Aim
This study is looking for a common pathogenicity between SARS-CoV-2 and Plasmodium species, in individuals with certain HLA serotypes.
Methods
1
. Tblastx searches of SARS-CoV-2 are performed by limiting searches to five Plasmodium species that infect humans.
2
. Aligned sequences in the respective organisms’ proteomes are searched with blastp.
3
. Binding predictions of the identified SARS-CoV-2 peptide to HLA supertype representatives are performed.
4
. Blastp searches of predicted epitopes that bind strongly to the identified HLA allele are performed by limiting searches to
H. sapiens
and Plasmodium species, separately.
5
. Peptides with minimum 60% identity to the predicted epitopes are found in results.
6
. Peptides among those, which bind strongly to the same HLA allele, are predicted.
7
. Step-
4
is repeated by limiting searches to
H. sapiens
, followed by the remaining steps until step-
7
, for peptides sourced by Plasmodium species after step
-6
.
Results
SARS-CoV-2 peptide with single letter amino acid code CFLGYFCTCYFGLFC has the highest identity to
P. vivax
. Its YFCTCYFGLF part is predicted to bind strongly to HLA-A*24:02. Peptides in the human proteome both homologous to YFCTCYFGLF and with a strong binding affinity to HLA-A*24:02 are YYCARRFGLF, YYCHCPFGVF, and YYCQQYFFLF. Such peptides in the Plasmodium species’ proteomes are FFYTFYFELF, YFVACLFILF, and YFPTITFHLF. The first one belonging to
P. falciparum
has a homologous peptide (YFYLFSLELF) in the human proteome, which also has a strong binding affinity to the same HLA allele.
Conclusion
Immune responses to the identified-peptides with similar sequences and strong binding affinities to HLA-A*24:02 can be related to autoimmune response risk in individuals with HLA-A*24:02 serotypes, upon getting infected with SARS-CoV-2 or
P. falciparum
.