Immunotherapy approaches on innate immunity for SARS-Cov-2

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused fatal outbreaks of pneumonia. The similarity of S protein of SARS-CoV-2 with SARS-CoV and RaTG13 is about 76% and 97%, respectively. Also its potential receptor-binding domain (RBD) shows similarity with approximately 74% and 90.1% for SARS-CoV and RaTG13, respectively. SARS-CoV-2 has been shown to use the SARS-CoV receptor ACE2 for entry and serine protease TMPRSS2 for S protein priming. Sialic acids are primarily expressed by vertebrates and some microbial pathogens improving the ability to avoid immune system of vertebrate host. Interactions of sialic acid-binding Ig-like lectins (Siglecs) with their ligands play an important role in modulating immune cell function activities as their regulators. Therefore, while Siglecs help immune cells to distinguish between self and non-self, non-self ligands of some sialylated pathogens can recognize Siglecs and reduce immune cell responses or escape from immune surveillance. In this review, innate immunity in SARS-Cov-2 infection was discussed through Siglecs, especially Siglec-7, Siglec-3, NKG2A and neuraminidases. Keywords: SARS-Cov-2; siglecs; NK cells; NKG2A; neuraminidases.