Association of interleukin 10 and interferon gamma gene polymorphisms with enterovirus 71 encephalitis in patients with hand, foot and mouth disease

Yang, Jing; Zhao, Ning; N, Su; Sun, Jian-Lan; Lv, Teng; Chen, Zongbo

doi:10.3109/00365548.2011.649490

Cited by 35 publications

(21 citation statements)

References 29 publications

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“…Compared to mice with IFNAR deficiency alone, mice with both IFNAR and IFN-␥ receptor (IFN-␥R) deficiency display increased susceptibility to EV71 infection (37), indicating a protective role for IFN-␥. In contrast, expression and gene polymorphism of IFN-␥ have been shown to associate with EV71-induced pulmonary edema and encephalitis in patients (18,38), and exogenous administration of three cytokines (IL-6, IL-13, and IFN-␥) together exacerbates EV71-induced pulmonary abnormality with edema in mice (39). Infection by EV71 may alter IFN-␥ responses, leading to escape from both antiviral strategies and immunopathogenesis.…”

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confidence: 99%

Enterovirus 71 Proteins 2A and 3D Antagonize the Antiviral Activity of Gamma Interferon via Signaling Attenuation

Wang

Chen

Chang

et al. 2015

J Virol

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Enterovirus 71 (EV71) infection causes severe mortality involving multiple possible mechanisms, including cytokine storm, brain stem encephalitis, and fulminant pulmonary edema. Gamma interferon (IFN-␥) may confer anti-EV71 activity; however, the claim that disease severity is highly correlated to an increase in IFN-␥ is controversial and would indicate an immune escape initiated by EV71. This study, investigating the role of IFN-␥ in EV71 infection using a murine model, showed that IFN-␥ was elevated. Moreover, IFN-␥ receptor-deficient mice showed higher mortality rates and more severe disease progression with slower viral clearance than wild-type mice. E nterovirus 71 (EV71) is a single-stranded RNA virus in the Picornaviridae family. The EV71 genome encodes four structural proteins, VP1 to VP4, and seven nonstructural proteins, 2A to 2C and 3A to 3D (1). Numerous studies have investigated the functions of viral proteins in viral replication and virulence (2). During EV71 infection, capsid VP proteins mediate virus entry by binding to cellular receptors, human scavenger receptor class B and P-selectin glycoprotein ligand 1 (3). Additionally, VP proteins participate in the assembly of viral particles (4). The 3C protein, a chymotrypsin-like protease, reduces host cell transcription dramatically by inhibiting cell polyadenylation (5) and induces caspase-regulated neural cell apoptosis (6). To develop specific anti-EV71 drugs, a number of small molecules targeting viral proteins have been designed, such as the 3C inhibitor rupintrivir and the 3D inhibitor aurintricarboxylic acid (ATA) (7-9).EV71 infection typically causes mild, self-limiting hand-footand-mouth disease; however, patients sometimes have significant morbidity and mortality resulting from hemorrhagic pulmonary edema following acute central nervous system-related cardiopulmonary failure and brain stem encephalitis (2,10,11). In addition to the direct cytotoxicity caused by EV71 infection (12-16) and the resultant virulence factors (6, 17), host factors such as the aberrant production of cytokines that is detected during EV71-associated pulmonary edema can also lead to disease. In infected

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confidence: 99%

Enterovirus 71 Proteins 2A and 3D Antagonize the Antiviral Activity of Gamma Interferon via Signaling Attenuation

Wang

Chen

Chang

et al. 2015

J Virol

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“…To our knowledge, only three genetic association studies have addressed susceptibility genes that related to EV71 infection (Chang et al 2008;Yang et al 2001Yang et al , 2012. Some of the results, however, could not be replicated in subsequent studies in other populations.…”

Section: Discussionmentioning

confidence: 96%

“…Individual susceptibility to EV71 infection seems to be variable (Chang et al 2008;Yang et al 2001Yang et al , 2012. Patients with EV71 infection displayed wide clinical spectrum, ranging from asymptomatic or mild hand-foot-mouth disease (HFMD) to severe neurological disease.…”

