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Avian Viral Immunosuppressive Disease

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A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Animal Viruses".

Deadline for manuscript submissions: closed (30 September 2022) | Viewed by 17397

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Prof. Dr. Yulong Gao

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Guest Editor

Harbin Veterinary Research Institute, The Chinese Academy of Agricultural Sciences, Harbin 150069, China
Interests: avian immunosuppressive disease; epidemiology; immune suppression; immune escape; vaccine; diagnosis; eradication

Dr. Suyan Wang

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Guest Editor

Harbin Veterinary Research Institute, The Chinese Academy of Agricultural Sciences, Harbin 150069, China
Interests: avian immunosuppressive disease; genetic variation; pathogenesis; immune suppression; immune escape; vaccine; diagnosis

Special Issue Information

Dear Colleagues,

Avian immunosuppressive diseases refer to avian diseases caused by pathogens that target and damage the immune organs or cells of birds after infection. Viral immunosuppressive pathogens that cause immunosuppression in chickens include infectious bursal disease virus (IBDV), avian leukemia virus (ALV), Marek’s disease virus (MDV), chicken infectious anemia virus (CIAV), reticuloendotheliosis virus (REV), avian reovirus (ARV), avian adenovirus (FAdV), etc. The infection of chickens with these viruses not only causes death, but also increases susceptibility to other microbial infections and the risk of failure in subsequent vaccination against other diseases, leading to serious economic losses. This Research Topic focuses on these avian immunosuppressive viruses, aimed at stimulating new ideas on how to improve the prevention and control strategies of these avian immunosuppressive diseases. Moreover, submissions on studies focusing on the basic biology, epidemiology, genetic variation, pathogenic potential, immune suppression, and immune escape of these viruses are highly welcome.

Prof. Dr. Yulong Gao
Dr. Suyan Wang
Guest Editors

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Keywords

avian immunosuppressive disease
epidemiology
genetic variation
pathogenesis
immune suppression
immune escape
vaccine
diagnosis
eradication

Published Papers (10 papers)

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Research

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13 pages, 1361 KiB

Open AccessArticle

Development of a One-Step Real-Time TaqMan Reverse Transcription Polymerase Chain Reaction (RT-PCR) Assay for the Detection of the Novel Variant Infectious Bursal Disease Virus (nVarIBDV) Circulating in China

by Chenyan Wang, Bo Hou, Guoqing Shao and Chunhe Wan

Viruses 2023, 15(7), 1453; https://doi.org/10.3390/v15071453 - 27 Jun 2023

Cited by 3 | Viewed by 1552

Abstract

The novel variant IBDV (nVarIBDV, especially genotype A2dB1) mainly affects broilers in China. It causes an infection characterized by the atrophy of the bursa, a decrease in the level of lymphocytes, proliferation of fibrous tissue around the follicle, and severe atrophy of the follicle in the bursa. Poultry vaccinated with live IBDV vaccines do not have the challenge present with bursa atrophy, which is misdiagnosed for nVarIBDV because of the lack of other gross clinical symptoms. The present study sought to explore the potential and reliability of the real-time TaqMan analysis method for the detection and discrimination of the nVarIBDV genotype from that of the non-nVarIBDV, especially in live vaccine strains. This method will help monitor vaccinated poultry to control and manage infection with the nVarIBDV IBDVs. The nucleotide polymorphism in the 5′-UTR region and the vp5/vp2 overlapping region of the segment A sequences of IBDV were used to establish a one-step real-time TaqMan reverse transcription polymerase chain reaction (RT-PCR) method in this study. The results showed that the method accurately distinguished the nVarIBDV and non-nVarIBDV strains (especially live vaccine strains), and there were no cross-reactions with the infectious bronchitis virus (IBV), Newcastle disease virus (NDV), avian influenza virus (AIV), infectious laryngotracheitis virus (ILTV), fowlpox virus (FPV), Mycoplasma gallisepticum (M. gallisepticum), Mycoplasma synoviae (M. synoviae), and IBDV-negative field samples. The method showed a linear dynamic range between 10² and 10⁷ DNA copies/reaction, with an average R² of 0.99 and an efficiency of 93% for nVarIBDV and an average R² of 1.00 and an efficiency of 94% for non-nVarIBDV. The method was also used for the detection of 84 clinical bursae of chickens vaccinated with the live vaccine. The results showed that this method accurately distinguished the nVarIBDV and non-nVarIBDV strains (vaccine strains), compared with a strategy based on the sequence analysis of HVRs at the vp2 gene or the reverse transcription PCR (RT-PCR) for the vp5 gene. These findings showed that this one-step real-time TaqMan RT-PCR method provides a rapid, sensitive, specific, and simple approach for detection of infections caused by nVarIBDV and is a useful clinical diagnostic tool for identifying and distinguishing nVarIBDV from non-nVarIBDV, especially live vaccine strains. Full article

