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MERS-CoV infection in humans is associated with a pro-inflammatory Th1 and Th17 cytokine profile

Open access
Mahallawi, Waleed H., Khabour, Omar F., Zhang, Qibo, Makhdoum, Hatim M., Suliman, Bandar A.·2018·Cytokine

Abstract

HIGHLIGHTSMERS is caused by a single‐stranded RNA virus named MERS‐corona virus.Infection with MERS‐CoV elicits a type‐I and type‐II interferon response.MERS‐CoV infected patients show a prominent Th1 and Th17 cytokine profile.MERS‐CoV infection induces the expression of IL‐10. ABSTRACT The Middle East respiratory syndrome coronavirus (MERS‐CoV) has been recognized as a highly pathogenic virus to humans that infects the respiratory tract and is associated with high morbidity and mortality. Studies in animal models suggest that MERS‐CoV infection induces a strong inflammatory response, which may be related to the severity of disease. Data showing the cytokine profiles in humans during the acute phase of MERS‐CoV infection are limited. In this study, we have analyzed the profile of cytokine responses in plasma samples from patients with confirmed MERS‐CoV infections (n=7) compared to healthy controls (n=13). The cytokine profiles, including T helper (Th) 1, Th2 and Th17 responses, were analyzed using cytometric bead array (CBA). A prominent pro‐inflammatory Th1 and Th17 response was clearly seen in patients with MERS‐CoV infection, with markedly increased concentrations of IFN‐&ggr;, TNF‐&agr;, IL‐15 and IL‐17 compared to controls. IL‐12 expression levels showed no difference between patients with MERS‐CoV infection and the healthy controls despite the significantly increased levels of IFN‐&agr;2 and IFN‐&ggr; (P<.01). No changes were observed in the levels of IL‐2, IL‐4, IL‐5, IL‐13, and TGF‐&agr; (P>.05). Our results demonstrate a marked pro‐inflammatory cytokine response during the acute phase of MERS‐CoV infection in humans.

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Metadata

Authors
Mahallawi, W. H., Khabour, O. F., Zhang, Q., Makhdoum, H. M., & Suliman, B. A.
Venue
Cytokine
Publisher
Elsevier BV
Published
2018-04
Volume
104
Pages
8-13
ISSN
1043-4666 (ISSN-L)
OpenAlex
W2790127336
Cited by
558
References
2
FWCI
68.82
Type
journal article
Language
en
Open access
green

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