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Results indicate that N-specific siRNA can inhibit virus replication.
The mechanism by which IL-17-producing cells may inhibit virus clearance is not clear.
In vitro, six DsiRNAs were shown to inhibit virus replication using cell proliferation tests.
One of the antibodies did inhibit virus infection, albeit with modest potency.
Antibodies can also coordinate other components of the host's immune response that destroys virus-infected cells, even when they cannot inhibit virus infection directly.
Inhibitor compounds that specifically bind capsid proteins could inhibit virus replication at steps of assembly, receptor recognition or uncoating.
However, p53 is also known to inhibit virus replication via enhanced type I interferon (IFN) antiviral responses.
The potential of RNA interference (RNAi) to inhibit virus propagation has been well established in recent years.
Since we demonstrated that IL-27-mediated induction of cell surface BST-2 expression is observed up to 24 48 h post-stimulation, it is possible that these enhanced levels of BST-2 may function to inhibit virus release.
This study showed that dsRNA against WSSV genes orf89, vp28 and vp26 were highly effective to inhibit virus replication and suggest an essential role in WSSV infection.
The CRISPR-Cas9 system is a newly developed genome-engineering tool used to inhibit virus infection by targeting the conserved regions of the viral genomic DNA.
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