(This article belongs to the Special Issue Avian Viral Immunosuppressive Disease)

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13 pages, 1569 KiB

Open AccessArticle

Current Epidemiology and Co-Infections of Avian Immunosuppressive and Neoplastic Diseases in Chicken Flocks in Central China

by Lu-Ping Zheng, Man Teng, Gui-Xi Li, Wen-Kai Zhang, Wei-Dong Wang, Jin-Ling Liu, Lin-Yan Li, Yongxiu Yao, Venugopal Nair and Jun Luo

Viruses 2022, 14(12), 2599; https://doi.org/10.3390/v14122599 - 22 Nov 2022

Cited by 10 | Viewed by 1350

Abstract

The avian immunosuppressive and neoplastic diseases caused by Marek’s disease virus (MDV), avian leucosis virus (ALV), and reticuloendotheliosis virus (REV) are seriously harmful to the global poultry industry. In recent years, particularly in 2020–2022, outbreaks of such diseases in chicken flocks frequently occurred in China. Herein, we collected live diseased birds from 30 poultry farms, out of 42 farms with tumour-bearing chicken flocks distributed in central China, to investigate the current epidemiology and co-infections of these viruses. The results showed that in individual diseased birds, the positive infection rates of MDV, ALV, and REV were 69.5% (203/292), 14.4% (42/292), and 4.7% (13/277), respectively, while for the flocks, the positive infection rates were 96.7% (29/30), 36.7% (11/30), and 20% (6/30), respectively. For chicken flocks, monoinfection of MDV, ALV, or REV was 53.3% (16/30), 3.3% (1/30), and 0% (0/30), respectively, but a total of 43.3% (13/30) co-infections was observed, which includes 23.3% (7/30) of MDV+ALV, 10.0% (3/30) of MDV+REV, and 10.0% (3/30) of MDV+ALV+REV co-infections. Interestingly, no ALV+REV co-infection or REV monoinfection was observed in the selected poultry farms. Our data indicate that the prevalence of virulent MDV strains, partially accompanied with ALV and/or REV co-infections, is the main reason for current outbreaks of avian neoplastic diseases in central China, providing an important reference for the future control of disease. Full article

(This article belongs to the Special Issue Avian Viral Immunosuppressive Disease)

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15 pages, 3708 KiB

Open AccessArticle

Synergistic Immunosuppression of Avian Leukosis Virus Subgroup J and Infectious Bursal Disease Virus Is Responsible for Enhanced Pathogenicity

by Weiguo Chen, Sheng Chen, Yu Nie, Wenxue Li, Hongxin Li, Xinheng Zhang, Feng Chen and Qingmei Xie

Viruses 2022, 14(10), 2312; https://doi.org/10.3390/v14102312 - 21 Oct 2022

Cited by 6 | Viewed by 1637

Abstract

In recent years, superinfections of avian leukosis virus subgroup J (ALV-J) and infectious bursal disease virus (IBDV) have been frequently observed in nature, which has led to the increasing virulence in infected chickens. However, the reason for the enhanced pathogenicity has remained unclear. In this study, we demonstrated an effective candidate model for studying the outcome of superinfections with ALV-J and IBDV in cells and specific-pathogen-free (SPF) chicks. Through in vitro experiments, we found that ALV-J and IBDV can establish the superinfection models and synergistically promote the expression of IL-6, IL-10, IFN-α, and IFN-γ in DF-1 and CEF cells. In vivo, the weight loss, survival rate, and histopathological observations showed that more severe pathogenicity was present in the superinfected chickens. In addition, we found that superinfections of ALV-J and IBDV synergistically increased the viral replication of the two viruses and inflammatory mediator secretions in vitro and in vivo. Moreover, by measuring the immune organ indexes and blood proportions of CD3⁺, CD4⁺, and CD8α⁺ cells, our results showed that the more severe instances of immunosuppression were observed in the superinfected chickens. In the present study, we concluded that the more severe immunosuppression induced by the synergistic viral replication of ALV-J and IBDV is responsible for the enhanced pathogenicity. Full article

