Novel Function of Avian p53 in Binding to ALV-J LTR Contributes to Its Antiviral Roles

Duan, Yueyue; Cao, Liyan; Yuan, Cong; Suo, Xuepeng; Kong, Xiangyu; Gao, Yulong; Li, Xiangtong; Zheng, Haixue; Wang, Xiaomei; Wang, Qi

doi:10.1128/mbio.03287-21

Cited by 8 publications

(3 citation statements)

References 24 publications

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“…Although some studies suggest that p53 inhibits viral replication by affecting innate immune factors, the potential association between chp53 and those innate immune factors remains unclear ( 76 , 130 ). However, a recent study indicates that p53 recruits the histone deacetylase 1 and 2 (HDAC1/2) complex to the ALV-J long terminal repeat (LTR) region which regulates viral replication to switch off gene expression ( 131 , 132 ), suggesting that p53 inhibits ALV replication not only by activating innate immune response but also by inhibiting ALV-J LTR activity. Current information is still insufficient to determine the proportion of chp53 effect on suppression of ALV-J replication via innate immunity or regulating LTR of ALV.…”

Section: Innate Immune Evasion By Avian Leukosis Virus (Alv)mentioning

confidence: 99%

Advances on Innate Immune Evasion by Avian Immunosuppressive Viruses

Wang

Zheng

2022

Front. Immunol.

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Innate immunity is not only the first line of host defense against pathogenic infection, but also the cornerstone of adaptive immune response. Upon pathogenic infection, pattern recognition receptors (PRRs) of host engage pathogen-associated molecular patterns (PAMPs) of pathogens, which initiates IFN production by activating interferon regulatory transcription factors (IRFs), nuclear factor-kappa B (NF-κB), and/or activating protein-1 (AP-1) signal transduction pathways in host cells. In order to replicate and survive, pathogens have evolved multiple strategies to evade host innate immune responses, including IFN-I signal transduction, autophagy, apoptosis, necrosis, inflammasome and/or metabolic pathways. Some avian viruses may not be highly pathogenic but they have evolved varied strategies to evade or suppress host immune response for survival, causing huge impacts on the poultry industry worldwide. In this review, we focus on the advances on innate immune evasion by several important avian immunosuppressive viruses (infectious bursal disease virus (IBDV), Marek’s disease virus (MDV), avian leukosis virus (ALV), etc.), especially their evasion of PRRs-mediated signal transduction pathways (IFN-I signal transduction pathway) and IFNAR-JAK-STAT signal pathways. A comprehensive understanding of the mechanism by which avian viruses evade or suppress host immune responses will be of help to the development of novel vaccines and therapeutic reagents for the prevention and control of infectious diseases in chickens.

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Section: Innate Immune Evasion By Avian Leukosis Virus (Alv)mentioning

confidence: 99%

Advances on Innate Immune Evasion by Avian Immunosuppressive Viruses

Wang

Zheng

2022

Front. Immunol.

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“…In addition to the signalling pathway, several host proteins have been confirmed to inhibit viral replication. The oncogene p53 transcription factor recruits histone deacetylase 1 and 2 (HDAC1/2) to shut off the promoter activity of ALV integration region ( 75 ). Chicken tripartite motif-containing 62 (TRIM62) inhibits ALV-J replication through the SPRY structural domain ( 76 ), and chicken TRIM25, a member of the same tripartite motif (TRIM) family, also inhibits ALV-A replication by regulating MDA5 -mediated type I IFN response ( 77 ).…”

Section: Cellular Factors Affecting Alv Replicationmentioning

confidence: 99%

Avian Leucosis Virus-Host Interaction: The Involvement of Host Factors in Viral Replication

Táng

Chang

et al. 2022

Front. Immunol.

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Avian leukosis virus (ALV) causes various diseases associated with tumor formation and decreased fertility. Moreover, ALV induces severe immunosuppression, increasing susceptibility to other microbial infections and the risk of failure in subsequent vaccination against other diseases. There is growing evidence showing the interaction between ALV and the host. In this review, we will survey the present knowledge of the involvement of host factors in the important molecular events during ALV infection and discuss the futuristic perspectives from this angle.

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“…Globally, avian leukosis viruses (ALVs) cause severe economic losses to the poultry industry because of their infectiousness and retroviral properties [ 1 ]. Based on the host range [ 2 ], antibody neutralization and receptor interference studies [ 3 ], ALVs that infect chickens can be divided into subgroups A, B, C, D, E, J and K. Among these subgroups, subgroup J (ALV-J), which was first isolated from meat-type breeder chickens in 1988 [ 4 ], is the most prevalent in chickens [ 5 – 7 ]. Following the initiation of a nationwide eradication program (NEP) in 2008, the infection rate of exogenous ALVs in China decreased significantly [ 8 ].…”

Section: Introductionmentioning

confidence: 99%

The coinfection of ALVs causes severe pathogenicity in Three-Yellow chickens

Wang,

Wang

et al. 2024

BMC Vet Res

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The coinfection of ALVs (ALV-J plus ALV-A or/and ALV-B) has played an important role in the incidence of tumors recently found in China in local breeds of yellow chickens. The study aims to obtain a better knowledge of the function and relevance of ALV coinfection in the clinical disease of avian leukosis, as well as its unique effect on the pathogenicity in Three-yellow chickens. One-day-old Three-yellow chicks (one day old) were infected with ALV-A, ALV-B, and ALV-J mono-infections, as well as ALV-A + J, ALV-B + J, and ALV-A + B + J coinfections, via intraperitoneal injection, and the chicks were then grown in isolators until they were 15 weeks old. The parameters, including the suppression of body weight gain, immune organ weight, viremia, histopathological changes and tumor incidence, were observed and compared with those of the uninfected control birds. The results demonstrated that coinfection with ALVs could induce more serious suppression of body weight gain (P < 0.05), damage to immune organs (P < 0.05) and higher tumor incidences than monoinfection, with triple infection producing the highest pathogenicity. The emergence of visible tumors and viremia occurred faster in the coinfected birds than in the monoinfected birds. These findings demonstrated that ALV coinfection resulted in considerably severe pathogenic and immunosuppressive consequences.

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Novel Function of Avian p53 in Binding to ALV-J LTR Contributes to Its Antiviral Roles

Abstract: Rous sarcoma virus (RSV)/ALV was the first retrovirus to be discovered, which was really the first hint that cancer, or a tumor, could be transmitted by a virus. The specific mechanisms that regulate ALV replication during infection remain poorly understood.

Cited by 8 publications

References 24 publications

Advances on Innate Immune Evasion by Avian Immunosuppressive Viruses

Advances on Innate Immune Evasion by Avian Immunosuppressive Viruses

Avian Leucosis Virus-Host Interaction: The Involvement of Host Factors in Viral Replication

The coinfection of ALVs causes severe pathogenicity in Three-Yellow chickens

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