Chapter 4 Flashcards

1
Q

Restriction Factors

A

anti-viral proteins that are produced in the host and counteract or ‘restrict’ viral replication.

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2
Q

Innate Immunity

A

Native/non-specific immunity. Has no memory response. Cytokines, phagocytes, NK cells, TLRs, and complement.

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3
Q

Adaptive Immunity

A

Acquired/specific immunity. Has memory. Mediated by T cells and B cells.

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4
Q

Cellular components

A

Macrophages, Neutrophils, NK cells

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5
Q

Cytokines

A

Small proteins that are secreted by cells to mediate immune functions of other cells

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6
Q

Antiviral Cytokines

A

IFN-α and IFN-β are the type I interferon’s that are primarily involved in anti-viral innate immunity.

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7
Q

Other Innate Cytokines

A

TNF-α stimulates the activity of macrophages and neutrophils. IL-1 and IL-6 are also pro-inflammatory cytokines. They in turn stimulate adaptive immunity cytokines like INF- γ and IL-12.

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8
Q

Complement

A

Small proteins that are present in the serum and help to destroy infected cells.

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9
Q

Phagocytes

A

Include several types of white blood cells such as dendritic cells, macrophages, neutrophils and natural killer cells [NK cells]. They seek and destroy invaders. Some also destroy damaged body cells.

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10
Q

Antigen Presenting Cells

A

Include dendritic cells, macrophages and monocytes. B cells can also present antigen.

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11
Q

NK Cells

A

Natural killer cells. Induce cell death by apoptosis.

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12
Q

Complement Pathway

A

If activated, complement binds to the Fc regions, recruits the membrane attack complex (MAC) to lyse the infected cells e.g HSV

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13
Q

CMV

A

Produces an MHC-1 homolog that engages the NK cell inhibitory receptor to generate a DON’T KILL signal.

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14
Q

HIV

A

Nef protein - upregulates the inhibitory signal to NK cells

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15
Q

HSV

A

produce envelope glycoproteins that bind Fc non-spedifically. Therefore it prevents ADCC as well as complement mediated lysis of free virus.

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16
Q

Classical

A

Requires Antibody

17
Q

Alternative

A

Does not require antibody. C3 is spontaneously cleaved.

18
Q

Lectin

A

Requires mannose binding protein.

19
Q

Complement Fixation

A

Binding of C3b to protein and carbohydrates on the viral surface. Then it recruits the MAC

20
Q

Acute Phase Proteins

A

Indicate inflammation is occuring in the body.

21
Q

PRRs

A

Pathogen recognition receptors on cells. (TLRs)

22
Q

PAMPs

A

Pathogen associated molecular patterns (DsRNA, CpG, DNA, LPS)

23
Q

Interferons

A

Proteins that inhibit viral replication

24
Q

PKR

A

Transcription factor

25
Q

Viroceptors

A

Viruses can secrete analogs of cytokine receptors or regulatory factors to bind up secreted cytokines or inhibit secretion.

26
Q

Virokines

A

Viruses can secrete analogs of immune regulators such as cytokines.

27
Q

Immune-escape Mutants

A

Genetic variation leading to antigenic variation, common in RNA viruses which have higher mutation rates (ex: HIV or Rhinoviruses)

28
Q

Glycosylation

A

Coating the surface antigens with sugars to render them as poor immunogens. (ex: HIV GP120)

29
Q

Hide Receptor Binding Sites

A

Rhinoviruses- the receptor binding site is in a canyon that cannot be accessed by antibodies, has over 100 different serotypes.

30
Q

Hide in Immune Privileged Sites

A

Polyoma viruses like Jc simian virus 40 hide in the kidney tubules, HSV - hides in neurons

31
Q

Immune Privileged Sites

A

Nervous system, brain, and Fetus

32
Q

Influenza

A

Leads to release of pro-inflammatory cytokines by the innate immune system that result in fever, body-aches etc.

33
Q

HBV

A

Tissue damage is due to the CD8 + T cells and pro-inflammatory cytokines that attack virus infected tissues.

34
Q

Coxsackievirus B3

A

Myocarditis due to the CD8 + T cell immune response and TNF-alpha and IL-1beta. Coxsackie B4 attacks the pancreas and is believed to trigger diabetes but is not proven.

35
Q

Herpes Stromal Keratitis

A

HSV-1 coat proteins cross-react with corneal antigens, leading to destruction

36
Q

Multiple Sclerosis

A

Been associated with several viruses but viral etiology is not proven.

37
Q

Guillain-Barre Syndrome

A

HCMV and Clostridium jejuni produce antibodies that are cross reactive to GM2 a ganglioside present on motor neurons. Results in limb weakness and paralysis.