Health Science Journal

Keywords

SARS-CoV-2; Genom of SARS-CoV-2; Gene mutation; COVID-19

Letter

It has been stated that the COVID-19 pandemic is caused by the corona virus (2019-nCoV) or severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) [1]. We first need to understand the structure of the SARS-CoV-2 genome that is causing the COVID-19 pandemic. In the review, the SARS-CoV-2 genome contained 29.903 nucleotides (nt). The SARS-CoV-2 genome consists of the: 5’ UTR, ORF 1ab gene, S gene, ORF 3a gene, E gene, M gene, ORF 6 gene, ORF 7a gene, ORF 7b gene, ORF 8 gene, N gene, ORF 10 gene and 3’ UTR [2]. The 5 'UTR consists of 265 nt, is a non-coding sequence. The ORF 1ab gene consists of 21.290 nt which encodes the ORF1a polyprotein and the ORF1ab polyprotein. The ORF 1ab gene ID is 43740578 (updated on 3rd January 2021 at https://www.ncbi.nlm.nih.gov/gene/43740578). The S gene consists of 3.822 nt which encodes the surface glycoprotein. The S gene ID is 43740568 (updated on 3rd January 2021 at https://www.ncbi.nlm.nih.gov/gene/43740568). The ORF 3a gene consists of 828 nt which encodes of ORF 3a protein. The gene ID of ORF 3a gene is 43740569 (updated on 3rd January 2021 at https://www.ncbi.nlm.nih.gov/gene/43740569). The E gene consists of 228 nt which encodes of envelope protein. The gene ID of E gene is 43740570 (updated on 3rd January 2021 at https://www.ncbi.nlm.nih.gov/gene/43740570). The M gene consists of 669 nt which encodes of membrane glycoprotein. The gene ID of M gene is 43740571 (updated on 3rd January 2021 at https://www.ncbi.nlm.nih.gov/gene/43740571). The ORF 6 gene consists of 186 nt which encodes of ORF 6 protein (viral accessory protein). The gene ID of ORF 6 gene is 43740572 (updated on 3rd January 2021 at https://www.ncbi.nlm.nih.gov/gene/43740572). The ORF 7a gene consists of 366 nt which encodes of ORF7a protein (viral accessory protein). The gene ID of ORF 7a gene is 43740573 (updated on 3rd January 2021 at https://www.ncbi.nlm.nih.gov/gene/43740573). The ORF 7b gene consists of 132 nt which encodes of ORF 7b protein (viral accessory protein). The gene ID of ORF 7b gene is 43740574 (updated on 3rd January 2021 at https://www.ncbi.nlm.nih.gov/gene/43740574). The ORF 8 gene consists of 193 nt which encodes of ORF 8 protein. The gene ID of ORF 8 gene yaitu 43740577 (updated on 3rd January 2021 at https://www.ncbi.nlm.nih.gov/gene/43740577). The N gene consists of 908 nt which encodes of nucleocapsid phosphoprotein. The Gene ID of N gene is 43740575 (updated on 3rd January 2021 at https://www.ncbi.nlm.nih.gov/gene/43740575). The ORF 10 gene consists of 117 nt which encodes of ORF 10 protein. The gene ID of ORF 10 is 43740576 (updated on 3rd January 2021 at https://www.ncbi.nlm.nih.gov/gene/43740576). The 3’ UTR consists of 229 nt which is non-coding sequence.

We know that gene mutations in SARS-CoV-2 can occur in all genes that make up the genome of SARS-CoV-2. Due to mutations in the SARS-CoV-2 gene, various variants of SARS-CoV-2 appear. Several variants of SARS-CoV-2 recorded since December 2020 include of B.1.1.7, B.1.351, B. 1.429, B.1.1.28, B.1.617 and B.1.618 variants.

The B.1.1.7 variant of SARS-CoV-2 was formerly known as VUI- 202012/01 (Variant Under Investigation-2020-month 12/variant 01). The B.1.1.7 variant debuted in the UK in December 2020 [3]. Subsequently, the B.1.1.7 variant was known as 20V/501Y.V1 [4] with mutation characteristics 69-70 del, 145 del, N501Y, A570D, D614G, P681H, T716I, S982A and D1118H [5]. The B.1.1.7 variant has a fast spreading rate [4] and increases the risk of death by 30% [6].

The B.1.351 variant was first discovered in South Africa [7]. The B.1.351 variant is here in after known as the 20H/501Y.V2 variant. Mutation characteristics of B.1.351 variant include D80A, D215G, K417N, E484K, N501Y, D614G and A701V [5]. It has also been reported that B.1.351 variant has a significantly greater affinity for the ACE2 receptor compared with the SARS-CoV-2 that caused COVID-19 outbreak in Wuhan, China [8].

The B.1.429 variant was first discovered in California, USA. Mutation characteristic of B.1.429 variant occurs in the ORF 1a, ORF 1b and S genes. Mutation of I4205V occurs in the ORF1a gene, D1183Y occurs in the ORF1b gene and S13I, W152C, L452R occurs in the S gene [5]. It was reported that the B.1.429 variant had a rapid deployment in the United States [9].

The B.1.1.28 variant also known as P.1. variant. These variant discovered in North Brazilia [10]. The B.1.1.28 variant also identification in Japan, and known as 20 J/501Y.V3. Characteristic of B.1.1.28 variant has gene mutation such as L18F, T20N, P26S, D138Y, R190S, K417T, E484K, N501Y, D614G, H655Y, T1027I and V1176F. Further also reported that a sample of someone returning from Africa to Japan in March 2021 who were positive for SARS-CoV-2 with the D614G mutation [5]. In addition, a variant with D614G mutation in the S gene of SARS-CoV-2 has also been reported in Pakistan [11].

Variants of B.1.617 and B.1.618 have been identified in India. The two variants are a concern in the development of COVID-19 cases in India [12]. The B.1,617 variant has mutation characteristics in the S gene, namely: L452R, E484Q, D614G. In addition to the B.1.617 variant, also identified the B.1.617.1 variant with characteristics of mutations in the S gene are T95I, G142D, E154K, L452R, E484Q, D614G, P681R and Q1071H. Beside that, another variant was first detected in India, namely the B.1.617.2 variant (delta variant) [13]. Mutation characteristic of B.1.618 variant such as Δ145-146, E484K and D614G [14].

The appearance of SARS-CoV-2 variants that mentioned above, We have to be more careful to avoid COVID-19. People who have comorbidities of COVID-19 include diabetic ketoacidosis and hypertension [15], heart disease [16], as well as diabetes mellitus and hypertension [17] to be more careful to avoid COVID-19. We have also written about the importance of implementing health protocols at the community level to prevent the transmission of SARS-CoV-2 [18].

Funding

We did not receive funds to complete this article

Competing Interests

We declare that there is no conflict of interest in the writing of this paper. The author completed the ICMJE form, download from http://www.icmje.org/disclosure-of-interest/

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