The proteins of SARS-CoV-2 and the antigen of Plasmodium falciparum share immunodominant epitopes . Generally, Plasmodium vivax infects host red blood cells via the Duffy antigen . Antibodies against band 3 and spectrin accumulate during Plasmodium vivax infection and are associated with anemia . The disease triggers the autoimmune response. Hemoglobin levels are inversely related to those of anti-band 3 or anti-spectrin antibodies. Anemic patients have higher IgG levels for band 3 and spectrin than non-anemic patients. Plasmodium vivax can also infect host cells via other mechanisms in Duffy-negative populations . Tryptophan-threonine-rich antigen (TryThrA) is a Plasmodium falciparum homologue of the erythrocyte membrane pypAg-1 antigen produced by Plasmodium yoelii. TryThrA is a tryptophan-rich antigen expressed by various Plasmodium species' merozoites. TR-Ags from Plasmodium can be combined with normal human red blood cells. The process can be slowed down by the serum of a malaria patient . Through the tryptophan-rich threonine antigen (PfTryThrA), Plasmodium falciparum infects host red blood cells . PvTRAg38 (P. vivax tryptophan-rich antigen) binds to red blood cell receptors sensitive to chymotrypsin . PvTRAg38 promotes Parasite growth by binding to the two red blood cell receptors Basigin and Band 3, via their P2 and P4 regions, respectively . Band 3 protein is also a parasite protein's chymotrypsin-sensitive red blood cell receptor . In COVID-19 patients, studies have revealed that the function of red blood cell membrane proteins such as band 3 is impaired . It demonstrates that the SARS-CoV-2 virus protein interacts with the structural proteins of red blood cells via TryThrA and other Plasmodium falciparum antigens. Some viral proteins also contain tryptophan-rich motifs. The tryptophan-rich region at the immunodeficiency virus gp41(36) proximal membrane end is involved in hydrophobic subunit interactions . It is required for the fusion of ENV proteins and viral infectivity . The carboxyl-terminal tryptophan-rich motif of the hepatitis B virus small envelope protein is critical for hepatitis D virus particle assembly . When influenza virus RNA's 5' end sequence is bound to the polymerase, the tryptophan-rich cap-binding sequence on the enzyme's PB2 subunit is activated . Shared antigens cause Cross-reactions between viral and malaria infections. The association between malaria and the risk of death in patients with the Ebola virus suggests that the P. falciparum parasite and the Ebola virus have an intra-host interaction . Semi-monkeys were not protected from malaria by recombinant vaccinia virus expressing Plasmodium falciparum antigens . Only the monoclonal antibody (MAb) to TNF-, on the other hand, inhibited malaria antigen-induced HIV-1 replication. By contrast, the monoclonal antibody does not affect IL-6 production . Malaria antigens promote HIV-1 replication by increasing viral mRNA expression and activating viral transcription directed by long-terminal repeats . TNF-, IFN-, MIF, MCP-1, and IL-10 have been detected in patients with falciparum and vivax malaria . Plasmodium-infected patients exhibit positive immunoglobulin IgM and IgG responses . Tumor necrosis factor (TNF-) and interleukin 6 levels were increased in response to malaria antigen stimulation (IL-6). TNF-and IL-6 are also the primary cytokines in COVID-19 patients. Besides, patients with acute malaria infection exhibit a high degree of cross-reactivity with the SARS-CoV-2 spike protein subunit 1 (S1) . The receptor-binding domain (RBD) and the N-terminal domain (NTD) are the two central regions targeted by neutralizing antibodies in Spike S1 . Acute malaria infections can induce cross-reactions with the S1 Spike protein via antibodies binding to the terminal sialic acid of complex glycans . As a result, the SARS-COV-2 virus must infect host cells via Plasmodium falciparum antigens such as TryThrA and induce the production of cytokines.