Even after more than two years of intensive research, not all of the pathophysiological processes of Coronavirus Disease 2019 (COVID-19), induced by severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) infection, have been fully elucidated. The initial virus-host interaction at the respiratory epithelium plays a crucial role in the course and progression of the infection, and is highly dependent on the glycosylation pattern of the host cell and of the secreted mucins. Glycans are polysaccharides that can be attached to proteins and thereby add to their stability and functionality. Lectins are glycan-binding proteins that recognize specific glycan motifs, and lectin histochemistry is a suitable tool to visualize and examine glycosylation pattern changes in tissues. In this study we used lectins with different glycan-specificities for the visualization of glycosylation pattern changes in the respiratory tract of SARS-CoV-2 infected Golden Syrian hamsters. While some lectins (LEL, STL) enable the visualization of the damage to alveolar type 1 pneumocytes, other lectins, e.g., GSLI, visualized the loss and subsequent hyperplasia of type 2 pneumocytes. UEAI staining was co-localized with KI67, a proliferation marker. Double staining of lectins LEL, STL and WGA with specific immune cell markers (Iba1, CD68) showed co-localization and the dominant infiltration of monocyte-derived macrophages into infected alveolar tissue. The elucidation of the glycosylation pattern of the respiratory tract cells in uninfected and infected Golden Syrian hamsters revealed physiological and pathological aspects of the disease that may open new possibilities for therapeutic development.

即使经过两年多的深入研究，由严重急性呼吸综合征冠状病毒2 型 (SARS-CoV-2) 感染引起的 2019 冠状病毒病 (COVID-19) 的所有病理生理过程仍未完全阐明。呼吸道上皮的最初病毒与宿主的相互作用在感染的过程和进展中起着至关重要的作用，并且高度依赖于宿主细胞和分泌的粘蛋白的糖基化模式。聚糖是可以附着在蛋白质上的多糖，从而增加其稳定性和功能性。凝集素是识别特定聚糖基序的聚糖结合蛋白，凝集素组织化学是可视化和检查组织中糖基化模式变化的合适工具。在这项研究中，我们使用具有不同聚糖特异性的凝集素来可视化感染 SARS-CoV-2 的金色叙利亚仓鼠呼吸道中糖基化模式的变化。虽然一些凝集素（LEL、STL）能够使肺泡1 型肺细胞的损伤可视化，但其他凝集素（例如 GSLI）使2 型肺细胞的损失和随后的增生可视化。UEAI 染色与增殖标记物 KI67 共定位。凝集素 LEL、STL 和 WGA 与特异性免疫细胞标记物（Iba1、CD68）的双重染色显示单核细胞来源的巨噬细胞共定位并主要浸润到受感染的肺泡组织中。阐明未感染和感染的金色叙利亚仓鼠呼吸道细胞的糖基化模式揭示了该疾病的生理和病理方面，可能为治疗开发开辟新的可能性。