Ecology and Epidemiology of Newcastle Disease. Necropsy Techniques and Collection of Samples.
OIE, FAO and NRL for AI: Friedrich-Loeffler-Institut
Conventional Diagnosis of Avian Influenza. Molecular Diagnosis of Avian Influenza. Molecular Diagnosis of Newcastle Disease Virus. Back Matter Pages Isolation and pathotyping of Newcastle disease viruses from field outbreaks among chickens in the southern part of Egypt Global Veterinaria, Molecular epidemiology of avian influenza virus and incidence of H5 and H9 virus subtypes among poultry in Egypt in Acta Virologica, Advancement in vaccination against Newcastle disease: recombinant HVT NDV provides high clinical protection and reduces challenge virus shedding with the absence of vaccine reactions.
Onset and long-term duration of immunity provided by a single vaccination with a turkey herpesvirus vector ND vaccine in commercial layers. Veterinary Immunology and Immunopathology. Virus Genes, Improved vaccination against Newcastle disease by an in ovo recombinant HVT-ND combined with an adjuvanted live vaccine at day-old. Vaccine, Further evidence of antigenic drift and protective efficacy afforded by a recombinant HVT-H5 vaccine against challenge with two antigenically divergent Egyptian clade 2.
International symposium of Avian Influenza. A simple method of estimating fifty percent end points. American Journal ofEpidemiology, Characterization of Newcastle disease virus isolatesby reverse transcription PCR coupled to directnucleotide sequencing and development of sequencedatabase for pathotype prediction and molecular epidemiological analysis.
Journal of ClinicalMicrobiology, Identification of sensitive and specificavian influenza polymerase chain reaction methodsthrough blind ring trials organized in the EuropeanUnion. Journal Management System.
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The identical thermal profile was adapted in order to detect both the distinct viruses within the same run. During the experiment, no clinical sign was observed in the groups under study groups which were treated with Newcastle or influenza viruses individually or in combination. The results of weighting the chickens showed that there was no significant difference between the groups and all chickens grew naturally Table 3.
Blood samples taken from all groups were examined in terms of antibody titres against AI and ND viruses. The results indicated that the antibody titre was negative in the control group, while it was positive in all groups to which the secondary virus was administered simultaneously or with an interval of 3 days. The results also demonstrated that in the group that the influenza virus was inoculated individually, the antibody titre of influenza and Newcastle was 4 and 5 Log 2 after 14 days, respectively Figure 1.
The highest rate was reported when both viruses were received commonly. Different time points show the viral shedding so that the blue square is related to single infected birds groups : B and C , the red square is related to co-infected birds with both viruses group D , the green triangle is related to sequential infected birds group E and the purple multiplication is related to group F. By comparing the number of viral shedding particles using RRT-PCR technique at different times after the inoculation, the shedding pattern in OP area showed that the type of infection and exposure of the virus to the host tissue play a major role in virus replication.
However, viral shedding was reported to be distinctly low in the early days in chickens of group F LPAIV three days after l NDV and the highest rate of AIV shedding was observed on the fifth day after the secondary inoculation, i. In group C, where H9N2 was inoculated individually, viral shedding showed a reduction in the fourth to sixth days after the inoculation while such a reduction was not observed in other groups which had been treated with both viruses simultaneously Figure 2 a. The influenza virus shedding in the cloacal area was studied in all groups and the results indicated that the highest shedding rate was related to groups C, D, and E in the second to fourth days after the inoculation, while this peak in group F was found on the tenth day after the inoculation, i.
According to the results of this study, there was a difference between the groups regarding the shedding rate of l NDV Figure 2 c. As the results indicated, shedding was observed on the second and third day after the inoculation in the group in which l NDV was administered alone group B and in the groups where the virus was inoculated simultaneously or with an interval of 3 days groups D and F. On the other hand, the lowest shedding rate was observed in group E where l NDV was injected three days after the administration of LPAIV, as the highest virus titre was measured on the fourth day after the secondary inoculation the seventh day Figure 2 c.
The l NDV shedding in CL area was recorded from group B on the fourth to the sixth day three days after the secondary inoculation while the highest shedding rate in groups E and F was observed only on the sixth day and it had a downward trend gradually until the tenth day in group D Figure 2 d. All control groups were reported to be negative in terms of the presence of the virus in the swab sample of OP and CL.
These viruses are circulating in poultry in many parts of the world, especially in Iran, and chickens are susceptible tanks of them.
It was mentioned that in co-infection with these viruses, one virus prevents the growth of the other, Ge et al. Co-infection and viral interference depend on factors such as bird species, type of virus, timing inoculation, and virus inoculation type, also tissue tropism, latency, dose, virulence and biological properties of pathogens and altered immune response are important, Pantin-Jackwood et al.
