ARTICLE NEWS B (Canarypox-like virus) B1 B2 B3 B4 APVs affecting wild canaries, crows, finches, bustards, penguins, house sparrows, apapanes, grackles, song thrush and common murre Starlingpox and mynahpox virus Virginian pox viruses Macqueen’s bustard Replication of Fowlpox virus: The replication of FWPV occurs at the cytoplasm of the cell. During replication, inclusion bodies are develop which are the sites of virion assembly. The FWPV are identified in two forms – intracellular matured virus (IMV) and extracellular enveloped virus (EEV). Both these forms could productively infect cells by binding with the cellular membranes. Upon binding, the nucleocapsid is released into the cytoplasm of the cell. The released nucleocapsid encode early promoters that initiates transcription of early viral genes with the help of virus mediated RNA polymerase and transcription factors. The transcription of early viral genes induce extracellular modulators (viral growth factors, cytokine inhibitors), intracellular modulators (apoptosis inhibition, anti-viral state blockade, signalling modulators, host range factors) and initiate uncoating of the nucleocapsid which releases the genome. The genome encodes intermediate and late genes, which initiates transcription of intermediate and late gene viral products. During virion assembly, IMV is accumulated in the cytoplasm. The IMV obtains an envelope from Golgi body, to form intracellular enveloped virus (IEV). The release of IMV and IEV occurs either through cytolysis or virus induced exocytosis or by budding. The IEV upon being released from the cell is known as EEV. Tropism of Fowlpox virus: The tropism of FWPV is determined by three factors: entry into cells, ability to replicate and cause disease in the host. Based on these three factors, the hosts are classified into permissive and semi-permissive or abortive hosts. The permissive host include avian species, in which entry of FWPV is successful, replication of FWPV is complete and onset of disease is exhibited by clinical signs. The semi-permissive or abortive host include mammalian species, in which entry of FWPV is unrestricted, replication of FWPV is abortive and thus pathogenesis is absent. Fowlpox virus as vaccine vector: FWPV evolved as the most potential vector for poultry vaccines, because of the strategic prospects they have reported to offer, which includes: (i) the number of potential insertion sites they offer, (ii) their capacity to harbour large heterologous genes without altering its genome stability, (iii) their ability to replicate in the cytoplasm independent of host cell enzyme machinery eliminating the possibilities of insertional mutagenesis, (iv) their ability to undergo homologous recombination, (v) their ability to express high levels of heterologous genes, (vi) their ability to induce effective antibody-mediated immune response with high levels of protective antibodies and lasting cell-mediated immune response; and (vii) their ability to induce both T-helper cell and cytotoxic T-lymphocyte response. In poultry, FWPV was used as a vaccine vector to deliver S1 glycoprotein of IB virus, VP2 gene of IBD virus, haemagglutinin gene of AI virus, gB protein of ILT virus, envelope antigen of avian leucosis or sarcoma virus and MD virus. FWPV evolved as a vaccine vector in mammalian species due to its abortive replication in mammalian cells. It was used as a vaccine vector to deliver glycoprotein G of rabies virus and F protein of measles virus. It was reported that cellmediated immune response was induced against both the diseases, whereas humoral immune response was induced only against rabies virus and not measles virus. Further, it was used in Human Immunodeficiency virus and in oncolytic therapy. Limitations of usage of Fowlpox virus as vaccine vector: The major limitation of use of FWPV as a vaccine vector in poultry is the pre-existing immunity to FWPV. The pre-existing immunity is imparted either by prior exposure or by maternal immunity. Though previous infection reduces the efficiency of FWPV vaccine vectors, maternal antibody was neither reported to affect the replication of FWPV nor reported reduced expression of heterologous genes. References: 1.Jarmin, S., R. Manvell, R.E. Gough, S.M. Laidlaw and M.A. Skinner. 2006. Avipoxvirus phylogenetics: identification of a PCR length polymorphism that discriminates between the two major clades. J. Gen. Virol., 87:2191–2201. 2. Davidson, I., I. Shkoda and S. Perk. 2008. Integration of the reticuloendotheliosis virus envelope gene into the poultry fowlpox virus genome is not universal. J. Gen. Virol.,89 (10): 2456 – 2460. 3. Skinner, M.A., S.M. Laidlaw, I. Eldaghayes, P. Kaiser and M.G. Cottingham. 2005. Fowlpox virus as a recombinant vaccine vector for use in mammals and poultry. Expert Rev Vaccines., 4: 63 – 76. 4. Weli, S. C.and M. Tryland. 2011. Avipoxviruses: infection biology and their use as vaccine vectors. Virol. J. 8: 49. 60 February, <strong>2019</strong>
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