Significant role of host sialylated glycans in the infection and spread of severe acute respiratory syndrome coronavirus 2

• Published in: PLoS pathogens Vol. 18; no. 6; p. e1010590
• Main Authors: Saso, Wakana, Yamasaki, Masako, Nakakita, Shin-ichi, Fukushi, Shuetsu, Tsuchimoto, Kana, Watanabe, Noriyuki, Sriwilaijaroen, Nongluk, Kanie, Osamu, Muramatsu, Masamichi, Takahashi, Yoshimasa, Matano, Tetsuro, Takeda, Makoto, Suzuki, Yasuo, Watashi, Koichi
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 01.06.2022; Public Library of Science (PLoS)
• Subjects: ACE2; Acids; Angiotensin; Angiotensin-converting enzyme 2; Biology and life sciences; Cell surface; Coronaviruses; COVID-19; Epidemics; Infections; Medicine and health sciences; Middle East respiratory syndrome; Peptidyl-dipeptidase A; Physical Sciences; Polysaccharides; Respiratory diseases; Severe acute respiratory syndrome; Severe acute respiratory syndrome coronavirus 2; Sialic acids; Viral diseases; Viral infections
• ISSN: 1553-7374; 1553-7366; 1553-7374
• DOI: 10.1371/journal.ppat.1010590

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been transmitted across all over the world, in contrast to the limited epidemic of genetically- and virologically-related SARS-CoV. However, the molecular basis explaining the difference in the virological characteristics among SARS-CoV-2 and SARS-CoV has been poorly defined. Here we identified that host sialoglycans play a significant role in the efficient spread of SARS-CoV-2 infection, while this was not the case with SARS-CoV. SARS-CoV-2 infection was significantly inhibited by α2-6-linked sialic acid-containing compounds, but not by α2–3 analog, in VeroE6/TMPRSS2 cells. The α2-6-linked compound bound to SARS-CoV-2 spike S1 subunit to competitively inhibit SARS-CoV-2 attachment to cells. Enzymatic removal of cell surface sialic acids impaired the interaction between SARS-CoV-2 spike and angiotensin-converting enzyme 2 (ACE2), and suppressed the efficient spread of SARS-CoV-2 infection over time, in contrast to its least effect on SARS-CoV spread. Our study provides a novel molecular basis of SARS-CoV-2 infection which illustrates the distinctive characteristics from SARS-CoV.