Dynamics of cellular and humoral immune responses following duck Tembusu virus infection in ducks

Thontiravong, Aunyaratana; Nedumpun, Teerawut; Ninvilai, Patchareeporn; Tunterak, Wikanda; Techakriengkrai, Navapon; Banlunara, Wijit; Suradhat, Sanipa

doi:10.1111/tbed.14467

Cited by 7 publications

(3 citation statements)

References 40 publications

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“…This difference may be attributed to the distinct viral replication capacity of each cluster in ducks. It should be noted that although the severity of disease gradually declined over the course of cluster 1 DTMUV infection, no obvious correlation was observed between neutralizing antibody titers and viral loads in blood and tissues, which contrasted with those observed in cluster 2.1 DTMUV [10,29]. This suggested that other immunological mechanisms, particularly cellular immune response, may be involved in the control of cluster 1 DTMUV infection in ducks, which warrants further investigation.…”

Section: Discussionmentioning

confidence: 85%

Pathogenesis of Cluster 1 Duck Tembusu Virus in Ducks Reveals the Impact of Viral Genotype on Pathogenicity and Disease Severity

Tunterak,

Rungprasert,

Wannaratana

et al. 2023

Transboundary and Emerging Diseases

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Duck Tembusu virus (DTMUV), an emerging avian pathogenic flavivirus, causes severe neurological disorders and acute egg drop syndrome in ducks. Currently, several clusters of DTMUV, including clusters 1, 2, and 3, have been identified and caused outbreaks in Asia. However, most of the DTMUV pathogenesis evaluation has mainly focused on cluster 2, while limited information is available on the pathogenesis of other DTMUV clusters, particularly cluster 1. In this study, the pathogenesis of a cluster 1 DTMUV was investigated in Cherry Valley ducks and compared to our previously reported cluster 2.1 DTMUV. Our results demonstrated that cluster 1 DTMUV was generally less pathogenic than cluster 2.1 DTMUV in ducks as evidenced by slower body weight loss, lower morbidity and mortality rates, and milder pathological changes. Concordantly, delayed viremia, reduced viral loads in blood and tissues, and shorter shedding period with lower viral loads were also observed in cluster 1 DTMUV inoculated ducks compared with those reported in cluster 2.1 DTMUV. In addition, we also found that cluster 1 DTMUV exhibited significant antigenic difference compared to cluster 2.1 DTMUV. Altogether, our findings suggest distinct pathogenicity and antigenicity between cluster 1 and 2.1 DTMUVs in ducks, highlighting the potential association between DTMUV genotype and pathogenicity/disease severity. This study enhances our understanding of DTMUV pathogenesis in ducks and provides useful information for the design and development of effective DTMUV vaccines.

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Section: Discussionmentioning

confidence: 85%

Pathogenesis of Cluster 1 Duck Tembusu Virus in Ducks Reveals the Impact of Viral Genotype on Pathogenicity and Disease Severity

Tunterak,

Rungprasert,

Wannaratana

et al. 2023

Transboundary and Emerging Diseases

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“…In ducks infected with DTMUV, there was a significant negative correlation between the levels of CD4+ and CD8+ T, B, and non-T and -B lymphocytes and the viral load in the blood and target organs (spleen). Additionally, significant neutralizing antibody responses were observed [126]. DTMUV infection upregulates suppressor of cytokine signaling 1 (SOCS1), leading to ubiquitination and proteasomal degradation of IRF7, ultimately inhibiting the production of type I IFNs and promoting viral replication [127].…”

