PSGL-1 restricts HIV-1 infectivity by blocking virus particle attachment to target cells | Zendy

Yajing Fu | Zendy; Sijia He | Zendy; Abdül Waheed | Zendy; Deemah Dabbagh | Zendy; Zheng Zhou | Zendy; Benjamin Trinité | Zendy; Zhao Wang | Zendy; Jieshi Yu | Zendy; Dan Wang | Zendy; Feng Li | Zendy; David N. Levy | Zendy; Hong Shang | Zendy; Eric O. Freed | Zendy; Yuntao Wu | Zendy

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PSGL-1 restricts HIV-1 infectivity by blocking virus particle attachment to target cells

Author(s) -

Yajing Fu,

Sijia He,

Abdül Waheed,

Deemah Dabbagh,

Zheng Zhou,

Benjamin Trinité,

Zhao Wang,

Jieshi Yu,

Dan Wang,

Feng Li,

David N. Levy,

Hong Shang,

Eric O. Freed,

Yuntao Wu

Publication year - 2020

Publication title -

proceedings of the national academy of sciences

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 5.011

H-Index - 771

eISSN - 1091-6490

pISSN - 0027-8424

DOI - 10.1073/pnas.1916054117

Subject(s) - infectivity , blocking (statistics) , virology , human immunodeficiency virus (hiv) , virus , chemistry , particle (ecology) , biology , computer science , computer network , ecology

Significance PSGL-1 and CD43 are surface glycoproteins expressed on blood CD4 T cells to bind to selectins for T cell tethering, rolling, and migration into inflamed tissues. The PSGL-1 level is greatly up-regulated during inflammation. Here we found that PSGL-1 and CD43 expression inhibits HIV spreading infection. Mechanistically, PSGL-1 blocks the binding of virus particles to target cells. PSGL-1–mediated suppression of virus infectivity extends to another retrovirus—murine leukemia virus—and to influenza A virus. These results further our understanding of virus–host interactions and help elucidate mechanisms by which cellular host factors regulate viral infection and pathogenesis.

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