Anemic pathogenesis of chicken infectious anemia

Liu, Z.G.; Zhou, Zhaoqing; Wan, Xiaoxiao; Zheng, Shancui; Yang, L.P.

doi:10.1016/s0928-4680(98)80893-6

Cited by 2 publications

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“…The means of PCV values for the infected chicks with CAV/CA1 and CAV/SK4 were 0.19 and 0.21; receptively, with a significant reduction (P \ 0.0001) in comparison with the negative control group (0.36). Therefore, these results supported the hypothesis that the CAV is directly cytotoxic for bone marrow hematopoietic precursor cells in young chicks [18]. That is in agree with previous studies which reported that CAV causes reduction in the production of mature red blood cells (erythropoiesis) and myelopoiesis leading to hypoplasia, anaemia and panleukopenia [6].…”

Section: Discussionsupporting

confidence: 92%

Full genome sequences of chicken anemia virus demonstrate mutations associated with pathogenicity in two different field isolates in Egypt

Abdel-Mawgod¹,

Adel²,

Arafa³

et al. 2018

VirusDis.

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Chicken anemia virus (CAV) is an important pathogen associated with immunosuppression in chicken. In this study, out of samples collected from 115 commercial poultry farms, 12 samples were CAV positive by PCR. Partial sequence and phylogenetic analysis of VP1 gene revealed that the detected viruses were clustered to genotype I (n = 3) and genotype II (n = 9). Motifs of both low (E144) and high pathogenic strains (T89, I125, Q141) were found in the three viruses of genotype I. Whereas genotype II viruses demonstrated the characteristic motifs of highly pathogenic strains (I75, T89, I125, Q141, and Q144). Three isolates representative of both genotypes (CAV/CA1, CAV/GZ1 and CAV/SK4) were selected for full genome sequencing and results revealed that the VP2 gene had two substitutions at V153 and E 175, while VP3 gene had only one substitution at C118. To evaluate virus pathogenicity, two isolates from each genotype (CAV/SK4 of genotype I and CAV/CA1 of genotype II) were intramuscularly inoculated in two groups of one-day-old specific pathogen free chicks. Eighteen days post inoculation, PCR detected CAV in 75 and 90% of chicks in group I and II; respectively. Mortalities in inoculated chicks were 5 and 20% and packed cell volume values were 0.21 and 0.19; respectively. CAV/CA1 and CAV/SK4 isolates showed pathogenic evidences at the level of genetic (Q141 and 394Q) with variable degree of virulence. In conclusion, the study reports the circulation of at least two genotypes of CAV among chicken population with mutation associated with pathogenicity.

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Section: Discussionsupporting

confidence: 92%

Full genome sequences of chicken anemia virus demonstrate mutations associated with pathogenicity in two different field isolates in Egypt

Abdel-Mawgod¹,

Adel²,

Arafa³

et al. 2018

VirusDis.

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“…Immunodepression caused by CIAV infection has dramatic effects on the poultry birds as it increases their susceptibility to secondary infections (viral, bacterial or fungal origin), depresses vaccinal immunity against other pathogens, complications like vaccinal reactions, aggravates residual pathogenicity of attenuated vaccine viruses and emergence of variant virus and most importantly leads to vaccination failure (Liu et al, 1997;Pascucci, 1997;Todd, 2000;Dhama et al, 2008). The important concurrent infections associated with CIAV infection include MD, ND, FP, ILT, IBD, etc.…”

Section: Discussionmentioning

confidence: 99%

Downregulation in cytokines profiles and immunopathological changes in chicks infected with chicken infectious anaemia virus

Basaraddi¹,

Dhama²,

Wani³

et al. 2013

Afr. J. Microbiol. Res.

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The present study was designed to study cytokine profile and lymphocytic proliferation activity in chicken infectious anaemia virus (CIAV) infected chicks at various intervals of clinically susceptible age. Briefly, ninety specific pathogen free (SPF) chicks were divided into five experimental groups (A to E). Groups A to D were inoculated with 0.5 ml of 10 4.5 TCID 50 of CIAV intramuscularly at 1, 14, 21 and 28-dayold, respectively, while group E served as uninfected control. Comparative cytokine gene expression levels of interleukin (IL)-1β, IL-10, IL-12β and granulocyte macrophage-colony stimulating factor (GM-CSF) were measured at 4 and 7 days post infection (dpi) by qRT-PCR. Also, lymphocytic proliferation activity was measured at 1, 2 and 3 week post infection (wpi) by lymphocyte transformation test (LTT). The down regulatory changes in cytokines and depressed cell mediated immune (CMI) responses were observed in chicks of all infected groups (A to D), which were significantly (p<0.05) low as compared to control group. Higher intensities and more pronounced effects on cytokine downregulation and blastogenic responses of lymphocytes were seen at younger ages. Apoptosis in thymic DNA as detected by nucleosomal fragmentation was highest on 7 and 10 dpi and lowest on 14 dpi, which correlated with down regulated cytokine profile in all infected groups. The development of clinical signs and lesions along with PCR testing confirmed the establishment of CIAV infection in experimental chicks. Increased apoptosis, decreased PCV, depletion of lymphocytes, down regulated cytokine profile and reduced lymphocyte activity explain involvement of thymic and hematopoietic precursor cells leading to CMI suppression caused by CIAV. Altogether, immunopathological changes were more severe in chicks infected at younger ages as compared to later ages of the clinically susceptible period. However, further studies are suggested regarding the impact of viral load on the various cytokine profiles and revealing more about immunopathogenesis of CIAV both in young and adult birds.

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Anemic pathogenesis of chicken infectious anemia

Cited by 2 publications

References 0 publications

Full genome sequences of chicken anemia virus demonstrate mutations associated with pathogenicity in two different field isolates in Egypt

Full genome sequences of chicken anemia virus demonstrate mutations associated with pathogenicity in two different field isolates in Egypt

Downregulation in cytokines profiles and immunopathological changes in chicks infected with chicken infectious anaemia virus

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