The importance of inflammasome, and related cytokines IL-1ß and IL-18, in host defense against pathogens is well documented, however, at the same time, dysregulation of inflammasome has been associated to multifactorial diseases characterized by chronic inflammation (i.e.: metabolic disorders, cardiovascular diseases, neurodegenerative diseases, autoimmunity, cancer). Inflammasome activation has been described in response to HIV-1 and possibly contributes to the resistance against virus establishment, however, on the other hand, when viral infection becomes chronic, independently from antiretroviral therapy, the increase constitutive activation of inflammasome has been eventually associated to a worse prognosis, raising the question about the role played by inflammasome and/or some specific receptors in this context. Due to the chance to imply targeted therapies that inhibit inflammasome activation and/or cytokines release, it will be important to define the impact of the complex in the pathogenesis of HIV. The purpose of this review is to depict the double-faced inflammasome role in HIV-1 infection, trying to unveil whether besides its role in first line defense against the virus, it exerts a harmful effect during the chronic phase of infection.

中文翻译：

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HIV感染中的炎症小体：光影。

炎症小体及相关的细胞因子IL-1ß和IL-18在抵抗病原体的宿主中的重要性已得到充分证明，但是，与此同时，炎症小体的失调与以慢性炎症为特征的多因素疾病（例如，代谢紊乱）有关，心血管疾病，神经退行性疾病，自身免疫性疾病，癌症）。炎症小体激活已被描述为对HIV-1的反应，并可能有助于抵抗病毒的建立，但是，另一方面，当病毒感染呈慢性时，独立于抗逆转录病毒疗法，炎症小体的组成型激活增加最终与预后较差，这引发了关于炎性体和/或某些特定受体在这种情况下所起的作用的问题。由于有可能暗示抑制炎症小体活化和/或细胞因子释放的靶向疗法，因此确定复合物在HIV发病机理中的影响将非常重要。这篇综述的目的是描述在HIV-1感染中炎症分子的双重作用，试图揭示它除了在针对病毒的一线防御中的作用之外，是否在感染的慢性阶段发挥了有害作用。