Increasing evidence points to host Th17 inflammatory responses as contributing to the severe lung pathology and mortality of lower respiratory tract infections from coronaviruses. This includes host inflammatory and cytokine responses to COVID-19 caused by the SARS-2 coronavirus (SARS CoV2). From studies conducted in laboratory animals, there are additional concerns about immune enhancement and the role of potential host immunopathology resulting from experimental human COVID-19 vaccines. Here we summarize evidence suggesting there may be partial overlap between the underlying immunopathologic processes linked to both coronavirus infection and vaccination, and a role for Th17 in immune enhancement and eosinophilic pulmonary immunopathology. Such findings help explain the link between viral-vectored coronavirus vaccines and immune enhancement and its reduction through alum adjuvants. Additional research may also clarify links between COVID-19 pulmonary immunopathology and heart disease.

越来越多的证据表明，宿主Th17的炎症反应可导致严重的肺部疾病和冠状病毒引起的下呼吸道感染的死亡。这包括由SARS-2冠状病毒（SARS CoV2）引起的宿主对COVID-19的炎症反应和细胞因子反应。从对实验动物的研究中，人们对免疫增强和由实验性人类COVID-19疫苗产生的潜在宿主免疫病理学的作用还有其他担忧。在这里，我们总结了证据，表明与冠状病毒感染和疫苗接种相关的潜在免疫病理过程之间可能存在部分重叠，并且Th17在免疫增强和嗜酸性粒细胞肺免疫病理学中的作用。这些发现有助于解释病毒载体冠状病毒疫苗与免疫增强及其通过明矾佐剂减少之间的联系。其他研究也可能阐明COVID-19肺部免疫病理学与心脏病之间的联系。