tetano
Editor, Senior Moderator
PLoS Pathog
. 2022 Jun 14;18(6):e1010590.
doi: 10.1371/journal.ppat.1010590. eCollection 2022 Jun.
Significant role of host sialylated glycans in the infection and spread of severe acute respiratory syndrome coronavirus 2
Wakana Saso[SUP] 1 2 3 [/SUP], Masako Yamasaki[SUP] 1 4 [/SUP], Shin-Ichi Nakakita[SUP] 5 [/SUP], Shuetsu Fukushi[SUP] 6 [/SUP], Kana Tsuchimoto[SUP] 7 [/SUP], Noriyuki Watanabe[SUP] 1 [/SUP], Nongluk Sriwilaijaroen[SUP] 8 9 [/SUP], Osamu Kanie[SUP] 10 [/SUP], Masamichi Muramatsu[SUP] 1 [/SUP], Yoshimasa Takahashi[SUP] 7 [/SUP], Tetsuro Matano[SUP] 2 3 [/SUP], Makoto Takeda[SUP] 11 [/SUP], Yasuo Suzuki[SUP] 9 [/SUP], Koichi Watashi[SUP] 1 4 7 12 13 [/SUP]
Affiliations
Abstract
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.
. 2022 Jun 14;18(6):e1010590.
doi: 10.1371/journal.ppat.1010590. eCollection 2022 Jun.
Significant role of host sialylated glycans in the infection and spread of severe acute respiratory syndrome coronavirus 2
Wakana Saso[SUP] 1 2 3 [/SUP], Masako Yamasaki[SUP] 1 4 [/SUP], Shin-Ichi Nakakita[SUP] 5 [/SUP], Shuetsu Fukushi[SUP] 6 [/SUP], Kana Tsuchimoto[SUP] 7 [/SUP], Noriyuki Watanabe[SUP] 1 [/SUP], Nongluk Sriwilaijaroen[SUP] 8 9 [/SUP], Osamu Kanie[SUP] 10 [/SUP], Masamichi Muramatsu[SUP] 1 [/SUP], Yoshimasa Takahashi[SUP] 7 [/SUP], Tetsuro Matano[SUP] 2 3 [/SUP], Makoto Takeda[SUP] 11 [/SUP], Yasuo Suzuki[SUP] 9 [/SUP], Koichi Watashi[SUP] 1 4 7 12 13 [/SUP]
Affiliations
- PMID: 35700214
- DOI: 10.1371/journal.ppat.1010590
Abstract
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.