(This article belongs to the Special Issue Avian Viral Immunosuppressive Disease)

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12 pages, 3543 KiB

Open AccessArticle

A20 Enhances the Expression of the Proto-Oncogene C-Myc by Downregulating TRAF6 Ubiquitination after ALV-A Infection

by Xueyang Chen, Xingming Wang, Yuxin Yang, Chun Fang, Jing Liu, Xiongyan Liang and Yuying Yang

Viruses 2022, 14(10), 2210; https://doi.org/10.3390/v14102210 - 7 Oct 2022

Viewed by 1423

Abstract

Hens infected with avian leukosis virus subgroup A (ALV-A) experience stunted growth, immunosuppression, and potentially, lymphoma development. According to past research, A20 can both promote and inhibit tumor growth. In this study, DF-1 cells were infected with ALV-A rHB2015012, and Gp85 expression was measured at various time points. A recombinant plasmid encoding the chicken A20 gene and short hairpin RNA targeting chicken A20 (A20-shRNA) was constructed and transfected into DF-1 cells to determine the effect on ALV-A replication. The potential signaling pathways of A20 were explored using bioinformatics prediction, co-immunoprecipitation, and other techniques. The results demonstrate that A20 and ALV-A promoted each other after ALV-A infection of DF-1 cells, upregulated A20, inhibited TRAF6 ubiquitination, and promoted STAT3 phosphorylation. The phosphorylated-STAT3 (p-STAT3) promoted the expression of proto-oncogene c-myc, which may lead to tumorigenesis. This study will help to further understand the tumorigenic process of ALV-A and provide a reference for preventing and controlling ALV. Full article

(This article belongs to the Special Issue Avian Viral Immunosuppressive Disease)

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9 pages, 1392 KiB

Open AccessArticle

The Interaction between B87 Vaccine Strain and BC6/85 of Infectious Bursa Disease Virus in SPF Chickens

by Ling Chen, Xiaoyue Yang, Yafen Song and Taozhen Jiang

Viruses 2022, 14(10), 2111; https://doi.org/10.3390/v14102111 - 23 Sep 2022

Viewed by 1162

Abstract

This study was initiated to determine the interaction between two infectious bursal disease virus (IBDV) strains in the early stages of infection by detection and quantification of IBDV RNA in lymphoid and non-lymphoid tissues. SPF chickens were inoculated with single infection or dual infection by the mild strain B87 followed by the pathogenic strain BC6/85 at 0, 1, 2, and 3 days post-inoculation (dpi) with B87. Real-time RT-PCR assays were developed to examine the viral loads of the tissues collected at various time intervals. The results reveal that B87 could delay the time point of positive detection of the BC6/85 strain in the bursa of Fabricius from 1 dpi to 3 dpi, indicating that B87 interfered with the replication of BC6/85. The interference occurred when BC6/85 was inoculated at 2 dpi and 3 dpi with the B87 strain. Moreover, BC6/85 could affect the proliferation and duration of B87 in SPF chickens. The rates of positive detection for B87 decreased significantly during dual infection. The investigation of the interaction between the two strains is important for the implementation of appropriate control measures. Full article

(This article belongs to the Special Issue Avian Viral Immunosuppressive Disease)

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11 pages, 3902 KiB

Open AccessArticle

Complete Genome Analysis and Animal Model Development of Fowl Adenovirus 8b

by Aijing Liu, Yu Zhang, Jing Wang, Hongyu Cui, Xiaole Qi, Changjun Liu, Yanping Zhang, Kai Li, Li Gao, Xiaomei Wang, Yulong Gao and Qing Pan

