The paper entitled “The impact of COPD and smoking history on the severity of COVID‐19: A systemic review and meta‐analysis.” published in Journal of Medical Virology on 15 April 2020.1 The results revealed the pooled odds ratio (OR) of chronic obstructive pulmonary disease and the development of severe coronavirus disease 2019 (COVID‐19) was 4.38 (fixed‐effect model, 95% confidence interval [CI]: 2.34‐8.20), while the OR of ongoing smoking was 1.98 (fixed‐effect model, 95% CI: 1.29‐3.05). However, in the sensitivity analysis, by excluding each study one by one showed that the study from Guan et al2 was a major source of heterogeneity. After excluding this study, the effect of smoking on the severity of COVID‐19 became insignificant with the OR of 1.55 (95% CI: 0.83‐ 2.87). The authors identified seven studies2-8 with data on smoking history and severity of COVID‐19. The searching for English and Chinese database was up to 22 March 2020.

In this letter, the author used the keywords “smoking,” “tobacco,” “smoker,” “COVID‐19,” “novel coronavirus,” and “SARS CoV‐2” to search PubMed on 16 April 2020. One new study published by Wang et al9 was identified. The updated meta‐analysis was performed by RevMan Ver. 5.3. The pooled OR of the fixed‐effect model was 2.16 (95% CI: 1.45‐3.22). The heterogeneity was smaller than that of the original analysis (I²: 39% vs 44%). The sensitivity analysis excluding the study from Guan et al2 revealed a pooled OR of 1.89 (95% CI: 1.10‐3.24) (Figure 1). The heterogeneity increased in the sensitivity analysis (I² = 48%). The new study from Wang et al9 contributed a positive effect to the meta‐analysis (OR: 3.93, 95% CI: 1.30‐11.93) and resulted in the statistical significance. The study from Guan et al2 contributed to most of the cases in the meta‐analysis (1085 out of 1851 cases). By excluding this study, the results were more robust.

The possible mechanisms linking smoke to the outcome of COVID‐19 were under study. A recent review10 suggested smokers are vulnerable to respiratory infection because of impaired immunity. Smoking can upregulate angiotensin‐converting enzyme‐2 receptor, the known receptor for the severe acute respiratory syndrome (SARS)‐coronavirus, and also possible for SARS‐CoV‐2 causing COVID‐19.

The results of the updated meta‐analysis further confirmed the impact of smoking history on the severity of COVID‐19.

这篇题为“慢性阻塞性肺病和吸烟史对 COVID-19 严重程度的影响：系统评价和荟萃分析”的论文。2020 年 4 月 15 日发表在Journal of Medical Virology上。1结果显示，慢性阻塞性肺病和 2019 年严重冠状病毒病 (COVID-19) 发展的汇总优势比 (OR) 为 4.38（固定效应模型，95%置信区间 [CI]：2.34-8.20），而持续吸烟的 OR 为 1.98（固定效应模型，95% CI：1.29-3.05）。然而，在敏感性分析中，通过逐一排除每项研究表明，Guan 等人的研究2是异质性的主要来源。排除本研究后，吸烟对 COVID-19 严重程度的影响变得不显着，OR 为 1.55（95% CI：0.83-2.87）。作者确定了七项研究2-8，其中包含有关吸烟史和 COVID-19 严重程度的数据。检索中英文数据库至2020年3月22日。

在这封信中，作者使用关键词“吸烟”、“烟草”、“吸烟者”、“COVID-19”、“新型冠状病毒”和“SARS CoV-2”于 2020 年 4 月 16 日搜索 PubMed。一项新研究由 Wang 等人9发表。更新后的荟萃分析由 RevMan Ver. 进行。5.3. 固定效应模型的汇总 OR 为 2.16（95% CI：1.45-3.22）。异质性小于原始分析的异质性（I ²：39% vs 44%）。不包括 Guan 等人2研究的敏感性分析显示合并 OR 为 1.89（95% CI：1.10-3.24）（图 1）。敏感性分析中的异质性增加（I ²  = 48%）。Wang 等人的新研究9对荟萃分析产生了积极影响（OR：3.93，95% CI：1.30-11.93）并具有统计学意义。Guan 等人2的研究促成了荟萃分析中的大多数病例（1851 例中的 1085 例）。通过排除这项研究，结果更加稳健。

正在研究将烟雾与 COVID-19 的结果联系起来的可能机制。最近的一项评论10表明，由于免疫力受损，吸烟者容易受到呼吸道感染。吸烟可以上调血管紧张素转换酶-2 受体，这是已知的严重急性呼吸综合征 (SARS) 冠状病毒受体，也可能上调引起 COVID-19 的 SARS-CoV-2。

更新后的荟萃分析结果进一步证实了吸烟史对 COVID-19 严重程度的影响。