Section: Innate Immune Responsesmentioning

confidence: 99%

Advancements in Research on Duck Tembusu Virus Infections

Cheng,

Wang,

et al. 2024

Viruses

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Duck Tembusu Virus (DTMUV) is a pathogen of the Flaviviridae family that causes infections in poultry, leading to significant economic losses in the duck farming industry in recent years. Ducks infected with this virus exhibit clinical symptoms such as decreased egg production and neurological disorders, along with serious consequences such as ovarian hemorrhage, organ enlargement, and necrosis. Variations in morbidity and mortality rates exist across different age groups of ducks. It is worth noting that DTMUV is not limited to ducks alone; it can also spread to other poultry such as chickens and geese, and antibodies related to DTMUV have even been found in duck farm workers, suggesting a potential risk of zoonotic transmission. This article provides a detailed overview of DTMUV research, delving into its genomic characteristics, vaccines, and the interplay with host immune responses. These in-depth research findings contribute to a more comprehensive understanding of the virus’s transmission mechanism and pathogenic process, offering crucial scientific support for epidemic prevention and control.

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“…Using duck models of TMUV infection, the TMUV-induced cellular immune response is beginning to be understood. TMUV induces significant up-regulation of IL-2 and IFN-γ at 7 days post infection (pi) ( 9 , 28 ), and significant increases in numbers of CD4 + and CD8 + T cells at 5 days pi ( 29 ). The E, prM/E, and C proteins were shown to induce cellular immune response by measurement of the expression of cytokines (e.g., IL-2, IL-4, IL-6, IFN-γ, and TNF-α) or the change of CD4 + and CD8 + T cell numbers in ducks following immunization with subunit vaccine, DNA vaccine, and live vector vaccine ( 13 , 14 , 17 , 19 , 20 , 22 , 27 ).…”

Section: Introductionmentioning

confidence: 99%

The difference in CD4+ T cell immunity between high- and low-virulence Tembusu viruses is mainly related to residues 151 and 304 in the envelope protein

et al. 2022

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Tembusu virus (TMUV) can result in a severe disease affecting domestic ducks. The role of T cells in protection from TMUV infection and the molecular basis of T cell-mediated protection against TMUV remain largely uncharacterized. Here, we used the high-virulence TMUV strain Y and the low-virulence TMUV strain PS to investigate the protective role for TMUV-specific CD4+ and CD8+ T cells. When tested in a 5-day-old Pekin duck model, Y and PS induced comparable levels of neutralizing antibody, whereas Y elicited significantly stronger cellular immune response relative to PS. Using a duck adoptive transfer model, we showed that both CD4+ and CD8+ T cells provided significant protection from TMUV-related disease, with CD8+ T cell conferring more robust protection to recipient ducklings. For TMUV, CD4+ T cells mainly provided help for neutralizing antibody response, whereas CD8+ T cells mainly mediated viral clearance from infected tissues. The difference in T cell immunity between Y and PS was primarily attributed to CD4+ T cells; adoptive transfer of Y-specific CD4+ T cells resulted in significantly enhanced protective ability, neutralizing antibody response, and viral clearance from the brain relative to PS-specific CD4+ T cells. Further investigations with chimeric viruses, mutant viruses, and their parental viruses identified two mutations (T151A and R304M) in the envelope (E) protein that contributed significantly to TMUV-specific CD4+ T cell-mediated protective ability and neutralizing antibody response, with more beneficial effects being conferred by R304M. These data indicate T cell-mediated immunity is important for protection from disease, for viral clearance from tissues, and for the production of neutralizing antibodies, and that the difference in CD4+T cell immunity between high- and low-virulence TMUV strains is primarily related to residues 151 and 304 in the E protein.

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Dynamics of cellular and humoral immune responses following duck Tembusu virus infection in ducks

Cited by 7 publications

References 40 publications

Pathogenesis of Cluster 1 Duck Tembusu Virus in Ducks Reveals the Impact of Viral Genotype on Pathogenicity and Disease Severity

Pathogenesis of Cluster 1 Duck Tembusu Virus in Ducks Reveals the Impact of Viral Genotype on Pathogenicity and Disease Severity

Advancements in Research on Duck Tembusu Virus Infections

The difference in CD4+ T cell immunity between high- and low-virulence Tembusu viruses is mainly related to residues 151 and 304 in the envelope protein

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