Influenza A IgM ELISA Kit (DEIA355)

Regulatory status: For research use only, not for use in diagnostic procedures.

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serum, plasma
Species Reactivity
Intended Use
The InfluenzaA IgM Antibody ELISA Test Kit has been designed for the the detection and the quantitative determination of specific IgM antibodies against Influenza A in serum and plasma.
Contents of Kit
1. Microtiter Strips
2. Calibrator A (Negative Control)
3. Calibrator B (Cut-Off Standard)
4. Calibrator C (Weak positive Control)
5. Calibrator D (Positive Control)
6. Enzyme Conjugate
7. Substrate
8. Stop Solution
9. Sample Diluent
10. Washing Buffer
11. Plastic Foils
For more detailed information, please download the following document on our website.
Intra-assay-Precision: 8.5%
Inter-assay-Precision: 6.5%
Inter-Lot-Precision: 3.8-6.1%
1.09 U/mL


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Zinc Finger CCCH-Type Antiviral Protein 1 Restricts the Viral Replication by Positively Regulating Type I Interferon Response


Authors: Zhang, Baoge; Goraya, Mohsan Ullah; Chen, Na; Xu, Lifeng; Hong, Yan; Zhu, Meiyi; Chen, Ji-Long

Zinc finger CCCH-type antiviral protein 1 (ZC3HAV1) is a host antiviral factor that can repress translation and promote degradation of specific viral mRNAs. In this study, we found that expression of ZC3HAV1 was significantly induced by infection with influenza A virus (IAV) and Sendai virus (Sev). It was shown that deficiency of IFNAR resulted in a dramatic decrease in the virus-induced expression of ZC3HAV1. Furthermore, transfection with poly(I:C) and treatment with interferon beta (IFN-beta) induced the ZC3HAV1 expression. Interference with the endogenous expression of ZC3HAV1 enhanced the replication of influenza virus by impairing the production of IFN-beta and MxA, following the infection of influenza virus. In contrast, ectopic expression of ZC3HAV1 significantly restricted the replication of influenza virus by increasing the IFN-beta expression. In addition, ZC3HAV1 also promoted the induction of tumor necrosis factor and interleukin 6. These results suggest that ZC3HAV1 is induced by IFN-beta/IFNAR signaling during IAV and Sev infection and involved in positive regulation of IFN-dependent innate antiviral response.

The Impact of TCR Signal Strength on Resident Memory T Cell Formation during Influenza Virus Infection


Authors: Fiege, Jessica K.; Stone, Ian A.; Fay, Elizabeth J.; Markman, Matthew W.; Wijeyesinghe, Sathi; Macchietto, Marissa G.; Shen, Steven; Masopust, David; Langlois, Ryan A.

Resident memory T cells (T-RM) in the lung are vital for heterologous protection against influenza A virus (IAY). Environmental factors are necessary to establish lung T-RM; however, the role of T cell-intrinsic factors like TCR signal strength have not been elucidated. In this study, we investigated the impact of TCR signal strength on the generation and maintenance of lung T-RM after IAV infection. We inserted high- and low-affinity OT-I epitopes into IAV and infected mice after transfer of OT-I T cells. We uncovered a bias in T-RM formation in the lung elicited by lower affinity TCR stimulation. TCR affinity did not impact the overall phenotype or long-term maintenance of lung T-RM. Overall, these findings demonstrate that T-RM formation is negatively correlated with increased TCR signal strength. Lower affinity cells may have an advantage in forming T-RM to ensure diversity in the Ag-specific repertoire in tissues.

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