Course review

C3.2 Defence against disease

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Learning objective

C3.2.1—Pathogens cause infectious diseases

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• Pathogens are disease-causing viruses, bacteria, fungi, protists, or parasites • Archaea are not currently known to cause human infectious diseases

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Learning objective

C3.2.2—Skin and mucous membranes

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• Keratinized skin, shedding, lysozyme, mucus, and cilia are primary defences • Mucous membranes protect respiratory and digestive surfaces

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Learning objective

C3.2.3—Blood clotting

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• Platelets and damaged tissue release clotting factors at wounds • Thrombin converts fibrinogen to fibrin, trapping blood cells and sealing entry points

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Learning objective

C3.2.4—Innate vs. adaptive immune system

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• Innate immunity is broad, rapid, and does not become more specific over life • Adaptive immunity is antigen-specific and produces memory cells

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Learning objective

C3.2.5—Phagocytes

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• Phagocytes use amoeboid movement to reach infection sites • They recognize, engulf, and digest pathogens using lysosomal enzymes

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Learning objective

C3.2.6—Lymphocytes

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• B-cells produce antibodies after activation; T-cells assist or destroy infected cells • Lymphocytes originate in bone marrow and circulate through blood, lymph, and lymph nodes

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Learning objective

C3.2.7—Antigens

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• Antigens are non-self molecules that trigger specific immune responses • They are often proteins or glycoproteins recognized by antibodies or lymphocyte receptors

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Learning objective

C3.2.8—B-lymphocyte activation

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• B-cells bind antigen, internalize it, and present it with MHC proteins • Helper T-cells activated by the same antigen stimulate B-cell activation

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Learning objective

C3.2.9—Clones of plasma cells

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• Activated B-cells divide by mitosis through clonal selection • Plasma cells rich in rough ER secrete large amounts of one specific antibody

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Learning objective

C3.2.10—Immunity from memory cells

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• Memory B- and T-cells remain after the primary response declines • Re-exposure triggers faster, stronger secondary immunity

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Learning objective

C3.2.11—HIV transmission

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• HIV is transmitted through infected blood, semen, vaginal fluids, or breast milk • Transmission risk depends on fluid exchange, barriers, and viral load

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Learning objective

C3.2.12—HIV infection and AIDS

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• HIV infects helper T-cells using CD4 receptors and reverse transcriptase • AIDS results when helper T-cell loss weakens antibody production and immune coordination

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Learning objective

C3.2.13—Antibiotics

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• Antibiotics block bacterial processes absent from eukaryotic cells • They do not treat viruses; antivirals target viral replication processes

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Learning objective

C3.2.14—Antibiotic resistance evolution

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• Antibiotic use selects resistant variants that survive and reproduce • Multi-resistant strains arise through mutation, plasmids, and overuse of antibiotics

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Learning objective

C3.2.15—Zoonoses

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• Zoonoses transfer from animal reservoirs to humans, sometimes through vectors • Examples include rabies, tuberculosis, Japanese encephalitis, and COVID-19

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C3.2.16—Vaccines and immunization

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• Vaccines contain weakened/inactivated pathogens, antigens, or genetic instructions • Immunization produces active artificial immunity and memory cells

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Learning objective

C3.2.17—Herd immunity

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• Herd immunity indirectly protects susceptible people when many are immune • Thresholds depend on transmission route and pathogen contagiousness

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C3.2.18—COVID-19 pandemic data evaluation

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• Evaluate COVID-19 data using source reliability, trends, and controlled comparisons • Calculate percentage change, percentage difference, incidence, and vaccine efficacy

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