P122 Dengue virus targets the adaptor protein MITA to subvert host innate immunity

Yu, Chia-Yi; Chang, Tsung-Hsien; Liang, Jian-Jong; Chiang, Ruei-Lin; Lee, Y.-L.; Liao, Ching‐Len; Lin, Yin-Shoiou

doi:10.1016/j.cyto.2012.06.214

Cited by 3 publications

(3 citation statements)

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“…The NS2B protein of DENV identifies cGAS for lysosomal degradation. On the other hand, the protease activity of the NS2B-NS3 complex cleaves STING, thereby inhibiting the production of type I IFN at an optimal level [ 162 , 180 ]. During DENV infection, the JAK-STAT signaling cascade is downregulated by NS4B, specifically by hijacking STAT1 activation by an unknown mechanism yet to unfold [ 181 ].…”

Section: Immune Evasion In the Vertebrate Hostmentioning

confidence: 99%

Mechanism of Immune Evasion in Mosquito-Borne Diseases

et al. 2023

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In recent decades, mosquito-borne illnesses have emerged as a major health burden in many tropical regions. These diseases, such as malaria, dengue fever, chikungunya, yellow fever, Zika virus infection, Rift Valley fever, Japanese encephalitis, and West Nile virus infection, are transmitted through the bite of infected mosquitoes. These pathogens have been shown to interfere with the host’s immune system through adaptive and innate immune mechanisms, as well as the human circulatory system. Crucial immune checkpoints such as antigen presentation, T cell activation, differentiation, and proinflammatory response play a vital role in the host cell’s response to pathogenic infection. Furthermore, these immune evasions have the potential to stimulate the human immune system, resulting in other associated non-communicable diseases. This review aims to advance our understanding of mosquito-borne diseases and the immune evasion mechanisms by associated pathogens. Moreover, it highlights the adverse outcomes of mosquito-borne disease.

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Section: Immune Evasion In the Vertebrate Hostmentioning

confidence: 99%

Mechanism of Immune Evasion in Mosquito-Borne Diseases

et al. 2023

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“…DENV also has the capacity to directly interfere with IFN induction that is triggered by the activated cGAS/STING pathway as a result of the release of mtDNA into the cytoplasm following DENV infection [114] (Figure 1). Indeed, DENV NS2B marks cGAS for lysosomal degradation and DENV NS2B-NS3 protease cleaves STING to suppress type I IFN induction [54,58,114,115]. Interestingly, DENV NS2B3 cannot process either mouse or nonhuman primate STING orthologs, suggesting that this pathogen has evolved towards an optimal pathogenicity in its natural hosts [54,59].…”

Section: Interference With the Cgas/sting Pathwaymentioning

confidence: 99%

The Interplay between Dengue Virus and the Human Innate Immune System: A Game of Hide and Seek

et al. 2019

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With 40% of the world population at risk, infections with dengue virus (DENV) constitute a serious threat to public health. While there is no antiviral therapy available against this potentially lethal disease, the efficacy of the only approved vaccine is not optimal and its safety has been recently questioned. In order to develop better vaccines based on attenuated and/or chimeric viruses, one must consider how the human immune system is engaged during DENV infection. The activation of the innate immunity through the detection of viruses by cellular sensors is the first line of defence against those pathogens. This triggers a cascade of events which establishes an antiviral state at the cell level and leads to a global immunological response. However, DENV has evolved to interfere with the innate immune signalling at multiple levels, hence dampening antiviral responses and favouring viral replication and dissemination. This review elaborates on the interplay between DENV and the innate immune system. A special focus is given on the viral countermeasure mechanisms reported over the last decade which should be taken into consideration during vaccine development.Vaccines 2019, 7, 145 2 of 21 serotypes (1-4) in one given restricted geographic area [4,5]. While there is an unmet medical need regarding strategies against dengue, the incidence of this disease is expected to geographically expand in the future considering that the arthropod vector is colonizing northern European and American territories with temperate climates. Clinical ManifestationDENV infection is characterized by a mixed clinical presentation that ranges from an asymptomatic disease to a mild febrile prodrome all the way to a severe hemorrhagic fever and shock syndrome. All infected individuals, asymptomatic or not, can transmit DENV to Aedes mosquitoes during a blood meal, making it difficult to precisely estimate the actual size of the reservoir at any given time. DENV infection severity is classified according to the World Health Organization (WHO) 1997 and 2009 guidelines [6]. Dengue "without warning signs" (or dengue fever) regroups at-risk individuals with fever and at least two of the following signs and symptoms: nausea/vomiting, rash, headaches, eye pain, muscle aches, joint pain, leukopenia, or positivity at the tourniquet test. Dengue "with warning signs of severe infection" (or dengue hemorrhagic fever) includes in addition to the previous signs and symptoms abdominal pain, persistent vomiting, ascites, pleural effusion, mucosal bleeding, lethargy or restlessness, hepatomegaly, and an increase in hematocrit paired with rapid decrease in platelet count. Lastly, severe dengue (or dengue shock) occurs when the infection leads to severe plasma leakage, massive bleeding, and multiple organ failures. As of now, the therapeutic arsenal against DENV infection is fairly limited and only consists of supportive care and intravenous fluid therapy.From a host-pathogen interaction point of view, it is interesting to note that, in the majority of DENV-...

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“…Other than being involved in viral polyprotein processing, the NS2B-3 protease also cleaved host proteins and plays a role in immune evasion. DENV NS2B-3 protease cleaves human stimulator of the interferon gene (STING) and inhibits type I interferon pathway (Aguirre et al, 2012;Rodriguez-Madoz et al, 2010;Yu et al, 2012). Furthermore, DENV NS2B-3 protease also cleaves two mitofusins which are responsible for mitochondrial fusions, the disruption of the mitochondrial dynamics leads to an attenuated mitochondrial antiviral signalling (MAVS) and its downstream pathways (Yu et al, 2015).…”

Section: N-terminal Protease Domainmentioning

confidence: 99%

Understanding the molecular basis of flavivirus replication process for antiviral therapeutics development

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P122 Dengue virus targets the adaptor protein MITA to subvert host innate immunity

Cited by 3 publications

References 0 publications

Mechanism of Immune Evasion in Mosquito-Borne Diseases

Mechanism of Immune Evasion in Mosquito-Borne Diseases

The Interplay between Dengue Virus and the Human Innate Immune System: A Game of Hide and Seek

Understanding the molecular basis of flavivirus replication process for antiviral therapeutics development

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