The researchers revealed a novel coronavirus in the Chinese population on
7th January 2020, named severe acute respiratory syndrome coronavirus-2 (SARSCoV-2). The previous coronaviruses proved merely the tip of the iceberg after the
emergence of the recently identified SARS-CoV-2. The potential of pandemic status
significantly revealed the concealed capabilities of virulence and contagiousness of the
betacoronaviruses group. This book chapter discusses the landscape of host genetic
factors correlating with SARS-CoV-2. All SARS-CoV-2 genes code for the structural
and non-structural proteins that have distinct interactions with host proteins. NSP13 is
associated with centrosome and insulin signals in humans, NSP5 is associated with the
ATPases of host cells, and NSP9 is associated with the nuclear pore's host proteins.
The ORF8ab and ORF8b avoid the host immune responses and inhibit the signaling
cascade of INF-β. Cytokine storm is associated with TLR2, FOXO1, and MYC genes
of SARS-CoV-2 that further cause host cell death during infection. STAT1, IFIH1,
IRF9, OAS1-3, and PML are associated with the immune response to SARS-CoV-2
infection, particularly the production of type I interferon. The SARS-CoV-2 entry is
affected by the TMEM106B gene, and this gene can prevent virus-induced cell death.
Replication of SARS-CoV-2 reduces due to deletions in TMEM106B and VAC14
genes. Genetic variants also influence the host susceptibility in the major
histocompatibility complex antigen loci (HLA). The susceptibility of COVID-19 is
considerably associated with the genetic variation in HLA and plays a significant role
in identifying populations at higher risk.
Keywords: SARS-CoV-2, COVID-19, Host, Genetic factors, GWAS, TWAS, HLA, Virus-host interactions.
