Infections And Immunity Flashcards

1
Q

What are the features of acute inflammation?

A
  • Resolve quickly
  • Harmful stimuli removed
  • Initial tissue destruction
  • Followed by healing
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2
Q

What are the features of chronic inflammation?

A
  • Prolonged inflammation
  • Harmful stimuli remain
  • Simultaneous tissue destruction
    and healing
  • Serious consequences
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3
Q

What are infectious diseases?

A

Caused by diverse living agents that replicate in their hosts

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4
Q

What is the determining factor for pathogenesis of infectious disease?

A

The interaction between host and micro-organism(s)

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5
Q

What routes of entry into the host?

A

Respiratory

Skin

Swallowed

Congenital

Blood

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6
Q

Is the route of entry important?

A

Does not necessarily correlate with the disease induced by a virus.

Some viral diseases were made localised others manifest in systemic symptoms.

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7
Q

What is viral cytopathicity?

A

Damage or alterations to host cells caused by viral infection.

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8
Q

What kinds of viral cytopathic effects are there?

A

Host protein synthesis shut off

Cell death

Cell fusion

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9
Q

What are non-cytopathic virus?

A

Cause less obvious damage that can affect physiologic function of the cells

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10
Q

What are the Initial Interactions Between Host and Virus?

A

Attachment

Entry

Uncoating

Replication

Assembly

Release

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11
Q

What is attachment?

A

The virus attached to specific receptors on the surface of host cells.

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12
Q

What is entry?

A

The virus gains entry into the host cell, either through direct fusion with the cell membrane (enveloped viruses) or receptor-mediated endocytosis.

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13
Q

What is uncoating?

A

The viral genome is released from its protective capsid or envelope and enters the host cell’s cytoplasm or nucleus, depending on the virus type.

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14
Q

What is replication?

A

The viral genome is replicated using the host cell’s machinery. This may involve transcription of viral genes to produce viral RNA or DNA, translation of viral proteins, and replication of viral nucleic acids.

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15
Q

What is assembly?

A

Newly synthesized viral components are assembled into complete virions (virus particles) within the host cell.

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16
Q

What is release?

A

Mature virions are released from the host cell, either by cell lysis, budding from the cell membrane (enveloped viruses), or exocytosis.

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17
Q

What are the key features of innate immunity?

A

Pre-existing non-specific mechanism.

React rapidly

Can trigger other defensive mechanisms

Recruit immune cells

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18
Q

What are the components of innate immunity?

A

Engulfing pathogens

Slow down pathogens replication

Bind to pathogen

Kill infected cells

19
Q

What types of cells engulf pathogens?

A

Macrophages

Monocytes

Neutrophils

20
Q

What kinds of cells in innate immunity kill cells?

A

Natural Killer (NK) cells

21
Q

What do CD8+ recognise?

A

MHC-I and 8-10 mer peptide via the T cell receptor

22
Q

How do CD8+(cytotoxic) cells kill infected cells?

A

Directly through perforin and FasL

Secrete antiviral cytokines

23
Q

What do CD4+ (helper) cells recognise?

A

MCH-II and 12-15 mer peptide via the T cell receptor

24
Q

What is the role of CD4+ (helper) cells?

A

Promote B-cell responses

Provide help to aid CD4+ T cell expansion.

Role of Tregs

25
Q

How are antibodies bound to the cells?

A

Initial secretion of IgM

Affinity maturation and antibody class switching to IgA

26
Q

Why is affinity maturation important?

A

Promote tighter binding to target antigen

27
Q

Where is IgG?

A

In serum

28
Q

Where is IgA?

A

A mucous membrane surface

29
Q

What is the role of antibodies?

A

Antibodies bind and neutralize free infective virus.

Antibodies could also bind to viral protein expressed on the cell surface.

30
Q

What is the purpose of the antibody binding to viral protein on cell surface?

A

Promotes the killing of infected cells via the complement attack and enhance phagocytosis via crosslinking Fc-receptor.

31
Q

What is protective immunity?

A

Immune memory

32
Q

Why is immune memory important?

A

Protect s from reinfection by the same pathogen

33
Q

What is the process of protective immunity?

A

Pathogen specific T- cells persist at a stable level.

Virus-specific B-cells persist.

Long lasting IgG in serum

34
Q

What are the viral immune evasions strategies?

A
  • High replication rate and rapid evolution
  • Modulation of cytokine responses
  • Lack of immunogenicity
  • Induction of Tolerance
35
Q

Why is high replication rate for viruses?

A

Ability to produce new virus particle and spread to new host before specific immune response.

Virus could overwhelm host immune system.

36
Q

Why is rapid evolution important for viruses?

A

No proofreading activity.

Immunological selection pressures select mutant good for survival.

37
Q

What is the CTL escape?

A

Mutations in T-cell epitopes can result in virus not being recognized by T-cells

38
Q

What is the antibody escape?

A

Evolution of surface proteins can allow re-infection of “immune” hosts

39
Q

What is Modulation or Hijacking of Cytokine Responses?

A

Modulation or hijacking of cytokine responses occurs when pathogens manipulate the host’s immune system, often leading to excessive inflammation or immune evasion.

This can result in severe complications, including cytokine storms.

40
Q

Define immunogenicity?

A

Ability of a substance to provoke an immune response in the body.

41
Q

What kinds of things reduce immunogenicity?

A

Reduction in amount of viral antigen presence

Infection in immune privileged sites

Prevents antigen presentation by infected cells

42
Q

Describe the down regulation of the MHC?

A

Disrupt the T-cell attack of infected cells by interfering antigen presentation

Cytomegalovirus protein US11 and US12 bind to MHC-I causing it to be retained in the ER.

US6 inhibits antigen transporter TAP prevents peptide loading onto MHC-I and downregulates MHC-I expression.

MHC-I deficient are NK targets

UL18 is a CMV homolog of MHC-I acting as a decoy for NK cells.

43
Q

What is clonal exhaustion?

A

Excessive amounts of viral antigen presented causing over-stimulation of TCR on T-cells results in peripheral deletion or anergy of virus specific T-cells.

44
Q
A