Issa Hawraa, Eid Ali H, Berry Bassam, Takhviji Vahideh, Khosravi Abbas, Mantash Sarah, Nehme Rawan, Hallal Rawan, Karaki Hussein, Dhayni Kawthar, Faour Wissam H, Kobeissy Firas, Nehme Ali, Zibara Kazem
PRASE and Biology Department, Faculty of Sciences - I, Lebanese University, Beirut, Lebanon.
College of Public Health, Phoenicia University, Zahrani, Lebanon.
Front Med (Lausanne). 2021 Mar 18;8:620990. doi: 10.3389/fmed.2021.620990. eCollection 2021.
Coronavirus disease-2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is currently the most concerning health problem worldwide. SARS-CoV-2 infects cells by binding to angiotensin-converting enzyme 2 (ACE2). It is believed that the differential response to SARS-CoV-2 is correlated with the differential expression of ACE2. Several reports proposed the use of ACE2 pharmacological inhibitors and ACE2 antibodies to block viral entry. However, ACE2 inhibition is associated with lung and cardiovascular pathology and would probably increase the pathogenesis of COVID-19. Therefore, utilizing ACE2 soluble analogs to block viral entry while rescuing ACE2 activity has been proposed. Despite their protective effects, such analogs can form a circulating reservoir of the virus, thus accelerating its spread in the body. Levels of ACE2 are reduced following viral infection, possibly due to increased viral entry and lysis of ACE2 positive cells. Downregulation of ACE2/Ang (1-7) axis is associated with Ang II upregulation. Of note, while Ang (1-7) exerts protective effects on the lung and cardiovasculature, Ang II elicits pro-inflammatory and pro-fibrotic detrimental effects by binding to the angiotensin type 1 receptor (AT1R). Indeed, AT1R blockers (ARBs) can alleviate the harmful effects associated with Ang II upregulation while increasing ACE2 expression and thus the risk of viral infection. Therefore, Ang (1-7) agonists seem to be a better treatment option. Another approach is the transfusion of convalescent plasma from recovered patients with deteriorated symptoms. Indeed, this appears to be promising due to the neutralizing capacity of anti-COVID-19 antibodies. In light of these considerations, we encourage the adoption of Ang (1-7) agonists and convalescent plasma conjugated therapy for the treatment of COVID-19 patients. This therapeutic regimen is expected to be a safer choice since it possesses the proven ability to neutralize the virus while ensuring lung and cardiovascular protection through modulation of the inflammatory response.
由严重急性呼吸综合征冠状病毒 2(SARS-CoV-2)引起的 2019 冠状病毒病(COVID-19)大流行是目前全球最令人担忧的健康问题。SARS-CoV-2 通过与血管紧张素转换酶 2(ACE2)结合来感染细胞。据信,对 SARS-CoV-2 的不同反应与 ACE2 的差异表达相关。一些报告提出使用 ACE2 药理抑制剂和 ACE2 抗体来阻断病毒进入。然而,ACE2 抑制与肺部和心血管病理相关,可能会增加 COVID-19 的发病机制。因此,有人提出利用 ACE2 可溶性类似物来阻断病毒进入,同时挽救 ACE2 活性。尽管这些类似物具有保护作用,但它们可能会形成病毒的循环储存库,从而加速其在体内的传播。病毒感染后 ACE2 水平会降低,这可能是由于病毒进入增加和 ACE2 阳性细胞的裂解所致。ACE2/血管紧张素(1-7)轴的下调与血管紧张素 II(Ang II)上调有关。值得注意的是,虽然血管紧张素(1-7)对肺和心血管系统具有保护作用,但 Ang II 通过与血管紧张素 1 型受体(AT1R)结合引发促炎和促纤维化的有害作用。事实上,AT1R 阻滞剂(ARBs)可以减轻与 Ang II 上调相关的有害影响,同时增加 ACE2 表达,从而增加病毒感染的风险。因此,血管紧张素(1-7)激动剂似乎是更好的治疗选择。另一种方法是输注症状恶化的康复患者的康复期血浆。事实上,由于抗 COVID-19 抗体的中和能力,这似乎很有前景。鉴于这些考虑因素,我们鼓励采用血管紧张素(1-7)激动剂和康复期血浆联合疗法来治疗 COVID-19 患者。这种治疗方案预计是一种更安全的选择,因为它具有已被证实的中和病毒的能力,同时通过调节炎症反应确保对肺和心血管系统的保护。