| Term | Definition |
|---|
| Host innate and Adaptive immune resonses | aimed at blocking infection and eliminating virus infected cells |
| Innate Immunity | Inhibits virus by Type I interferons and NK cell-mediated killing of infected cells |
| Interferons | Cytokines produced and secreted by somatic cells in response to a variety of stimuli including virus infection. They possess antiviral, immunomodulating, and anticancer properties. ARE NOT VIRUS SPECIFIC. |
| glycoproteins | Because interferons are this, they are orally inactive and therefore must be given parenterally. |
| Type I Interferons | induce an antiviral state in uninfected cells via inhibition of viral protein synthesis and simultaneously induce apoptosis in the virus infected cells. |
| MHC class I proteins and proteasome proteins | Type I interferons stimulate the production of these substances |
| IFN-alpha (Leukocyte interferon) | secreted by virus infected macrophages and other leukocytes. NOT HOST SPECIFIC |
| IFN-beta (Fibroblast interferon) | Secreted by virus infected fibroblasts and epithelial cell. HOST SPECIES SPECIFIC. |
| pH2 | Type I interferons are stable at this pH |
| RNA VIRUSES | are stronger inducers of IFN (RNA or DNA viruses ?) |
| Protein kinase | inactivates a viral initiation protein thereby preventing translation of viral mRNA |
| 2-5A synthetase | activates a ribonuclease that degrades viral mRNA |
| Type II Interferons (IFN-gamma) | secreted by antigen, mitogen, or cytokine stimulated T cells and NK cells. Labile at pH2 and is host specific. Has NO ANTIVIRAL ACTIVITY. Enhances expression of MHC I and II. |
| NK cells | Lyse infected cells not expressing or expressing few MHC class I proteins. Also lyse target cell cia antibody dependent cell mediated cytotoxicity (ADCC). |
| Adaptive Immunity | directed against viral capsid and envelope antigens |
| internal viral antigens | elicit protective CMI response |
| Surface antigens | elicit protective humoral and CMI responses |
| Antibody-mediated (humoral) immunity | antibodies are effective against viruses only during the extracellular stage of virus infection |
| Neutralizing Antibodies | prevent virus attachment and entry into host cells. They bind viral capsid or envelope proteins. |
| Opsonization | coating of virions by IgG may facilitate pinocytosis and intracellular killing by MACROPHAGES and neutrophils |
| Clumping of viruses | reduces the number of infectious units available for cell invasion |
| Complement activation | opsonization and possible direct lysis of enveloped viruses |
| Cell-Mediated Immunity | the intracellular replicative steps of viruses and virus-infected cells are major targets for this. It is also more important in recovery from non-cytolytic viruses |
| Plasticity | rapidly changing surface antigenic structure by mutation, genetic reassortment, or recombination. As a result, the virus becomes resistant to immunity generated by previous infection. |
| Multiplicity | antigenic variants with little or no cross-reactivity |
| immunosuppression | immunocompetent cells are either lysed or inactivated |
| virokines | protein homologue of ILs that suppresses cytokine production by Th1 CD4+ cells |
| viroreceptors | proteins encoded by poxviruses that are homologous to the receptors for several cytokines. The cytokine receptor homologues may bind cytokines and function as competitive antagonists f the cytokines |
| down regulation of class I MHC expression | inhibition of class I MHC-associated presentation of endogenous protein antigens. As a result, cells infected by such viruses become insusceptible to killing by CD8+ T cells. |
| Inhibition of complement activation | VCP (vaccina viral protein) binds to CD4b which inhibits the classical complement oathway. A glycoprotein component of herpes simplex viruses bind to C3b inhibiting both the classical and alternative pathways |
| Latency | viruses may become latent within infected cells. Viral antigens are scarce or absent on the cell surface |
| evasion of neutralizing antibodies | lg amts of soluble viral proteins are produced that soak up antibody |
| cell to cell spread (Type II spread) | cause adjacent cells to fuse together enabling the viral genome to spread from cell to cell without being exposed to the host's immune mediators |
Combine with other sets
Share on Facebook
Share on MySpace