The ongoing outbreak of coronavirus disease COVID-19 is significantly implicated by global heterogeneity in the genome organization of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The causative agents of global heterogeneity in the whole genome of SARS-CoV-2 are not well characterized due to the lack of comparative study of a large enough sample size from around the globe to reduce the standard deviation to the acceptable margin of error. To better understand the SARS-CoV-2 genome architecture, we have performed a comprehensive analysis of codon usage bias of sixty (60) strains to get a snapshot of its global heterogeneity. Our study shows a relatively low codon usage bias in the SARS-CoV-2 viral genome globally, with nearly all the over-preferred codons’ A.U. ended. We concluded that the SARS-CoV-2 genome is primarily shaped by mutation pressure; however, marginal selection pressure cannot be overlooked. Within the A/U rich virus genomes of SARS-CoV-2, the standard deviation in G.C. (42.91% ± 5.84%) and the GC3 value (30.14% ± 6.93%) points towards global heterogeneity of the virus. Several SARS-CoV-2 viral strains were originated from different viral lineages at the exact geographic location also supports this fact. Taking all together, these findings suggest that the general root ancestry of the global genomes are different with different genome’s level adaptation to host. This research may provide new insights into the codon patterns, host adaptation, and global heterogeneity of SARS-CoV-2.

Hypotrichosis is an uncommon type of alopecia (hair loss) characterized by coarse scalp hair caused by the reduced or fully terminated activity of the Lipase-H (LIPH) enzyme. LIPH gene mutations contribute to the development of irregular or non-functional proteins. Because several cellular processes, including cell maturation and proliferation, are inhibited when this enzyme is inactive, the hair follicles become structurally unreliable, undeveloped, and immature. This results in brittle hair, as well as altered hair shaft development and structure. Because of these nsSNPs, the protein’s structure and/or function may be altered. Given the difficulty in discovering functional SNPs in genes associated with disease, it is possible to assess potential functional SNPs before conducting broader population investigations. As a result, in our in silico analysis, we separated potentially hazardous nsSNPs of the LIPH gene from benign representatives using a variety of sequencing and architecture-based bioinformatics approaches. Using seven prediction algorithms, 9 out of a total of 215 nsSNPs were shown to be the most likely to cause harm. In order to distinguish between potentially harmful and benign nsSNPs of the LIPH gene, in our in silico investigation, we employed a range of sequence- and architecture-based bioinformatics techniques. Three nsSNPs (W108R, C246S, and H248N) were chosen as potentially harmful. The present findings will likely be helpful in future large population-based studies, as well as in drug discovery, particularly in the creation of personalized medicine, since this study provides an initial thorough investigation of the functional nsSNPs of LIPH.