Section: Introductionmentioning

confidence: 99%

Association of functional polymorphisms in the MxA gene with susceptibility to enterovirus 71 infection

Zhang

Chen

et al. 2013

Hum Genet

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Myxovirus resistance A (MxA) is an antiviral protein induced by type I interferons α and β (IFN-α and IFN-β) that can inhibit virus replication. We examined whether the MxA polymorphisms were related to the risk and severity of enterovirus 71 (EV71) infection in Chinese populations. The MxA C-123A and G-88T polymorphisms were genotyped in two independent case-control populations in China by polymerase chain reaction-based restriction fragment length polymorphism (PCR-RFLP) analysis. Multivariate logistic regression analysis was used to calculate adjusted odds ratios (ORs) and 95% confidence intervals (95% CIs). MxA messenger RNA was quantified by real-time quantitative PCR in peripheral blood mononuclear cells (PBMCs) from 45 healthy children and 19 patients with EV71 infection. Significantly decreased susceptibility to EV71 infection was observed for the -123A allele and -88T allele carriers, with ORs (95% CIs) estimated as 0.56 (0.39-0.81) and 0.64 (0.47-0.88), respectively, in the northern population. This association was confirmed in the southern population, with ORs (95% CIs) estimated as 0.58 (0.38-0.89) and 0.67(0.47-0.95), respectively. The A- 123T- 88 haplotype was also significantly associated with lower risk of EV71 infection in both the northern (OR = 0.62; 95% CI = 0.44-0.85) and the southern population (OR = 0.63; 95% CI = 0.43-0.92). Furthermore, we observed higher MxA messenger RNA levels in IFNβ1a-stimulated PBMCs from the -123A or -88T allele carriers compared with that from nocarriers. Our findings suggest that polymorphisms in the MxA promoter may play a role in mediating the susceptibility to EV71 infection in Chinese population.

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“…In recent years, many association studies between host genetic factors and EV71 infection have been performed. Our lab has previously demonstrated that polymorphisms in genes of IL-8, IL-10, IFN-γ, IL-6, IL-4, CXCL-10, CCL-2, TLR3, OAS3 and CPTII were associated with the susceptibility and/ or the severity of EV71 infection [24][25][26][27][28][29][30][31][32]. These cytokines/ chemokines and receptors are all necessary for an efficient inflammatory response.…”

Section: Introductionmentioning

confidence: 99%

Association of Interleukin-17F gene polymorphisms with susceptibility to severe enterovirus 71 infection in Chinese children

Guo

et al. 2018

Arch Virol

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Enterovirus 71 (EV71) is a single-strand RNA virus that causes hand, foot and mouth disease (HFMD) in infants and young children, leading to neurological complications with significant morbidity and mortality. Unfortunately, the pathogenesis of EV71 infection is not well understood. In this study, we investigated the IL-17F rs1889570 and rs4715290 gene polymorphisms in a Chinese Han population. Severe cases and cases with EV71 encephalitis had a significantly higher frequency of the rs1889570 T/T genotype and T allele. The serum IL-17F levels in rs1889570 T/T and C/T genotypes were also significantly elevated when compared to C/C genotypes. However, there was no significant difference observed in rs4715290 genotype distribution and allele frequency. These findings suggest that IL-17F rs1889570 gene polymorphisms are significantly associated with the susceptibility to severe EV71 infection in Chinese Han children.

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Association of interleukin 10 and interferon gamma gene polymorphisms with enterovirus 71 encephalitis in patients with hand, foot and mouth disease

Cited by 35 publications

References 29 publications

Enterovirus 71 Proteins 2A and 3D Antagonize the Antiviral Activity of Gamma Interferon via Signaling Attenuation

Enterovirus 71 Proteins 2A and 3D Antagonize the Antiviral Activity of Gamma Interferon via Signaling Attenuation

Association of functional polymorphisms in the MxA gene with susceptibility to enterovirus 71 infection

Association of Interleukin-17F gene polymorphisms with susceptibility to severe enterovirus 71 infection in Chinese children

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