Viruses 2022, 14(8), 1826; https://doi.org/10.3390/v14081826 - 20 Aug 2022

Cited by 2 | Viewed by 1731

Abstract

Inclusion body hepatitis (IBH), hydropericardium syndrome, and gizzard erosion associated with fowl adenovirus (FAdV) infection have caused notable economic losses worldwide. In 2020, severe IBH was observed in a layer chicken farm in Hebei Province, China. Liver samples were collected from layer chickens with severe IBH and virus isolation was performed in LMH cells. DNA sequence and bioinformatics analyses were conducted to determine the phylogenetic relationship and the pathogenicity assay was conducted in specific-pathogen-free (SPF) chickens. HeB20 strain was isolated and identified as FAdV-8b, and the complete genome was successfully sequenced (GenBank No. OK188966). Although widespread recombination in clinical strains has been reported within FAdVs, HeB20 showed some novel characteristics, and did not show any recombination, highlighting that recombinant and non-recombinant FAdV-8b coexist in the clinic poultry industry. Finally, pathogenicity animal model of HeB20 was developed and showed severe IBH and 10% mortality. Collectively, a new FAdV-8b strain (HeB20) was isolated and responsible for the severe IBH in layer chickens. Complete genome of HeB20 was sequenced and valuable for future epidemiological investigations. HeB20 was capable of inducing severe IBH and 10% mortality in SPF chickens; this animal model provides a powerful tool for the future vaccine development. Full article

(This article belongs to the Special Issue Avian Viral Immunosuppressive Disease)

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18 pages, 4255 KiB

Open AccessArticle

Stromal Interaction Molecule 1 Promotes the Replication of vvIBDV by Mobilizing Ca²⁺ in the ER

by Nana Yan, Yongqiang Wang, Zehua Chen, Aijing Liu, Yue Li, Bo Yang, Kai Li, Xiaole Qi, Yulong Gao, Li Gao, Changjun Liu, Yanping Zhang, Hongyu Cui, Qing Pan and Xiaomei Wang

Viruses 2022, 14(7), 1524; https://doi.org/10.3390/v14071524 - 13 Jul 2022

Cited by 2 | Viewed by 1627

Abstract

Infectious bursal disease virus (IBDV) is one of the main threats to the poultry industry worldwide. Very virulent IBDV (vvIBDV) is a fatal virus strain that causes heavy mortality in young chicken flocks. Ca²⁺ is one of the most universal and versatile signalling molecules and is involved in almost every aspect of cellular processes. Clinical examination showed that one of the characteristics of vvIBDV-infected chickens was severe metabolic disorders, and the chemical examination showed that their serum Ca²⁺ level decreased significantly. However, there are limited studies on how vvIBDV infection modulates the cellular Ca²⁺ level and the effect of Ca²⁺ level changes on vvIBDV replication. In our study, we found Ca²⁺ levels in the endoplasmic reticulum (ER) of vvIBDV-infected B cells were higher than that of mock-infected cells, and the expression level of stromal interaction molecule 1 (STIM1), an ER Ca²⁺ sensor, was significantly upregulated due to vvIBDV infection. The knock-down expression of STIM1 led to decreased Ca²⁺ level in the ER and suppressed vvIBDV replication, while the over-expressed STIM1 led to ER Ca²⁺ upregulation and promoted vvIBDV replication. We also showed that the inhibition of Ca²⁺-release-activated-Ca²⁺ (CRAC) channels could reduce vvIBDV infection by blocking Ca²⁺ from entering the ER. This study suggests a new mechanism that STIM1 promotes the replication of vvIBDV by mobilizing Ca²⁺ in the ER. Full article

(This article belongs to the Special Issue Avian Viral Immunosuppressive Disease)

