induces autophagy, which facilitates BVDV replication in MDBK cells and impairs the innate immune response. These findings might help to illustrate the pathogenesis of persistent infection caused by BVDV.

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Recent Advances on the Bovine Viral Diarrhea Virus Molecular Pathogenesis, Immune Response, and Vaccines Development.

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