Avian influenza viruses suppress innate immunity by inducing trans-transcriptional readthrough via SSU72

Zhao, Yan; Huang, Fengming; Zou, Zhen; Bi, Yuhai; Yang, Yang; Zhang, Cong; Liu, Qiang; Shang, Daozhen; Yan, Yongnian; Ju, Xiangwu; Song, Moshi; Xie, Peng; Li, Xiao; Tian, Mingyao; Tan, Shuguang; Lu, Huijun; Han, Zongsheng; Liu, Kangtai; Zhang, Yuqing; Liang, Junbo; Zhu, Lei; Zhang, Qingchao; Chang, Jian; Liu, William J.; Feng, Cong; Li, Tanshi; Zhang, Michael Q.; Wang, Xiaoyue; Gao, Lidong; Liu, Yingxia; Jin, Ningyi; Jiang, Chengyu

doi:10.1038/s41423-022-00843-8

Cited by 5 publications

(4 citation statements)

References 46 publications

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“…Compared with less virulent seasonal IAV, highly pathogenic avian influenza virus (HPAIV) H5N1, H5N6, and H7N9 can better bypass the innate immune response. Furthermore, through the molecular mechanism of the NS1-SSU72-trans-transcriptional readthrough (TRT)-STAT1/2 axis, AIV infection can reduce the expression of SSU72 and induce TRT, thereby weakening the innate immune response ( Figure 2B ) ( Zhao et al, 2022 ). Thus, restoring SSU72 expression could be a potential strategy for preventing AIV pandemics.…”

Section: Iav Escapes From Innate Immunementioning

confidence: 99%

Virus versus host: influenza A virus circumvents the immune responses

Su,

Chen,

et al. 2024

Front. Microbiol.

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Influenza A virus (IAV) is a highly contagious pathogen causing dreadful losses to humans and animals around the globe. As is known, immune escape is a strategy that benefits the proliferation of IAVs by antagonizing, blocking, and suppressing immune surveillance. The HA protein binds to the sialic acid (SA) receptor to enter the cytoplasm and initiate viral infection. The conserved components of the viral genome produced during replication, known as the pathogen-associated molecular patterns (PAMPs), are thought to be critical factors for the activation of effective innate immunity by triggering dependent signaling pathways after recognition by pattern recognition receptors (PRRs), followed by a cascade of adaptive immunity. Viral infection-induced immune responses establish an antiviral state in the host to effectively inhibit virus replication and enhance viral clearance. However, IAV has evolved multiple mechanisms that allow it to synthesize and transport viral components by “playing games” with the host. At its heart, this review will describe how host and viral factors interact to facilitate the viral evasion of host immune responses.

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Section: Iav Escapes From Innate Immunementioning

confidence: 99%

Virus versus host: influenza A virus circumvents the immune responses

Su,

Chen,

et al. 2024

Front. Microbiol.

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“…Yan Zhao et al have reported a novel mechanism employed by highly pathogenic avian IAV to further escape host innate immunity, which is through altering the transcriptional readthrough (TRT) [110]. The authors showed that NS1 binds to SSU72 (RNA polymerase II subunit A C-terminal domain phosphatase), leading to a reduction in its expression that eventually induces TRT and represses STAT1/2 mRNA expression, which enabled the virus to evade host antiviral immune responses [110]. IAV infection was also shown to induce the degradation of a sub-nuclear structure known as the Nuclear Domain-10 (ND-10) [111], which has been known to play a role in antiviral defense during IAV infection [112,113].…”

Section: Viral Ns1mentioning

confidence: 99%

Triggering Degradation of Host Cellular Proteins for Robust Propagation of Influenza Viruses

Xia,

Wang,

Hahm

2024

IJMS

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Following infection, influenza viruses strive to establish a new host cellular environment optimized for efficient viral replication and propagation. Influenza viruses use or hijack numerous host factors and machinery not only to fulfill their own replication process but also to constantly evade the host’s antiviral and immune response. For this purpose, influenza viruses appear to have formulated diverse strategies to manipulate the host proteins or signaling pathways. One of the most effective tactics is to specifically induce the degradation of the cellular proteins that are detrimental to the virus life cycle. Here, we summarize the cellular factors that are deemed to have been purposefully degraded by influenza virus infection. The focus is laid on the mechanisms for the protein ubiquitination and degradation in association with facilitated viral amplification. The fate of influenza viral infection of hosts is heavily reliant on the outcomes of the interplay between the virus and the host antiviral immunity. Understanding the processes of how influenza viruses instigate the protein destruction pathways could provide a foundation for the development of advanced therapeutics to target host proteins and conquer influenza.

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“…On the other hand, the SSU72 overexpression reduced lung damage and protected animals infected with H5N1 from inhibiting the antiviral gene expression. Hence, it was emphasized that SSU72 might act as a possible therapeutic target in the treatment of AIV infections [ 186 ].…”

Section: Immune Response To Avian Influenza Virusesmentioning

confidence: 99%

Immune Control of Avian Influenza Virus Infection and Its Vaccine Development

et al. 2023

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The avian influenza A virus (AIV) is naturally prevalent in aquatic birds, infecting different avian species and transmitting from birds to humans. Both AIVs, the H5N1 and H7N9 viruses, have the potential to infect humans, causing an acute influenza disease syndrome in humans, and are a possible pandemic threat. AIV H5N1 is highly pathogenic, whereas AIV H7N9 has comparatively low pathogenicity. A clear insight into the disease pathogenesis is significant to understand the host’s immunological response, which in turn facilitates the design of the control and prevention strategies. In this review, we aim to provide comprehensive details on the pathogenesis and clinical features of the disease. Moreover, the innate and adaptive immunological responses to AIV and the recent studies conducted on the CD8+ T cell immunity against AIVs are detailed upon. Further, the current status and advancement in the development of AIV vaccines, along with the challenges, are also discussed. The information provided will be helpful in combating the transmission of AIV from birds to humans and, thus, preventing severe outbreaks leading to pandemics worldwide.

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Avian influenza viruses suppress innate immunity by inducing trans-transcriptional readthrough via SSU72

Cited by 5 publications

References 46 publications

Virus versus host: influenza A virus circumvents the immune responses

Virus versus host: influenza A virus circumvents the immune responses

Triggering Degradation of Host Cellular Proteins for Robust Propagation of Influenza Viruses

Immune Control of Avian Influenza Virus Infection and Its Vaccine Development

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