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Review

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18 pages, 1150 KiB

Open AccessReview

Host Combats IBDV Infection at Both Protein and RNA Levels

by Shujun Zhang and Shijun Zheng

Viruses 2022, 14(10), 2309; https://doi.org/10.3390/v14102309 - 21 Oct 2022

Cited by 4 | Viewed by 1861

Abstract

Infectious bursal disease (IBD) is an acute, highly contagious, and immunosuppressive avian disease caused by infectious bursal disease virus (IBDV). In recent years, with the emergence of IBDV variants and recombinant strains, IBDV still threatens the poultry industry worldwide. It seems that the battle between host and IBDV will never end. Thus, it is urgent to develop a more comprehensive and effective strategy for the control of this disease. A better understanding of the mechanisms underlying virus–host interactions would be of help in the development of novel vaccines. Recently, much progress has been made in the understanding of the host response against IBDV infection. If the battle between host and IBDV at the protein level is considered the front line, at the RNA level, it can be taken as a hidden line. The host combats IBDV infection at both the front and hidden lines. Therefore, this review focuses on our current understanding of the host response to IBDV infection at both the protein and RNA levels. Full article

(This article belongs to the Special Issue Avian Viral Immunosuppressive Disease)

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11 pages, 1112 KiB

Open AccessReview

The Over-40-Years-Epidemic of Infectious Bursal Disease Virus in China

by Wenying Zhang, Xiaomei Wang, Yulong Gao and Xiaole Qi

Viruses 2022, 14(10), 2253; https://doi.org/10.3390/v14102253 - 14 Oct 2022

Cited by 24 | Viewed by 2401

Abstract

Infectious bursal disease (IBD) is an acute, highly contagious, immunosuppressive disease of chickens caused by the virus (IBDV), which critically threatens the development of the global chicken industry and causes huge economic losses. As a large country in the poultry industry, the epidemic history of IBDV in China for more than 40 years has been briefly discussed and summarized for the first time in this report. The first classic strain of IBDV appeared in China in the late 1970s. In the late 1980s and early 1990s, the very virulent IBDV (vvIBDV) rapidly swept across the entirety of China, threatening the healthy development of the poultry industry for more than 30 years. Variants of IBDV, after long-term latent circulation with the accumulation of mutations since the early 1990s, suddenly reappeared as novel variant strains (nVarIBDV) in China in the mid-2010s. Currently, there is a coexistence of various IBDV genotypes; the newly emerging nVarIBDV of A2dB1 and persistently circulating vvIBDV of A3B3 are the two predominant epidemic strains endangering the poultry industry. Continuous epidemiological testing and the development of new prevention and control agents are important and require more attention. This report is of great significance to scientific cognition and the comprehensive prevention and control of the IBDV epidemic. Full article

(This article belongs to the Special Issue Avian Viral Immunosuppressive Disease)

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Other

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9 pages, 1495 KiB

Open AccessBrief Report

Modeling Infectious Bursal Disease Virus (IBDV) Antigenic Drift In Vitro

by Amin S. Asfor, Vishwanatha R. A. P. Reddy, Salik Nazki, Joanna Urbaniec, Andrew J. Brodrick and Andrew J. Broadbent

Viruses 2023, 15(1), 130; https://doi.org/10.3390/v15010130 - 31 Dec 2022

Cited by 4 | Viewed by 1687

Abstract

Infectious bursal disease virus (IBDV) vaccines do not induce sterilizing immunity, and vaccinated birds can become infected with field strains. Vaccine-induced immune selection pressure drives the evolution of antigenic drift variants that accumulate amino acid changes in the hypervariable region (HVR) of the VP2 capsid, which may lead to vaccine failures. However, there is a lack of information regarding how quickly mutations arise, and the relative contribution different residues make to immune escape. To model IBDV antigenic drift in vitro, we serially passaged a classical field strain belonging to genogroup A1 (F52/70) ten times, in triplicate, in the immortalized chicken B cell line, DT40, in the presence of sub-neutralizing concentrations of sera from birds inoculated with IBDV vaccine strain 2512, to generate escape mutants. This assay simulated a situation where classical strains may infect birds that have suboptimal vaccine-induced antibody responses. We then sequenced the HVR of the VP2 capsid at passage (P) 5 and 10 and compared the sequences to the parental virus (P0), and to the virus passaged in the presence of negative control chicken serum that lacked IBDV antibodies. Two escape mutants at P10 had the same mutations, D279Y and G281R, and a third had mutations S251I and D279N. Furthermore, at P5, the D279Y mutation was detectable, but the G281R mutation was not, indicating the mutations arose with different kinetics. Full article

(This article belongs to the Special Issue Avian Viral Immunosuppressive Disease)

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