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Question 1

Why do different infections require different effector mechanisms?

Answer 1

Different pathogens vary in type, localization, and stage of infection.
The immune system must tailor responses to effectively clear pathogens while minimizing damage.

Question 2

How do pathogens escape host defense mechanisms?

Answer 2

Suppressing immune signaling (e.g., dampening interferon production).
Reducing MHC expression to evade cytotoxic T cells.
Mutation to evade antibody recognition.

Question 3

How can immune responses contribute to disease symptoms?

Answer 3

Overactive responses (e.g., cytokine storms) can cause tissue damage.
Chronic inflammation or immune dysregulation may worsen outcomes.

Question 4

Which cells present antigens via MHC class I and MHC class II?

Answer 4

MHC class I: Expressed by all nucleated cells; presents antigens to cytotoxic T cells (CD8+).
MHC class II: Expressed by antigen-presenting cells (APCs) like macrophages, dendritic cells, and B cells; presents antigens to helper T cells (CD4+).

Question 5

What are viruses, and why are they challenging for the immune system?

Answer 5

Obligate intracellular parasites.
Can exist extracellularly during certain stages, requiring both intracellular and extracellular immune responses.

Question 6

What are the roles of type I interferons (IFNα, IFNβ) in viral infections?

Answer 6

Induce an antiviral state in neighboring cells to prevent viral replication.
Increase NK cell cytotoxic activity by 20-100 fold.
Enhance antigen presentation via upregulation of MHC class I.

Question 7

How do natural killer (NK) cells combat viral infections?

Answer 7

Recognize stressed or infected cells using activating and inhibitory receptors.
Kill target cells via perforin and granzymes.
Bypass MHC-mediated antigen presentation, targeting cells that reduce MHC expression.

Question 8

How do cytotoxic T lymphocytes (CTLs) kill virus-infected cells?

Answer 8

Release cytotoxic granules containing perforin and granzymes to induce apoptosis.
Fas ligand on CTLs binds Fas on target cells to trigger programmed cell death.
No inflammation or virus release ensures a controlled response.

Question 9

What are the roles of antibodies in viral immunity?

Answer 9

Neutralize free viruses, preventing cell entry and spread.
Opsonize viruses to enhance phagocytosis.
Activate complement, leading to lysis of enveloped viruses.

Question 10

How does HIV evade and impair the immune system?

Answer 10

• Infects and depletes CD4 T cells, macrophages, and dendritic cells.
• Generates mutations to escape cytotoxic T cell recognition.
• Antibodies to HIV are not protective, leading to progressive immune system failure.

Question 11

How does CTL activity correlate with HIV disease progression?

Answer 11

Higher levels of CTL activity slow disease progression.
Mutations that allow the virus to escape CTL recognition accelerate progression to AIDS.

Question 12

What are the key immune responses against SARS-CoV-2?

Answer 12

Innate Immunity: Dampened type I interferon responses aid viral replication.
Viral proteins inhibit RIG-I (PRR) and activate NF-κB, promoting inflammation.
Adaptive Immunity:
Antibodies neutralize the virus and aid in preventing reinfection.
Cytotoxic T cells kill infected cells and limit viral replication.

Question 13

What causes severe COVID-19 outcomes?

Answer 13

Immune dysregulation, including cytokine storms.
Lymphopenia and eosinopenia.
Extensive pneumonia and lung damage, leading to acute respiratory distress syndrome (ARDS).

Question 14

Why are parasites particularly challenging for the immune system?

Answer 14

Parasites vary widely in size and complexity, from unicellular protozoa to multicellular helminths.
They often have complex life cycles, requiring different immune responses at different stages.

Question 15

What immune responses combat protozoa like Leishmania?

Answer 15

Cell-mediated immunity is critical.
Activated macrophages kill intracellular protozoa with the help of cytokines like IFNγ.

Question 16

What immune mechanisms target helminths?

Answer 16

IgE-mediated antibody responses trigger mast cell degranulation and inflammation.
Eosinophils mediate ADCC (antibody-dependent cell-mediated cytotoxicity).

Question 17

How does the immune system combat malaria at different stages?

Answer 17

Antibodies neutralize sporozoites and merozoites.
Cytotoxic T cells target infected liver cells.
RTS,S vaccine induces immunity against Plasmodium falciparum.

Question 18

Why must vaccines induce the correct immune response?

Answer 18

Different pathogens and stages of infection require specific effector mechanisms.
Mismatched responses may lead to ineffective protection or immune-mediated damage.

Question 19

What are the challenges in developing immunity against pathogens like COVID-19 and malaria?

