Santos G C Dos, Parra E R, Stegun F W, Cirqueira C S, Capelozzi V L
Universidade de São Paulo, Disciplina de Pneumologia, Departamento de Patologia, Faculdade de Medicina, São PauloSP, Brasil.
Braz J Med Biol Res. 2013 Nov;46(11):985-992. doi: 10.1590/1414-431X20132885. Epub 2013 Nov 18.
Idiopathic interstitial pneumonias include complex diseases that have a strong interaction between genetic makeup and environmental factors. However, in many cases, no infectious agent can be demonstrated, and these clinical diseases rapidly progress to death. Theoretically, idiopathic interstitial pneumonias could be caused by the Epstein-Barr virus, cytomegalovirus, adenovirus, hepatitis C virus, respiratory syncytial virus, and herpesvirus, which may be present in such small amounts or such configuration that routine histopathological analysis or viral culture techniques cannot detect them. To test the hypothesis that immunohistochemistry provides more accurate results than the mere histological demonstration of viral inclusions, this method was applied to 37 open lung biopsies obtained from patients with idiopathic interstitial pneumonias. As a result, immunohistochemistry detected measles virus and cytomegalovirus in diffuse alveolar damage-related histological patterns of acute exacerbation of idiopathic pulmonary fibrosis and nonspecific interstitial pneumonia in 38 and 10% of the cases, respectively. Alveolar epithelium infection by cytomegalovirus was observed in 25% of organizing pneumonia patterns. These findings were coincident with nuclear cytopathic effects but without demonstration of cytomegalovirus inclusions. These data indicate that diffuse alveolar damage-related cytomegalovirus or measles virus infections enhance lung injury, and a direct involvement of these viruses in diffuse alveolar damage-related histological patterns is likely. Immunohistochemistry was more sensitive than the histological demonstration of cytomegalovirus or measles virus inclusions. We concluded that all patients with diffuse alveolar damage-related histological patterns should be investigated for cytomegalovirus and measles virus using sensitive immunohistochemistry in conjunction with routine procedures.
特发性间质性肺炎包括一类复杂的疾病，其在基因构成与环境因素之间存在强烈的相互作用。然而，在许多病例中，无法证实存在感染因子，并且这些临床疾病会迅速进展至死亡。从理论上讲，特发性间质性肺炎可能由爱泼斯坦 - 巴尔病毒、巨细胞病毒、腺病毒、丙型肝炎病毒、呼吸道合胞病毒和疱疹病毒引起，这些病毒可能以极少量或特殊构型存在，以至于常规组织病理学分析或病毒培养技术无法检测到它们。为了检验免疫组织化学比单纯的病毒包涵体组织学显示能提供更准确结果这一假说，该方法被应用于37例取自特发性间质性肺炎患者的开胸肺活检标本。结果，免疫组织化学在特发性肺纤维化急性加重和非特异性间质性肺炎的弥漫性肺泡损伤相关组织学模式中分别在38%和10%的病例中检测到麻疹病毒和巨细胞病毒。在25%的机化性肺炎模式中观察到巨细胞病毒对肺泡上皮的感染。这些发现与核细胞病变效应相符，但未显示出巨细胞病毒包涵体。这些数据表明，弥漫性肺泡损伤相关的巨细胞病毒或麻疹病毒感染会加重肺损伤，并且这些病毒很可能直接参与了弥漫性肺泡损伤相关的组织学模式。免疫组织化学比巨细胞病毒或麻疹病毒包涵体的组织学显示更敏感。我们得出结论，对于所有具有弥漫性肺泡损伤相关组织学模式的患者，应结合常规程序使用敏感的免疫组织化学方法对巨细胞病毒和麻疹病毒进行检测。
