Microbiology · MU Sofia

37: Protective mechanisms in infectious diseases

Covers how the body defends against viral infections, starting with innate defences such as interferons, NK cells, phagocytosis, complement and fever, then adaptive humoral and cell-mediated responses including antibody actions and CD8+ and CD4+ T cell roles. It then outlines fungal defences: pattern recognition receptors, neutrophils and macrophages, and Th1 and Th17 responses, ending with general points on timing and immunodeficiency.

Inside: 3 sections · 3 labelled pictures · 14 flashcards · 5 min

Topic 37 of 113 in the MU Sofia syllabus for Microbiology (Dental Medicine, Year 2). The free AceMed note covers it in 3 sections, about 711 words (5 min of reading), with 14 flashcards.

In this note

  1. Protective mechanisms in infectious diseases, focusing on defense mechanisms in viral and fungal infections
  2. Defense Mechanisms in Viral Infections
  3. Defence Mechanisms in Fungal Infections

Defense Mechanisms in Viral Infections

Defense mechanisms against viral infections involve both rapid non-specific innate immunity and slower specific adaptive immunity.

  1. 1. Innate Immunity (Nonspecific Immune Defences / Natural Resistance)
  • Activated immediately upon pathogen penetration of outer barriers.
  • Interferons (IFNs): Crucial cytokines in the immune response to viral infections.
  • Cell-coded proteins. Three types: Type I (IFN-alpha from leukocytes, IFN-beta from fibroblasts) and Type II (IFN-gamma stimulated by Th1 lymphocytes and NK cells).
  • They do not directly affect viruses but induce cellular resistance mechanisms ("antiviral proteins") that interfere with specific steps in viral replication.
  • Infected cells release IFNs, which can protect neighbouring cells from viral infection by inducing an antiviral state.
  • Type I IFNs are primarily involved in antiviral responses.
  • Natural Killer (NK) cells: Part of innate immunity.
  • Recognize and kill virus-infected cells.
  • Can lyse virus-infected cells via apoptosis, potentially using perforins and granzymes.
  • Identify damaged or infected cells via MHC on the surface. They specialise in killing cells that have a reduced number of MHC I molecules.
  • Involved in phagocytosis and destruction of pathogens via NK and granulocytes.
  • Can produce IFN-gamma.
  • Phagocytosis: Ingestion and destruction of pathogens. Performed by macrophages and granulocytes.
  • Complement System: Important humoral factor.
  • The alternative pathway can activate and lead to the destruction of viral particles. Can be activated by antibodies binding to the virus.
  • Other Factors: Changes in pH and ion balance, as well as fever, play a role, potentially blocking certain temperature-sensitive replication steps.
  1. 2. Adaptive Immunity (Specific Immune Defences)
  • Develops after a latent period, typically 1-2 weeks.
  • Humoral Immunity: Mediated by antibody-producing B cells.
  • Antibodies can only attack viruses outside of their host cells, in the extracellular phase.
  • Primary role is preventing generalized infection, especially if present early (e.g., via vaccination).
  • Antibodies defend against viruses by:
  • Neutralization: Antibodies bind to viral particles, inhibiting their effect.
  • Blocking Adherence: Antibodies can block attachment and infection of naked viruses.
  • Agglutination: Cause clumping of the virus to make it an easier target.
  • Complement Activation: Antibodies can activate the complement system against the virus.
  • Activating Phagocytosis: Antibodies bind to Fc receptors on phagocytic cells, promoting phagocytosis.
  • Different antibody classes have roles: IgG and IgM are active in the bloodstream, IgA is active on mucosal surfaces. Secretory IgA in the nasal mucosa plays a role in local immunity.
  • Cell-Mediated Immunity (CMI): Involves T-lymphocytes (T helper cells, cytotoxic T cells) and macrophages.

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