Answer 19

High mutation rates and immune evasion strategies of viruses.
Complex life cycles and diverse forms of parasites.
Need for global cooperation and data sharing for vaccine development.

Question 20

What do interferons do in viral infections?

Answer 20

• Type I interferons (IFNα and IFNβ):
  1. Induce an antiviral state in neighboring cells, preventing viral nucleic acid production and replication.
  2. Increase natural killer (NK) cell cytotoxic activity.
  3. Enhance antigen presentation by upregulating MHC class I expression.
• Type II interferon (IFNγ):
  1. Secreted by T cells and NK cells.
  2. Inhibits TH2 responses (antibody-focused immunity) and promotes TH1 responses (cell-mediated killing).
  3. Activates macrophages and enhances pathogen killing.

Question 21

What is the role of natural killer (NK) cells, and how do they work?

Answer 21

Role:
NK cells are innate immune cells that target and kill virus-infected and stressed cells.
Mechanism:
Recognize stressed or infected cells via activating receptors (bind carbohydrate ligands).
Avoid killing healthy cells via inhibitory receptors that detect MHC class I.
Kill target cells by releasing perforin (forms pores in membranes) and granzymes (induce apoptosis).

Question 22

What is ADCC, and which immune cells are involved?

Answer 22

Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC):
Antibodies bind to antigens on the surface of infected or abnormal cells.
Effector cells with Fc receptors (e.g., NK cells, macrophages, eosinophils) bind the antibody.
These effector cells release cytotoxic substances to kill the target cell.

Question 23

What are the roles of antibodies in defending against infections?

Answer 23

1. Neutralisation
- Bind pathogens or toxins, preventing them from entering host cells or spreading
2. Opsonisation
- Coat pathogens, making them easier for phagocytes to engulf and destroy
3. Complement activation
- Trigger complement pathways, leading to lysis of pathogens (especially enveloped viruses)
4. ADCC
- Facilitate killing of infected cells by immune cells

Question 24

Compare TH1 and TH2 responses and their roles in different infections.

Answer 24

TH1 Response:
Promotes cell-mediated immunity.
Effective against intracellular pathogens like viruses and protozoa (e.g., Leishmania).
Produces cytokines like IFNγ to activate macrophages and enhance cytotoxic T cell responses.
TH2 Response:
Promotes humoral immunity (antibody production).
Effective against extracellular pathogens like helminths.
Produces cytokines like IL-4 to stimulate B cell activation and IgE production.

Question 25

Describe how the immune system clears SARS-CoV-2 during infection.

Answer 25

Innate Immunity:
Early production of interferons (IFNα, IFNβ) slows viral replication.
NK cells kill infected cells.
PRRs like RIG-I recognize viral RNA, triggering inflammatory responses (though SARS-CoV-2 dampens some of these mechanisms).
Adaptive Immunity:
Antibodies: Neutralize the virus, prevent cell entry, and enhance phagocytosis.
Cytotoxic T cells (CD8+): Kill infected cells by inducing apoptosis, limiting viral replication.
Helper T cells (CD4+): Support antibody production and macrophage activation.

Question 26

How do pathogens evade host defense mechanisms?

Answer 26

Through antigenic concealment, variation, immunosuppression, and interference with immune effector mechanisms.

Question 27

How can the immune response contribute to disease symptoms?

Answer 27

Overactive or misdirected immune responses (e.g., cytokine storms, autoimmune reactions) can cause significant pathology.

Question 28

How do some viruses conceal their antigens?

Answer 28

By inhibiting antigen presentation via MHC class I (e.g., herpes simplex virus, adenovirus).

Question 29

What are “privileged sites” in immune evasion?

Answer 29

Locations where pathogens evade immune detection, such as the CNS for latent Herpes zoster virus or hydatid cysts in Echinococcus infection.

Question 30

What is the “cloak effect” in immune evasion?

Answer 30

Pathogens coat themselves in host molecules to evade immune detection (e.g., Schistosomes).

Question 31

What are four types of antigenic variation?

Answer 31

Large antigenic diversity (e.g., Streptococcus pneumoniae).

Mutation (antigenic drift, e.g., flu, HIV).

Recombination (antigenic shift, e.g., flu).

Gene switching (e.g., Trypanosoma brucei).

Question 32

How does Streptococcus pneumoniae evade immunity?

Answer 32

By having over 91 capsular types, making it difficult for antibodies to recognize all strains.

Question 33

What is the difference between antigenic drift and shift?

Answer 33

Drift involves point mutations causing minor changes; shift involves genetic reassortment, leading to major changes and pandemics.

