Coronavirus disease 2019 (COVID-19) consists of a severe involvement of the lower respiratory tract leading to an acute respiratory syndrome. But there exist other infectious respiratory syndromes that have the same initial respiratory symptoms, show similar pattern in the size of the antigenic proteins and release comparable cytokines pathways, but with an unlike response magnitude. Here we propose that COVID-19 disease wrong response in the host immune system can be explained in the perspective of the antigen viral size. In COVID-19 sepsis, the < 70 kDa antigens activate the B-cell receptor (BCR), which modulates the shift in the pattern of T-helper 1 (Th1) to Th2 cytokines, increases the release of interleukin-10 (IL-10) and the up-regulation of the membrane form of tumor necrosis factor alpha (TNF-α), promoting the production of immunoglobulin G1 (IgG1)- and IgG3-neutralizing antibodies, but failing in IgG2a production and in developing long-lasting B-cell immune memory. The sustained infected cells lysis overfeeds high levels of viral proteins < 70 kDa, increases B-cell activation and, in the shift from a Th1 to a Th2 immune response, can trigger a cytokine storm. The continuous BCR activation increases IL-10 release that can lead to cytokine storm, apoptosis, and immune paralysis. Here, we propose a new vaccine design using the polymerization of viral antigens that could be ready in short time, would be cheap and easy to develop because it is based on classic technologies available in every country, is safe because it does not employ genetic material, and would able to promote long-lasting B-cell immune memory and IgG2a production.

中文翻译：

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小于70千道尔顿的病毒蛋白可防止COVID-19疫苗中长期持久的B细胞免疫记忆的发展和IgG2a的预防

2019年冠状病毒病（COVID-19）包括下呼吸道的严重感染导致急性呼吸道综合症。但是，还有其他传染性呼吸综合征，它们具有相同的初始呼吸道症状，抗原蛋白的大小显示出相似的模式，并释放出可比的细胞因子途径，但反应幅度却不同。在这里，我们建议可以从抗原病毒大小的角度解释宿主免疫系统中的COVID-19疾病错误反应。在COVID-19败血症中，<70 kDa的抗原激活B细胞受体（BCR），从而调节T辅助1（Th1）向Th2细胞因子模式的转变，增加白介素10（IL- 10）和肿瘤坏死因子α（TNF-α）的膜形式上调，促进产生免疫球蛋白G1（IgG1）和中和IgG3的抗体，但无法产生IgG2a和发展持久的B细胞免疫记忆。持续的受感染细胞裂解使高水平的<70 kDa病毒蛋白超载，增加B细胞活化，并在从Th1免疫反应转变为Th2免疫反应时触发细胞因子风暴。BCR的持续激活会增加IL-10的释放，从而导致细胞因子风暴，凋亡和免疫麻痹。在这里，我们提出了一种使用病毒抗原聚合的新型疫苗设计，这种疫苗设计可在短时间内准备就绪，价格便宜，易于开发，因为它基于每个国家/地区的经典技术，因此很安全，因为它不使用遗传材料，并能够促进持久的B细胞免疫记忆和IgG2a产生。