Sharma et al. presented hemagglutinin esterase as a structural protein on the SARS-CoV-2 surface in a recent review article in Biomedicine & Pharmacotherapy [1]. However, evidence suggests that the SARS-CoV-2 genome lacks the HE gene [2], [3], [4], [5], [6]. In addition, the authors did not presented envelope protein in structure of SARS-CoV-2 in [1].
Although most beta coronaviruses recognize 9-O-acetyl-SAs, this has changed as a result of coronavirus evolution. The hemagglutinin esterase (HE) gene was horizontally adapted from an influenza C-specific HEF and transferred to a beta coronavirus lineage A (OC43-CoV, HKU1-CoV, and Bovine-CoV). Cross-species transmission and HE evolution both contribute to HE adaptation. This proves viral compatibility with host glycans [7]. Thus, studying emerging viruses like SARS-CoV-2 may help us better understand the viral evolution process.
COVID-19 is caused by SARS-CoV-2, a beta-coronavirus of lineage B. It encodes four structural proteins: [1] the spike-surface glycoprotein [2], the small envelope protein [3], the membrane glycoprotein, and [4] the nucleocapsid protein, as well as several nonstructural proteins; however, HE is encoded by other betacoronaviruses in lineage A, including HCoV-OC43, HCoV-HKU1, BCoV, and MHV [2], [8].
In conclusion, evidence suggests that the SARS-CoV-2 genome lacks the HE gene, and thus HE cannot play a role in SARS-CoV-2 replication.
CRediT authorship contribution statement
Ahmad Hosseinzadeh adli: Conceptualization, Supervision. Sanaz Baghban Rahimi: Writing – review & editing.
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No data was used for the research described in the article.