CD59 association with infectious bronchitis virus particles protects against antibody-dependent complement-mediated lysis

Abstract

CD59 protein functions as a negative regulator of the terminal pathway of the complement system by binding to the C8/C9 factors. To date, little is known about the role of CD59 in coronavirus infectious bronchitis virus (IBV) infection. In this study, we discovered that CD59 was downregulated in IBV-infected cells and was associated with IBV virions. This association protected IBV particles from antibody-dependent complement-mediated lysis. IBV titres in the supernatant were significantly increased when CD59 proteins were overexpressed in cells followed by IBV infection, and this observation was further supported by knockdown or cleavage of CD59. Because no considerable change in IBV N protein and viral RNA levels was detected in total cell lysates prepared from the overexpression, knockdown or cleavage of CD59 groups, our data indicated that CD59 was involved in IBV particle release and that IBV had evolved a mechanism to utilize CD59 to evade complement-mediated destruction.

A multi-tissue study of immune gene expression profiling highlights the key role of the nasal epithelium in COVID-19 severity

“…CD59 is a non-IFN inducible protein that acts as inhibitor of complement-mediated lysis by disruption of the membrane attack complex. Its implication in viral complement evasion of many enveloped viruses ( Li and Parks, 2018 ), including coronaviruses ( Wei et al, 2017 ), has been demonstrated. This escape mechanism can be mediated by incorporating CD59 to the viral envelope, controlling cellular CD59 expression or producing a counterpart protein that mimics host CD59, or even use it as cell entry receptor ( Maloney et al, 2020 ).…”

A multi-tissue study of immune gene expression profiling highlights the key role of the nasal epithelium in COVID-19 severity

“…CD59 is a non-IFN inducible protein that acts as inhibitor of complement-mediated lysis by disruption of the membrane attack complex. Its implication in viral complement evasion of many enveloped viruses (97), including coronaviruses (98), has been demonstrated. This escape mechanism can be mediated by incorporating CD59 to the viral envelope, controlling cellular CD59 expression or producing a counterpart protein that mimics host CD59, or even use it as cell entry receptor (99).…”

Infectious Bronchitis Coronavirus Infection in Chickens: Multiple System Disease with Immune Suppression

“…The components of the complement pathway aid in the host immune response via complement- and antibody-mediated lysis of viruses [ 92 , 93 , 94 , 95 ]. Since host cells are shielded from lysis via this strategy due to the expression of CD59 in the host cell membrane, IBV is capable of incorporating CD59 into its envelop during exit from the host cells, negating lysis via complement- and antibody-dependent mechanisms [ 96 ]. Previous studies showed that IBV is vulnerable to attack by this strategy [ 97 ].…”