Abstract：
:Neutralizing antibodies (NAbs) are traditionally thought to inhibit virus infection by preventing virion entry into target cells. In addition, antibodies can engage Fc receptors (FcRs) on immune cells to activate antiviral responses. We describe a mechanism by which NAbs inhibit chikungunya virus (CHIKV), the most common alphavirus infecting humans, by preventing virus budding from infected human cells and activating IgG-specific Fcγ receptors. NAbs bind to CHIKV glycoproteins on the infected cell surface and induce glycoprotein coalescence, preventing budding of nascent virions and leaving structurally heterogeneous nucleocapsids arrested in the cytosol. Furthermore, NAbs induce clustering of CHIKV replication spherules at sites of budding blockage. Functionally, these densely packed glycoprotein-NAb complexes on infected cells activate Fcγ receptors, inducing a strong, antibody-dependent, cell-mediated cytotoxicity response from immune effector cells. Our findings describe a triply functional antiviral pathway for NAbs that might be broadly applicable across virus-host systems, suggesting avenues for therapeutic innovation through antibody design.
journal_name
Cell Host Microbejournal_title
Cell host & microbeauthors
Jin J,Galaz-Montoya JG,Sherman MB,Sun SY,Goldsmith CS,O'Toole ET,Ackerman L,Carlson LA,Weaver SC,Chiu W,Simmons Gdoi
10.1016/j.chom.2018.07.018subject
Has Abstractpub_date
2018-09-12 00:00:00pages
417-428.e5issue
3eissn
1931-3128issn
1934-6069pii
S1931-3128(18)30388-3journal_volume
24pub_type
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