A farm economic analysis in different dairy production systems in Bangladesh M M Uddin, M N Sultana, O A Ndambi T Hemmeand K J Peters Department of Animal. Full text Infectious bursal disease virus in poultry current status and future. Department of Pathobiology, Ontario Veterinary College, University of Guelph, Guelph, Canada 2. Clinic for Poultry, University of Veterinary Medicine Hannover, Hannover, Germany. Abstract Infectious bursal disease virus IBDV affects immature B lymphocytes of the bursa of Fabricius and may cause significant immunosuppression. It continues to be a leading cause of economic losses in the poultry industry. IBDV, having a segmented double stranded RNA genome, is prone to genetic variation. Therefore, IBDV isolates with different genotypic and phenotypic diversity exist. Understanding these features of the virus and the mechanisms of protective immunity elicited thereof is necessary for developing vaccines with improved efficacy. In this review, we highlighted the pattern of virus evolution and new developments in prophylactic strategies, mainly the development of new generation vaccines, which will continue to be of interest for research as well as field application in the future. Introduction. In all poultry producing regions of the world, infectious bursal disease virus IBDV continues to be a major constraint for poultry farmers. The consequences of immunosuppression associated with IBDV are vaccination failure and susceptibility of chickens to opportunistic pathogens. Bingo Call Sheet Template'>Bingo Call Sheet Template. It was also shown that IBDV infected birds may become a good propagator for other viral pathogens. For example, low pathogenic duck adapted avian influenza virus becomes more virulent when serially passaged in IBDV infected chickens. Moreover, highly virulent IBDV can cause high mortality in unprotected flocks. IBDV is a double stranded RNA ds. RNA virus,2 which targets immature B lymphocytes of the bursa of Fabricius BF, a primary lymphoid organ in avian species, and subsequently causes B cell depletion in bursal follicles. Macrophages may be susceptible to IBDV reviewed by Khatri and Sharma. IBDV positive T cell populations were detected in the BF. Efficient horizontal virus transmission between flocks through ingestion of feed and water contaminated with infectious feces is remarkable, once a rearing site has been contaminated. However, there are no indications of vertical transmission. USAID-livestock.jpg' alt='Poultry Production In Ethiopia Pdf' title='Poultry Production In Ethiopia Pdf' />The virus may use one or more putative host cell receptorsstructures such as N glycosylated polypeptides,5 heat shock proteins HSPs,6 41 integrin,7 or lipid raft endocytic pathways. Mononuclear phagocytic cells and lymphoid cells of the gut mucosa may serve as targets for initial IBDV infection and replication following oral exposure. Infected macrophages transport the virus to the BF, where extensive replication takes place. Psp Minis Iso. Virus spread from the bursa to other lymphoid organs may occur depending on the virulence of the infecting IBDV strain. Investment opportunities for 100 Investment Project Profiles Agriculture Manufacturing. ILRI undertakes research into animal health, genetics, forages, dairy smallholder systems, policy, impact assessment and production systems, focusing on developing. Increasing%20Food%20Security%20through%20FTF_0.JPG?itok=S84DvVD5' alt='Poultry Production In Ethiopia Pdf' title='Poultry Production In Ethiopia Pdf' />Since the first discovery of classical IBDV strains in the USA over 5. Our understanding of IBDV epidemiology has been much more comprehensive by today. Agriculture in Ethiopia is the foundation of the countrys economy, accounting for half of gross domestic product GDP, 83. Infectious bursal disease virus in poultry current status and future prospects Tamiru Negash Alkie,1 Silke Rautenschlein21Department of Pathobiology, Ontario. All major poultry producing regions report the coexistence of two or more strains of variable pathogenicity. A recent study addressing the global molecular epidemiology of IBDV from four continents revealed that 6. Poultry Production In Ethiopia Pdf' title='Poultry Production In Ethiopia