Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, as coronavirus disease 2019 (COVID-19) pandemic, has killed more than a million people worldwide, and researchers are constantly working to develop therapeutics in the treatment and prevention of this new viral infection. To infect and induced pathogenesis as observed in other viral infections, we postulated that SARS-CoV-2 may also require an escalation in the anabolic metabolism, such as glucose and glutamine, to support its energy and biosynthetic requirements during the infection cycle. Recently, the requirement of altered glucose metabolism in SARS-CoV-2 pathogenesis was demonstrated, but the role of dysregulated glutamine metabolism is not yet mentioned for its infection. In this perspective, we have attempted to provide a summary of possible biochemical events on putative metabolic reprograming of glutamine in host cells upon SARS-CoV-2 infection by comparison to other viral infections/cancer metabolism and available clinical data or research on SARS-CoV-2 pathogenesis. This systematic hypothesis concluded the vital role of glutaminase-1 (GLS1), phosphoserine aminotransferase (PSAT1), hypoxia-inducible factor-1 alpha (HIF-1α), mammalian target of rapamycin complex 1 (mTORC1), glutamine-fructose amidotransferase 1/2 (GFAT1/2), and transcription factor Myc as key cellular factors to mediate and promote the glutamine metabolic reprogramming in SARS-CoV-2 infected cells. In absence of concrete data available for SARS-CoV-2 induced metabolic reprogramming of glutamine, this study efforts to connect the gaps with available clinical shreds of evidence in SARS-CoV-2 infection with altered glutamine metabolism and hopefully could be beneficial in the designing of strategic methods for therapeutic development with elucidation using in vitro or in vivo approaches.

随着2019年冠状病毒病（COVID-19）大流行，严重的急性呼吸系统综合症冠状病毒2（SARS-CoV-2）感染已导致全球100万人丧生，研究人员正在不断努力开发治疗和预防这种疾病的疗法新的病毒感染。为了在其他病毒感染中观察到感染和诱发发病机理，我们假设SARS-CoV-2可能还需要增加合成代谢的代谢，例如葡萄糖和谷氨酰胺，以支持其在感染周期中的能量和生物合成需求。最近，已证明在SARS-CoV-2发病机理中需要改变葡萄糖代谢，但是由于其感染尚未提及谷氨酰胺代谢失调的作用。从这个角度来看，我们试图通过与其他病毒感染/癌症新陈代谢以及可用的临床数据或SARS-CoV-2发病机理的研究进行比较，总结SARS-CoV-2感染后宿主细胞中谷氨酰胺的假定代谢重编程的可能生化事件。这个系统的假设总结了谷氨酰胺酶1（GLS1），磷酸丝氨酸氨基转移酶（PSAT1），低氧诱导因子1α（HIF-1α），雷帕霉素复合物1（mTORC1）的哺乳动物靶标，谷氨酰胺-果糖酰胺基转移酶1 /的重要作用。 2（GFAT1 / 2）和转录因子Myc作为介导和促进SARS-CoV-2感染细胞中谷氨酰胺代谢重编程的关键细胞因子。在缺乏可用于SARS-CoV-2诱导的谷氨酰胺代谢重编程的具体数据的情况下，体外 要么 体内 方法。