Antibody-Dependent Enhancement (ADE) of SARS-CoV-2 Infection Requires FcγRIIB and Virus-Antibody Complex With Bivalent Interaction

2021 ◽  
Author(s):  
Shuang Wang ◽  
Junchao Wang ◽  
Xiaojuan Yu ◽  
Wen Jiang ◽  
Shuo Chen ◽  
...  
Keyword(s):  
Virus Antibody ◽  
Antibody Dependent Enhancement ◽  
Antibody Complex ◽  
Bivalent Interaction

A study on dissociation of Coxsackie B4 virus-antibody complex

Virology ◽  
1963 ◽  
Vol 20 (3) ◽  
pp. 457-463 ◽  
Author(s):  
Francisco Pinheiro ◽  
G.D. Hsiung
Keyword(s):  
Virus Antibody ◽  
Antibody Complex ◽  
Coxsackie B4 Virus

scholarly journals INFECTIOUS VIRUS-ANTIBODY COMPLEX IN THE BLOOD OF CHRONICALLY INFECTED MICE

1966 ◽  
Vol 124 (1) ◽  
pp. 81-97 ◽  
Author(s):  
Abner Louis Notkins ◽  
Suellen Mahar ◽  
Christina Scheele ◽  
Joel Goffman
Keyword(s):  
Infectious Virus ◽  
Neutralizing Antibody ◽  
Lactic Dehydrogenase ◽  
Resistant Virus ◽  
Virus Antibody ◽  
In Vitro Exposure ◽  
Antiviral Antibody ◽  
Antibody Complex

If viremic sera from mice chronically infected with lactic dehydrogenase virus (LDV) were first treated with ether or ultraviolet light to inactivate the infectious virus, neutralizing antibody could be demonstrated. Significant amounts of antibody, however, were not detected until the mice had been infected for about 2½ months and its presence did not result in the elimination of the chronic viremia. Virus isolated from sera containing neutralizing antibody was found to be relatively resistant to neutralization by anti-LDV. Further studies revealed that the resistant virus existed in the form of an infectious virus-antibody complex (sensitized virus). The presence of such a complex was demonstrated by the fact that the virus fraction which persisted after in vivo or in vitro exposure to mouse anti-LDV was readily neutralized by goat anti-mouse sera or goat anti-mouse γ-globulin, whereas virus that had not been previously exposed to mouse anti-LDV was completely resistant to neutralization by goat anti-mouse sera. These findings suggest that (a) sensitization may play an important role in the resistance and susceptibility of a virus to neutralization by antiviral antibody, and (b) an anti-γ-globulin may prove useful in neutralizing the resistant fraction and in demonstrating otherwise undetectable antiviral antibody.

Infectious influenza virus-antibody complex

1971 ◽  
Vol 34 (3) ◽  
pp. 209-213 ◽  
Author(s):  
E. Zalan ◽  
E. Borman ◽  
N. A. Labzoffsky
Keyword(s):  
Influenza Virus ◽  
Virus Antibody ◽  
Antibody Complex

scholarly journals HDAC6 regulates antibody-dependent intracellular neutralization of viruses via deacetylation of TRIM21

2020 ◽  
Vol 295 (42) ◽  
pp. 14343-14351 ◽  
Author(s):  
Songbo Xie ◽  
Linlin Zhang ◽  
Dan Dong ◽  
Ruixin Ge ◽  
Qianqian He ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Histone Deacetylase ◽  
Histone Deacetylase 6 ◽  
Virus Antibody ◽  
Ubiquitin Proteasome Pathway ◽  
Virus Accumulation ◽  
Tripartite Motif ◽  
Ubiquitin Proteasome ◽  
Antibody Complex ◽  
Proteasome Pathway

Tripartite motif–containing protein 21 (TRIM21) is a cytosolic antibody receptor that targets the internalized virus–antibody complex to the proteasome for degradation. However, the precise mechanism regulating TRIM21 activity is unknown. Here we show that TRIM21 is a substrate of histone deacetylase 6 (HDAC6) and that its function is regulated by acetylation. HDAC6 interacts with TRIM21 through its PRYSPRY motif and deacetylates TRIM21 at lysine 385 and lysine 387, thus promoting its homodimerization. Inhibiting HDAC6 activity increases TRIM21 acetylation, and hyperacetylation blocks TRIM21 dimerization and ubiquitination, preventing its binding to the virus–antibody complex and its degradation via the ubiquitin–proteasome pathway. HDAC6 depletion or inhibition increases virus accumulation in cells, indicative of an impaired capacity for antibody-dependent intracellular neutralization of viruses, whereas TRIM21 acetylation-deficient K385/387R mutant rescues HDAC6 depletion–caused ADIN impairment. These findings provide evidence for HDAC6 as a novel regulator of TRIM21-mediated intracellular innate immunity.

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