Viral Pathogenesis: Host Responses to Viral Infections II Flashcards

1
Q

Compare antibodies produced in primary and secondary responses

A

a. Antibody levels are effector T-cell activity gradually decline after an infection is cleared. Early reinfection is rapidly cleared by preformed immune reactants (IgG). Later reinfection leads to rapid increases in antibody and effector T cells due to immunological memory and infection can be mild or not apparent. Viral infection can be controlled by the host immune system with or without clearance of virus

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2
Q

List and describe major cell types involved in anti-viral responses (innate)

A

i. Mononuclear phagocytes - phagocytosis, release of inflammatory mediators, antigen presentation
ii. Dendritic cells - present antigens to T cells, stimulate B cell differentiation and proliferation, modulate adaptive immune response, secrete antiviral & immunoregulatory cytokines
iii. NK cells - contain virus infections before adaptive immune response generates antigen-specific cytotoxic T cells that can clear the infection Granulocytes release of inflammatory mediators

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3
Q

List and describe major cell types involved in anti-viral responses (adaptive)

A

i. B-Cells – immunoglobulin producing cells that are huge in the humoral response, bind antigen and are stimulated to divide and produce loads of the receptor on their surface as antibody
ii. T-Cell – effectors of the cell-mediated response, recognize MHC I and II on cell surfaces and bind
1. T cells are activated if a non-self antigen is being presented in an MHC receptor
produce cytokines, activate B-Cells, kill cells

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4
Q

efficacy of antibody anti-viral response.

A

Antibodies are ineffective once the virus enters a cell as they cannot gain access to bind them. Cytotoxic T-Cells and there CD8 receptors are key once the virus has entered a cell

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5
Q

efficacy of cell-mediated immunity in the anti-viral response.

A

Antibody mediated immunity usually serve to arrest an infection while a cell-mediated, adaptive immune response develops. Although, antibody mediated immunity can sometimes clear an infection, the job is usually left to the bigger guns of the cell-mediated immunity. Cell-mediated immunity harnesses many of the same effector mechanisms as the antibody response, but is able to target them with greater precision. antigen-specific T cells activate the microbicidal and cytokine-secreting properties of macrophages harboring pathogens, while antibodies activate complement, act as direct opsonins for phagocytes, and stimulate NK cells to kill infected cells. In addition, the adaptive immune response uses cytokines and chemokines, in a manner similar to that of innate immunity, to induce inflammatory responses that promote the influx of antibodies and effector lymphocytes to sites of infection

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6
Q

means of virus evasion/manipulation of host defenses by various viruses

A

a. Antigenic variation
b. Immune tolerance
c. Virus makes itself closely remember host proteins to such an extent that the host can no longer recognize self from virus and does not mount a response
d. Restricted expression of viral genes
e. Viral production of inhibitors or decoys
f. Down-regulation of host proteins
g. Infections of immunoprivileged sites like the brain
h. Direct infection of the immune system
i. inhibition of apoptosis and cell cycle control – also involved in tumorigenesis

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7
Q

Antigenic variation –

A

point mutations and genome shuffling that cause viruses to become unrecognizable to specific immune receptors

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8
Q

Immune tolerance –

A

molecular mimicry or infection prior to competent immune system

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9
Q

Restricted expression of viral genes –

A

going invisible to host defenses like in latent infections

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10
Q

viral production of inhibitors or decoys –

A

virus produces proteins which bind and block cellular mediators such as cytokines and antibody receptors. Some viruses even themselves mimic cellular mediators, but omit functions that would be stimulatory functions)

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11
Q

Down-regulation of host proteins –

A

main example is down regulation of MHC Class I to avoid detection by CTL – some viruses even have their own viral MHC that mimics Class I

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