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关于SARS的发病机制 ,目前尚有争议。有人认为SARS冠状病毒 (SARS CoV)与人类免疫缺陷病毒 (HIV)一样 ,主要是损伤人体的免疫器官 ,其发病与免疫器官的损伤有关 ,其依据是 :SARS患者的外周血淋巴细胞的计数减少 ,T淋巴细胞亚群CD4 + 和CD8+ 细胞数减少 ;病理学检查发现 ,除肺部损伤外 ,SARS死亡病例的尸检中可见脾脏萎缩、淋巴结出血及坏死等。本文作者综述了近一年来国内外发表的有关SARS发病机制的论文 ,认为SARS CoV并不直接损伤人体的免疫器官 ,因大多数SARS患者在发病 2周后 ,血液中可检测到特异性抗 SARS CoVIgM和IgG抗体 ;血浆中多种细胞因子如肿瘤坏死因子 (TNF α)和一些白细胞介素 (IL)明显升高 ,说明其机体体液免疫和细胞免疫是正常的 ;HIV感染者由于机体免疫功能损伤而导致慢性感染和各种机会性感染 ;与SARS患者发生的继发感染有别。由于SARS CoV的发现仅 1年时间 ,对其研究尚不充分 ,目前对SARS的发病机制尚难下最后结论。本刊发表此文的初衷是发扬学术民主 ,提倡“百家争鸣 ,百花齐放” ,以便进一步推动对SARS发病机制的研究。
There are still controversies about the pathogenesis of SARS. Some people think that SARS CoV (SARS CoV), like human immunodeficiency virus (HIV), is mainly an immune organ that damages the human body and its incidence is related to the damage of immune organs on the basis that the count of peripheral blood lymphocytes in patients with SARS is reduced , T lymphocyte subsets CD4 + and CD8 + cells decreased; pathological examination found that, in addition to lung injury, SARS death in the autopsy showed spleen atrophy, lymph node bleeding and necrosis. The paper reviews the papers published in the past year on the pathogenesis of SARS at home and abroad and concludes that SARS CoV does not directly damage the body’s immune organs since most SARS patients detect specific anti-SARS CoVIgM and IgG antibodies; a variety of plasma cytokines such as tumor necrosis factor (TNFα) and some interleukin (IL) were significantly increased, indicating that the body humoral immunity and cellular immunity is normal; HIV-infected patients due to immune function Damage caused by chronic infections and opportunistic infections; secondary infection with SARS patients are different. Because of the discovery of SARS CoV only 1 year, its research is not enough, the current pathogenesis of SARS is difficult to make the final conclusion. This article published in the original intention of this article is to promote academic democracy and promote “a hundred schools of thought, all flowers bloom,” in order to further promote the SARS pathogenesis research.