Rhinovirus species C (RV-C) causes more severe asthma attacks than other rhinovirus species. However, the modulation of RV-C replication by drugs has not been well studied. Primary human nasal epithelial (HNE) cells cultured on filter membranes with air-liquid interface methods were infected with RV-C03, and the levels of RV-C03 RNA collected from the airway surface liquid (ASL) of HNE cells were measured with a SYBR Green assay. Pretreatment of HNE cells with the specific vacuolar H⁺-ATPase inhibitor bafilomycin A₁ reduced the RV-C03 RNA levels in the ASL; inflammatory cytokines, including interleukin (IL)-1β, IL-6 and IL-8, in the supernatant; the mRNA expression of the RV-C receptor cadherin-related family member 3 (CDHR3) in the cells; and the number of acidic endosomes where RV-B RNA enters the cytoplasm. The levels of RV-C03 RNA in the ASL obtained from HNE cells with the CDHR3 rs6967,330 G/A genotype tended to be higher than those obtained from HNE cells with the G/G genotype. Pretreatment with the Na⁺/H⁺ exchanger inhibitor ethyl-isopropyl amiloride or either of the macrolides clarithromycin or EM900 also reduced RV-C03 RNA levels in the ASL and the number of acidic endosomes in HNE cells. In addition, significant levels of RV-A16, RV-B14 and RV-C25 RNA were detected in the ASL, and bafilomycin A₁ also decreased the RV-C25 RNA levels. These findings suggest that bafilomycin A₁ may reduce the release of RV-Cs and inflammatory cytokines from human airway epithelial cells. RV-Cs may be sensitive to drugs, including bafilomycin A₁, that increase endosomal pH, and CDHR3 may mediate virus entry through receptor-mediated endocytosis in human airway epithelial cells.

鼻病毒 C 种 (RV-C) 比其他鼻病毒种类引起更严重的哮喘发作。然而，药物对 RV-C 复制的调节尚未得到很好的研究。用气液界面法在滤膜上培养的原代人鼻上皮 (HNE) 细胞用 RV-CO3 感染，并用 SYBR 测量从 HNE 细胞的气道表面液体 (ASL) 收集的 RV-C03 RNA 水平绿色化验。^{用特异性液泡 H +} -ATPase 抑制剂巴弗洛霉素 A ₁预处理 HNE 细胞降低 ASL 中的 RV-C03 RNA 水平；上清液中的炎性细胞因子，包括白细胞介素 (IL)-1β、IL-6 和 IL-8；细胞中 RV-C 受体钙粘蛋白相关家族成员 3 (CDHR3) 的 mRNA 表达；以及 RV-B RNA 进入细胞质的酸性内体的数量。从具有 CDHR3 rs6967,330 G/A 基因型的 HNE 细胞获得的 ASL 中 RV-C03 RNA 的水平往往高于从具有 G/G 基因型的 HNE 细胞获得的水平。^{Na +} /H ⁺预处理交换抑制剂乙基异丙基阿米洛利或大环内酯类克拉霉素或 EM900 也降低了 ASL 中的 RV-C03 RNA 水平和 HNE 细胞中酸性内体的数量。此外，在 ASL 中检测到显着水平的 RV-A16、RV-B14 和 RV-C25 RNA，并且巴弗洛霉素 A ₁也降低了 RV-C25 RNA 水平。这些发现表明，巴弗洛霉素 A ₁可能会减少人气道上皮细胞释放 RV-Cs 和炎性细胞因子。RV-Cs 可能对增加内体 pH 值的药物（包括巴弗洛霉素 A ₁ ）敏感，并且 CDHR3 可能通过受体介导的人气道上皮细胞内吞作用介导病毒进入。