Interaction of a virus with<unk> es must prevent the virus from attaching to the host cell entry receptors. However, instead of preventing infection of the host cell, this process can facilitate viral infection of immune cells, causing<unk> . After binding the virus, the<unk>  interacts with Fc or complement receptors expressed on certain immune cells. These receptors promote virus-antibody internalization by the immune cells, which should be followed by the virus destruction. However, the virus might escape the<unk>  complex and start its replication cycle inside the immune cell avoiding the degradation. This happens if the virus is bound to a low-affinity<unk> . Different virus serotypes There are several possibilities to explain the phenomenon of enhancing intracellular virus survival: 1)<unk> es against a virus of one serotype binds to a virus of a different serotype. The binding is meant to neutralize the virus from attaching to the host cell, but the virus-antibody complex also binds to the Fc-region<unk>  receptor (FcγR) on the immune cell. The cell internalizes the virus for programmed destruction but the virus avoids it and starts its replication cycle instead. 2)<unk> es against a virus of one serotype binds to a virus of a different serotype, activating the classical pathway of the complement system. The complement cascade system binds C1Q complex attached to the virus surface protein via the<unk> es, which in turn bind C1q receptor found on cells, bringing the virus and the cell close enough for a specific virus receptor to bind the virus, beginning infection. This mechanism has been shown for Ebola virus in vitro and some flaviviruses in vivo. Conclusion When an<unk>  to a virus is unable to neutralize the virus, it forms sub-neutralizing virus-antibody complexes. Upon phagocytosis by macrophages or other immune cells, the complex may release the virus due to poor binding with the<unk> . This happens during acidification and eventual fusion of the phagosome with lysosomes. The escaped virus begins its replication cycle within the cell, triggering<unk> .
Antibody-dependent enhancement
Cross-tolerance
Reverse tolerance
Peripheral tolerance
Immune tolerance
Central tolerance
Desensitization 
Sensitization 