Abstract
BackgroundThe rapid spread of the COVID-19 demands immediate response from the scientific communities. Appropriate countermeasures mean thoughtful and educated choice of viral targets (epitopes). There are several articles that discuss such choices in the SARS-CoV-2 proteome, other focus on phylogenetic traits and history of the Coronaviridae genome/proteome. However none consider viral protein low complexity regions (LCRs). Recently we created the first methods that are able to compare such fragments.ResultsWe show that five low complexity regions (LCRs) in three proteins (nsp3, S and N) encoded by the SARS-CoV-2 genome are highly similar to regions from human proteome. As many as 21 predicted T-cell epitopes and 27 predicted B-cell epitopes overlap with the five SARS-CoV-2 LCRs similar to human proteins. Interestingly, replication proteins encoded in the central part of viral RNA are devoid of LCRs.ConclusionsSimilarity of SARS-CoV-2 LCRs to human proteins may have implications on the ability of the virus to counteract immune defenses. The vaccine targeted LCRs may potentially be ineffective or alternatively lead to autoimmune diseases development. These findings are crucial to the process of selection of new epitopes for drugs or vaccines which should omit such regions.
Highlights
The rapid spread of the COVID-19 demands immediate response from the scientific communities
The detailed description of the data sources and the methods used to identify and analyze low complexity regions in SARS-CoV-2 and human proteome is provided in Supplemental Material 9 “Materials and Methods”
In the step we identified which of the severe acute respiratory syndrome coronavirus (SARSCoV)-2 low complexity regions (LCRs) are similar to human LCRs (Fig. 1)
Summary
The rapid spread of the COVID-19 demands immediate response from the scientific communities. Appropriate countermeasures mean thoughtful and educated choice of viral targets (epitopes). The causative agent of the disease was a previously unknown Betacoronavirus named SARS-CoV-2. Some of the animal coronaviruses exhibited ability to transmit to human e.g. the severe acute respiratory syndrome coronavirus (SARSCoV) in 2003 and Middle East respiratory syndrome coronavirus (MERS-CoV) in 2012 had caused human epidemics [1, 2]. SARS-CoVs enters cells via the angiotensin-converting enzyme 2 (ACE2) receptor [3, 4]. The SARS-CoV-2 first infects airways and binds to ACE2 on alveolar epithelial cells. Both viruses are potent inducers of inflammatory cytokines [5]. To date there are no fully effective drugs or vaccines against SARS-CoV-2 [6, 10,11,12,13,14]
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