HSV Type 1 rec. gG1 IgG-ELISA Kit (DEIA05535)

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

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serum, citrate plasma
Species Reactivity
Intended Use
The HSV 1 recombinant gG1 IgG-ELISA allows the detection of HSV 1 infection in presence of antibodies to HSV 2 in human serum or plasma (citrate).
Contents of Kit
1. HSV Type 1 Coated Wells (IgG)
2. IgG Sample Diluent
3. Stop Solution
4. Washing Solution (20X conc.)
5. HSV Type 1 anti-IgG Conjugate
6. TMB Substrate Solution
7. HSV Type 1 IgG Positive Control
8. HSV Type 1 IgG Cut-off Control
9. HSV Type 1 IgG Negative Control
The reagents are stable up to the expiry date stated on the label when stored at 2-8°C. For more detailed information, please download the following document on our website.
The diagnostic sensitivity is >95 %.


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Interferon-Independent Activities of Mammalian STING Mediate Antiviral Response and Tumor Immune Evasion


Authors: Wu, Jianjun; Dobbs, Nicole; Yang, Kun; Yan, Nan

Type I interferon (IFN) response is commonly recognized as the main signaling activity of STING. Here, we generate the Sting1(S365A/S365A) mutant mouse that precisely ablates IFN-dependent activities while preserving IFN-independent activities of STING. Sting(S365A/S365A) mice protect against HSV-1 infection, despite lacking the STING-mediated IFN response. This challenges the prevailing view and suggests that STING controls HSV-1 infection through IFN-independent activities. Transcriptomic analysis reveals widespread IFN-independent activities of STING in macrophages and T cells, and STING activities in T cells are predominantly IFN independent. In mouse tumor models, T cells in the tumor experience substantial cell death that is in part mediated by IFN-independent activities of STING. We found that the tumor induces STING-mediated cell death in T cells to evade immune control. Our data demonstrate that mammalian STING possesses widespread IFN-independent activities that are important for restricting HSV-1 infection, tumor immune evasion and likely also adaptive immunity.

Viruses and atypical bacteria in the respiratory tract of immunocompromised and immunocompetent patients with airway infection


Authors: Reckziegel, Maria; Weber-Osel, Claudia; Egerer, Renate; Gruhn, Bernd; Kubek, Florian; Walther, Mario; Wilhelm, Stefanie; Zell, Roland; Krumbholz, Andi

Respiratory tract infections (RTI) can take a serious course under immunosuppression. Data on the impact of the underlying pathogens are still controversial. Samples from the upper (n = 322) and lower RT (n = 169) were collected from 136 children and 355 adults; 225 among them have been immunocompromised patients. Exclusion criteria were presence of relevant cultivable microorganisms, C-reactive protein > 20 mg/dl, or procalcitonin > 2.0 ng/ml. Samples were tested by PCR for the presence of herpesviruses (HSV-1/-2; VZV; CMV; HHV6; EBV), adenoviruses, bocaviruses, entero-/rhinoviruses (HRV), parechoviruses, coronaviruses, influenza viruses (IV), parainfluenza viruses as well as for pneumoviruses (HMPV and RSV), and atypical bacteria (Mycoplasma pneumoniae, M.p.; Chlamydia pneumoniae, C.p.). Viral/bacterial genome equivalents were detected in more than two-thirds of specimens. Under immunosuppression, herpesviruses (EBV 30.9%/14.6%, p < 0.001; CMV 19.6%/7.9%, p < 0.001; HSV-1: 14.2%/7.1%, p = 0.012) were frequently observed, mainly through their reactivation in adults. Immunocompromised adults tended to present a higher RSV prevalence (6.4%/2.4%, p = 0.078). Immunocompetent patients were more frequently tested positive for IV (15.0%/5.8%, p = 0.001) and M.p. (6.4%/0.4%, p < 0.001), probably biased due to the influenza pandemic of 2009 and an M.p. epidemic in 2011. About 41.8% of samples were positive for a single pathogen, and among them EBV (19.9%) was most prevalent followed by HRV (18.2%) and IV (16.6%). HSV-2 and C.p. were not found. Marked seasonal effects were observed for HRV, IV, and RSV. Differences in pathogen prevalence were demonstrated between immunocompetent and immunocompromised patients. The exact contribution of some herpesviruses to the development of RTI remains unclear.

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