Peters C J, Simpson G L, Levy H
Centers for Disease Control and Prevention, Atlanta, Georgia 30333, USA.
Annu Rev Med. 1999;50:531-45. doi: 10.1146/annurev.med.50.1.531.
Hantaviruses chronically infect rodents without apparent disease, but when they are spread by aerosolized excreta to humans, two major clinical syndromes result: hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS). Both diseases appear to be immunopathologic, and inflammatory mediators are important in causing the clinical manifestations. In HPS, T cells act on heavily infected pulmonary endothelium, and it is suspected that gamma interferon and tumor necrosis factor are major agents of a reversible increase in vascular permeability that leads to severe, noncardiogenic pulmonary edema. HFRS has prominent systemic manifestations. The retroperitoneum is a major site of vascular leak and the kidneys suffer tubular necrosis. Both syndromes are accompanied by myocardial depression and hypotension or shock. HFRS is primarily a Eurasian disease, whereas HPS appears to be confined to the Americas; these geographic distinctions correlate with the phylogenies of the rodent hosts and the viruses that coevolved with them.
汉坦病毒可长期感染啮齿动物而不引发明显疾病，但当病毒通过气溶胶化排泄物传播给人类时，会导致两种主要临床综合征：肾综合征出血热（HFRS）和汉坦病毒肺综合征（HPS）。这两种疾病似乎都与免疫病理有关，炎症介质在引发临床表现方面起着重要作用。在HPS中，T细胞作用于严重感染的肺内皮细胞，据推测，γ干扰素和肿瘤坏死因子是导致血管通透性可逆性增加的主要因素，进而导致严重的非心源性肺水肿。HFRS有明显的全身表现。腹膜后是血管渗漏的主要部位，肾脏会出现肾小管坏死。两种综合征均伴有心肌抑制和低血压或休克。HFRS主要是一种欧亚疾病，而HPS似乎局限于美洲；这些地理差异与啮齿动物宿主及其共同进化的病毒的系统发育有关。