Despite the severity, natural co-infections of lNDV and AIV are anticipated to occur in poultry, and the effects of such co-infections on several host responses such as viral shedding dynamic, seroconversion and clinical signs are not fully known in chickens, Costa-Hurdato et al. Even with the differences in the type of virus replication, co-infection of chickens with l NDV and LPAIV has not had significant effects on the increase or decrease of clinical symptoms, Pantin-Jackwood et al.
The clinical signs in birds depend on the species, age and virus type, para OIE, The main clinical signs are nasal discharge, cough, nervous signs, diarrhea, inappetance in laying birds, para OIE, Therefore, the host species is a factor that can influence the severity of clinical signs and amount of virus replication in such virus co-infections, Costa-Hurtado et al. According to the previous studies, no effect on clinical signs of co-infection with the two viruses was found in the present study.
The results clearly showed that viral titre on the OP route was distinctly more than viral titre on the CL route, these results are consistent with a previous study by Costa-Hurtado, that stated that LPAIV viral shedding is mainly in the OP route, Costa-Hurtado et al.
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In addition, shedding was lower in groups which were treated with viruses individually. Similarly to the previous studies, the findings of the present study prove that LPAIV is more pathogenic for chickens, as the presence of AIV in the host could delay or prohibit the replication of NDV.
Therefore, it is recommended that the severity and degree of interference depend on the amount and pathogenicity of the virus strain, Spackman et al. This suggests that Lasota, if inoculated individually or simultaneously, cannot interfere with the replication and shedding of H9N2 but can only slow down the process of viral replication.
In other words, due to the inoculation of Lasota before H9N2, the replication of the influenza virus had a slower process and the viral shedding was lower. These values were evaluated in the sixth to the tenth day after the inoculation Figure 2 a, b. By comparing the results of this study with qualitative achievements of previous studies, it can be stated that AIV virus is a more powerful agent than NDV in the interference between these two viruses.
Viral interference is a very important phenomenon in which one cell is infected with a virus, as the virus can prevent the replication of secondary viruses. In other words, it can suppress the shedding of a virus of the homologous or heterologous type which enters the cell, Dianzani, Several important mechanisms have been proposed to explain the viral interference: Competing by attachment interference. In this mechanism, receptors for the superinfecting virus are reduced or blocked, competing intracellular for replication of the host machinery, virus-induced interferon interference, Kimura et al.
Therefore, superficial cell receptors for AIV are glycoconjugates containing sialic acid, whereas these receptors for NDV are recommended to be ganglioside and N-glycoprotein, Rott, ; Ferreira et al. These findings suggest that both viruses may compete for the same target cell as Lasota can connect to the HN glycoprotein, LPAIV can connect to HA glycoprotein compounds because both of these compounds contain sialic acid, Costa-Hurtado et al.
Previous studies have explained that an inactivated particle of influenza can interfere with the replication of a live virus that later enters the cell. Replication of a virus following the activation of anti-viral immune responses, including immunomodulators or the use of immune cells, can influence the replication of other viruses in a similar area, Ge et al. As mentioned in the previous studies, Ge et al. Therefore, in confirmation of the previous studies, it is recommended that humoral response against co-infection may not be much effective in antibody titre courses.
In general, effects of viral interference depend on the adaptation of viruses to a host species, pathogenicity of viruses, time of co-infection, and environmental factors. Assessment and identification of the factors affecting the viral interference or understanding the factors that cause delay in the replication and infection of viruses will help us to better find the path of pathogenicity and transmission of these viruses in chickens.
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That understanding could also provide new plans of virus control programs, including new tools for identification and more improved protocols of vaccination. Birds are often infected with more than one infectious agents. Newcastle disease. Newcastle disease, other avian paramyxoviruses and pneumovirus infections. Diseases of poultry. Ames: Blackwell Publishing; Alexander DJ. An overview of the epidemiology of avian influenza. Vaccine ;25 30 Report on avian influenza in the eastern hemisphere during Avian Disease ;47 s3 Evaluation of pathogenic potential of avian influenza virus serotype H9N2 in chickens.
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Avian Disease ;47 s3 : Ames: Iowa State University; Journal of Virological Methods ; Capua I, Alexander DJ. Avian influenza and Newcastle disease: a field and laboratory manual. Rome: Springer Verlag; Avian influenza: recent developments. Avian Pathology ;33 4 Virus interference between H7N2 low pathogenic avian influenza virus and lentogenic Newcastle disease virus in experimental co-infections in chickens and turkeys.
Veterinary Research ; Surveillance for influenza viruses in poultry and Swine, West Africa,