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This Concept Map, created with IHMC CmapTools, has information related to: Answers_Viral path, viral proteins and glycoproteins changing the antigenic surface of the host cell's cytoplasmic membrane results in The infected cell is recognized as foreign and destroyed by the body's immune defenses., 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 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 down regulating several host proteins involved in attaching viral epitopes to MHC-I molecules, stimulating body cells to release inflammatory vasoactive peptides, bradykinins, histamines, etc. results in vasodilation and increased mucous secretion, inhibiting normal host cell DNA, RNA, or protein synthesis results in structural or functional defects in the infected host cell leading to cytolysis or altered cell functions, stimulating body cells to release inflammatory cytokines and chemokines results in inflammation, 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 Antibodies block viral adsorption to host cell receptors., Pathogenicity of Animal Viruses immune defenses against viruses Antibodies function as opsonins and sticking viruses to phagocytes., causing nicks or breaks in the host cell's chromosomes example congenital rubella syndrome, Pathogenicity of Animal Viruses damaging infected host cells stimulating body cells to release inflammatory cytokines and chemokines, NK cells recognize infected cells displaying stressed-induced proteins and not displaying MHC-I molecules on their surface and kill these cells. evade by producing microRNAs that down-regulate the production of stress-induced proteins; NK cell does not bind to infected cell, 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 playing a role in normal cells becoming malignant, Pathogenicity of Animal Viruses damaging infected host cells causing nicks or breaks in the host cell's chromosomes, Pathogenicity of Animal Viruses damaging infected host cells stimulating body cells to release inflammatory vasoactive peptides, bradykinins, histamines, etc., 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., Type-I interferons produced during innate immunity block viral replication. evade by producing microRNAs that block production of type-I interferons, Antibodies block viral adsorption to host cell receptors. evade by Antibodies function as opsonins and sticking viruses to phagocytes.