Pdf' />IBDV isolates are very virulent vv IBDV strains. However, other strains including variants are also gaining grounds and are the most prevailing in the USA. Besides biosecurity, vaccination is the most important measure to control IBDV in the field. Classical and variant strains have been used for many years, but extensive usage of live vaccines in the field is thought to favor the emergence of new strains. The emerging viruses evade vaccine induced immunity, and may in addition contribute their viral genome to reassortment and recombination events. In addition, some IBDV live vaccines are expected to maintain quasispecies nature, which in the face of selection pressure may favor the outgrowth of more virulent antigenic variants or mutants in the viral population. Understanding the current epidemiology of IBDV and the implementation of new prophylactic measures are vital to control IBDV. This review article bridges the current understanding of IBDV from epidemiological and immunological perspectives, to possible control measures and new developments in prophylactic strategies against IBDV. IBDV genome. IBDV has a bisegmented ds. RNA genome. 2 Segment A contains two partially overlapping open reading frames ORFs. The larger ORF encodes for a polyprotein PP, which is autocatalytically cleaved into the two structural proteins, virus protein VP2 and VP3, and a serine S protease, VP4. The PP is considered as the main mediator of IBDV induced immunosuppression and pathogenicity. VP2 contains the major antigenic sites responsible for induction of neutralizing antibodies Abs. VP5, which is encoded by the small ORF, is involved in the dissemination of the virus from infected cells. The crystal structure of VP2 indicates that most amino acid aa changes are localized in the exposed projection domain that contains the hypervariable region h. VP2. 1. 7 h. VP2 has two major hydrophilic domains namely major hydrophilic peak A aa 2. B aa 3. 143. 251. PBC aa 2. 192. 24 and PHI aa 3. The minor hydrophilic peak 1 aa 2. VP2 form loop PDE aa 2. PFG aa 2. 792. 84, respectively. Segment B encoded polymerase VP1 mediates viral RNA replication. The VP1 crystal structure shows three domains the N terminal aa 11. C terminal aa 6. IBDV is constantly evolving in the field with varying virulence. Historically, IBDV evolution has three major events the first description of a classical IBDV outbreak in 1. USA as well as the detection of vv. IBDV in late 1. 98. Europe. 1. 0,2. 3 While classical and variant strains dominated field outbreaks for nearly 5 decades in the USA, the first IBDV outbreak related to vv. IBDV in the USA was reported in 2. IBDV neutralizing Ab escape mutants that have been reported in most recurrent outbreaks in vaccinated flocks were the result of mutations at major hydrophilic peak A and B domains loop PBC and PHI of h. VP2. 2. 5,2. 6 Moreover, the emergence of reassortant field strains plays a significant role in current IBDV evolution. In recent years, IBDV field strains from different continents showed aa exchanges at minor hydrophilic peak domains loop PDE and PFG of h. VP2. 2. 72. 9 Single or combined mutations at these regions affect the virulence of IBDV field isolates. Experimentally, the substitution of aa at positions 2. Q2. 53. H, 2. 79 D2. N, and 2. 84 A2. T in the VP2 of vv. Dynasty Warriors 7 Psp English. IBDV isolates resulted in loss of virulence. However, a single aa mutation at position 2. H2. 53. QN or 2. R2. Q in VP2 markedly increased the virulence of an attenuated IBDV strain. In addition, mutation at position 2. D2. 12. N is common in most recent vv. IBDV isolates and may influence the structure of VP2 and consequently the antigenicity of the virus. Moreover, a S residue instead of glycine G at position 2. PDE was reported from vv. IBDV field isolates detected from chickens vaccinated with classical IBDV vaccines,3. Chickens vaccinated with a live Delaware Del E variant and challenged with a neutralizing Ab escape Del E mutant that contains S at position 2. In the USA, one third out of 3. IBDV field isolates failed to react with any of the known monoclonal Abs raised against VP2, which were used to identify IBDV strains for the last 2 decades and hence demonstrate enormous virus evolution.