Open reading frame 8 (ORF8) shows one of the highest levels of variability among accessory
proteins in Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), the causative agent of
Coronavirus Disease 2019 (COVID-19). It was previously reported that the ORF8
protein inhibits the presentation of
viral antigens by the major histocompatibility complex class I (MHC-I), which interacts with host factors involved in
pulmonary inflammation. The ORF8
protein assists SARS-CoV-2 in evading immunity and plays a role in SARS-CoV-2 replication. Among many contributing mutations, Q27STOP, a mutation in the ORF8
protein, defines the B.1.1.7 lineage of SARS-CoV-2, engendering the second wave of
COVID-19. In the present study, 47 unique truncated ORF8
proteins (T-ORF8) with the Q27STOP mutations were identified among 49,055 available B.1.1.7 SARS-CoV-2 sequences. The results show that only one of the 47 T-ORF8 variants spread to over 57 geo-locations in North America, and other continents, which include Africa, Asia, Europe and South America. Based on various quantitative features, such as
amino acid homology, polar/non-polar sequence homology, Shannon entropy conservation, and other physicochemical properties of all specific 47 T-ORF8
protein variants, nine possible T-ORF8 unique variants were defined. The question as to whether T-ORF8 variants function similarly to the wild type ORF8 is yet to be investigated. A positive response to the question could exacerbate future
COVID-19 waves, necessitating severe containment measures.