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This Concept Map, created with IHMC CmapTools, has information related to: Answers_Viral path, Antibodies block viral adsorption to host cell receptors. evade by Antibodies function as opsonins and sticking viruses to phagocytes., CTLs bind to viral epitopes on MHC-I molecules and trigger apoptosis of viral-infected cells. evade by down regulating several host proteins involved in attaching viral epitopes to MHC-I molecules, Pathogenicity of Animal Viruses damaging infected host cells inducing adjacent host cells to fuse together forming giant multinucleated cells or syncytias, Pathogenicity of Animal Viruses damaging infected host cells depleting the host cell of cellular materials essential for life or normal function, causing nicks or breaks in the host cell's chromosomes example congenital rubella syndrome, CTLs bind to viral epitopes on MHC-I molecules and trigger apoptosis of viral-infected cells. evade by producing microRNAs that blocks apoptosis of virus-infected cells, CTLs bind to viral epitopes on MHC-I molecules and trigger apoptosis of viral-infected cells. evade by inhibiting proteasomal activity, Pathogenicity of Animal Viruses damaging infected host cells stimulating body cells to release inflammatory cytokines and chemokines, CTLs bind to viral epitopes on MHC-I molecules and trigger apoptosis of viral-infected cells. evade by blocking the TAP transport of peptides into the endoplasmic reticulum, CTLs bind to viral epitopes on MHC-I molecules and trigger apoptosis of viral-infected cells. evade by blocking the formation of MHC-I molecules by the infected cell, stimulating body cells to release inflammatory vasoactive peptides, bradykinins, histamines, etc. results in vasodilation and increased mucous secretion, Pathogenicity of Animal Viruses immune defenses against viruses Antibodies function as opsonins and sticking viruses to phagocytes., Pathogenicity of Animal Viruses damaging infected host cells stimulating body cells to release inflammatory vasoactive peptides, bradykinins, histamines, etc., Type-I interferons produced during innate immunity block viral replication. evade by secreting molecules that bind and tie up cytokines, Pathogenicity of Animal Viruses immune defenses against viruses NK cells recognize infected cells displaying stressed-induced proteins and not displaying MHC-I molecules on their surface and kill these cells., Pathogenicity of Animal Viruses damaging infected host cells playing a role in normal cells becoming malignant, Type-I interferons produced during innate immunity block viral replication. evade by producing microRNAs that block production of type-I interferons, Pathogenicity of Animal Viruses damaging infected host cells inhibiting normal host cell DNA, RNA, or protein synthesis, Pathogenicity of Animal Viruses damaging infected host cells causing nicks or breaks in the host cell's chromosomes, Pathogenicity of Animal Viruses immune defenses against viruses CTLs bind to viral epitopes on MHC-I molecules and trigger apoptosis of viral-infected cells.
