Abstract
The emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and its rapid evolution has led to a global health crisis. Increasing mutations across the SARS-CoV-2 genome have severely impacted the development of effective therapeutics and vaccines to combat the virus. However, the new SARS-CoV-2 variants and their evolutionary characteristics are not fully understood. Host cellular components such as the ACE2 receptor, RNA-binding proteins (RBPs), microRNAs, small nuclear RNA (snRNA), 18s rRNA, and the 7SL RNA component of the signal recognition particle (SRP) interact with various structural and non-structural proteins of the SARS-CoV-2. Several of these viral proteins are currently being examined for designing antiviral therapeutics. In this review, we discuss current advances in our understanding of various host cellular components targeted by the virus during SARS-CoV-2 infection. We also summarize the mutations across the SARS-CoV-2 genome that directs the evolution of new viral strains. Considering coronaviruses are rapidly evolving in humans, this enables them to escape therapeutic therapies and vaccine-induced immunity. In order to understand the virus’s evolution, it is essential to study its mutational patterns and their impact on host cellular machinery. Finally, we present a comprehensive survey of currently available databases and tools to study viral–host interactions that stand as crucial resources for developing novel therapeutic strategies for combating SARS-CoV-2 infection.
Highlights
Introduction published maps and institutional affilThe outbreak of coronavirus disease (COVID-19) was caused by severe acute respiratory syndrome coronavirus (SARS-CoV-2)
Their study predicted that 12 different mutations in the SARS-CoV-2 spike, nucleocapsid, and membrane proteins might contribute to the generation of drift variants [147]
There is a notable paucity of databases containing protein–RNA interactions (PRI) or RNA interactions (RRI) data; we anticipate that new information from emerging studies will become available and an opportunity arises for existing or new databases to capture and integrate such datasets
Summary
Our knowledge of SARS-CoV-2 pathogenesis can be improved by a detailed understanding of various interactions between SARS-CoV-2 and its host cell during infection. The protein proteins in the SARS-Co-V-2 genome interact components of the host innate has been identified to interact with various host RNA factors to protect the viral genome from nucleases and pattern-recognition proteins (PRPs), thereby regulating the virion’s transcription, replication, and translation [74]. Similar to Nsp, another non-structural protein, Nsp, binds to host 18s ribosomal RNA that forms the structural component of the 40s ribosomal subunit [76] This interaction inhibits translation in the host’s mRNA upon SARSCoV-2 infection. Translation of SARS-CoV-2 RNA is protected from its own Nsp1-mediated translation inhibition by the first stem-loop (SL1) of its 50 leader sequence [75] Other host components, such as the signal recognition particle (SRP), play a crucial role during protein synthesis by binding to the 80s ribosome.
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