Question 34

How does Trypanosoma brucei evade the immune system?

Answer 34

Through gene rearrangement of its Variant-Specific Glycoprotein (VSG), leading to repeated waves of parasitemia.

Question 35

How does HIV cause immunosuppression?

Answer 35

By infecting and depleting CD4+ T cells, macrophages, and dendritic cells, weakening adaptive immunity.

Question 36

What role do regulatory T cells (Tregs) play in chronic infections?

Answer 36

They suppress immune responses, allowing persistent infections (e.g., Helicobacter pylori, Leishmania).

Question 37

How does the measles virus suppress immunity?

Answer 37

By infecting dendritic cells, causing apoptosis and reducing IL-12 production, which weakens NK cell and TH1 responses.

Question 38

How do pathogens interfere with antibody function?

Answer 38

By producing IgA proteases (e.g., Streptococcus pneumoniae), or Fc-binding proteins (e.g., Staphylococcal protein A).

Question 39

How do pathogens disrupt the complement system?

Answer 39

By producing enzymes to degrade complement components (e.g., Pseudomonas) or molecules that inhibit complement activation (e.g., Vaccinia virus).

Question 40

How does Mycobacterium tuberculosis evade phagocytosis?

Answer 40

By surviving within macrophages, avoiding lysosomal degradation.

Question 41

What causes cytokine storms, and what are their effects?

Answer 41

Excessive cytokine release (e.g., TNFα, IL-1) from macrophages leads to systemic inflammation, fever, and potentially fatal shock.

Question 42

How can immune responses cause tissue damage?

Answer 42

Overactive T cells or antibodies can contribute to pathologies like granulomas in TB or rashes in measles.

Question 43

What is an example of a pathogen triggering autoimmunity?

Answer 43

Streptococcus pyogenes M protein antibodies cross-reacting with heart tissue, leading to rheumatic fever.

Question 44

How does Ebola virus evade immune responses?

Answer 44

By infecting immune cells, inhibiting dendritic cell maturation, inducing apoptosis, and interfering with interferon signaling.

Question 45

What are the pathological effects of Ebola?

Answer 45

Cytokine storms, increased vascular permeability, disseminated intravascular coagulation, and widespread organ failure.

Question 46

List four ways pathogens evade immune responses:

Answer 46

Antigenic variation: Pathogens can alter their surface proteins to avoid detection by the immune system.
Inhibition of antigen presentation: Some pathogens can interfere with the host’s ability to present antigens on major histocompatibility complex (MHC) molecules.
Immune suppression: Pathogens may produce molecules that suppress the host’s immune responses (e.g., HIV).
Latency: Some pathogens, like herpesviruses, can enter a dormant state within the host, avoiding immune detection.

Question 47

What is the difference between antigenic drift and shift?

Answer 47

Antigenic drift: A gradual change in the virus’s surface proteins due to small mutations, leading to slight variations that can evade immunity over time (common in influenza).
Antigenic shift: A major, sudden change in the virus’s surface proteins, often due to genetic reassortment between different viral strains, leading to new, highly different strains that can cause pandemics.

Question 48

What type of genetic rearrangement causes major flu pandemics?

Answer 48

Antigenic shift, which occurs when different strains of the influenza virus exchange genetic material, creating a new strain with a novel combination of surface proteins.

Question 49

Which protein does Trypanosoma brucei rearrange to avoid clearance?

Answer 49

Variant Surface Glycoprotein (VSG). Trypanosoma brucei frequently changes the VSG protein on its surface to evade detection by the host’s immune system.

Question 50

Define immunopathology:

Answer 50

Immunopathology refers to the damage to the host’s tissues and organs caused by the immune system’s response to infection, often involving inflammation, cytokine release, and immune cell activity that harms the host.

Question 51

Give an example of a pathogen causing immunosuppression and explain how:

Answer 51

HIV is an example of a pathogen that causes immunosuppression. It targets and destroys CD4+ T cells, weakening the host’s immune response and making the body more vulnerable to opportunistic infections.

Question 52

What happens during a cytokine storm in sepsis?

Answer 52

A cytokine storm in sepsis occurs when the immune system overreacts to an infection, releasing an excessive amount of cytokines, which leads to widespread inflammation, tissue damage, organ failure, and potentially death.

Question 53

What makes Ebola a highly successful pathogen?

Answer 53

Ebola’s success is due to its ability to rapidly replicate in the host, cause severe damage to tissues, and evade immune detection. It also triggers an immune system dysregulation that contributes to the pathogenesis, leading to severe hemorrhagic fever and high mortality rates.