Viral and Bacterial Immunity: Defense Mechanisms

Immunity Against Viruses

Viruses are submicroscopic particles with a simple structure that depend on cells for replication. Their genetic material can be either RNA or DNA.

DNA Viruses

The infection process begins with the following steps:

  1. Collision and Viral Absorption: The virus attaches to the cell surface using specific receptor molecules. For example, the rabies virus uses acetylcholine receptors, rhinovirus uses integrin receptors, and influenza uses sialic acid molecules.
  2. Penetration: The cell engulfs the virus through endocytosis (viropexis).
  3. Uncoating: Once inside, the virus sheds its outer layer, exposing its genetic material.
  4. Synthesis: The cell’s machinery is hijacked to produce viral proteins and nucleic acids.
  5. Assembly: Viral components assemble to form new virus particles.
  6. Release: New viruses are released, either by budding from the cell membrane or by cell lysis (death).

RNA Viruses

Examples include Newcastle disease and foot-and-mouth disease viruses. RNA serves as a template for new viral RNA synthesis and acts as mRNA for viral protein synthesis. The initial steps (collision, absorption, penetration, and uncoating) are similar to DNA viruses.

In retroviruses (e.g., retroviridae), viral RNA is transcribed into DNA using reverse transcriptase. This DNA integrates into the host cell’s genome as a provirus, which can remain inactive for extended periods, causing persistent infections. Upon activation, the provirus is transcribed into mRNA, initiating viral replication and protein synthesis.

Some RNA viruses (e.g., retroviridae and some herpesviruses) can cause tumors. These viruses can induce minimal changes or lead to cell death and tumor formation.

Defense Against Viruses

Innate Immunity

  1. Genetic Resistance: Some species are inherently resistant to certain viruses due to the absence of specific receptor molecules.
  2. Chemical Barriers: Non-specific substances like lysozyme and bile, along with the alternative complement pathway, offer initial defense.
  3. Sentinel Cells: Cells like macrophages and dendritic cells recognize viral patterns (PAMPs) and initiate phagocytosis.
  4. Apoptosis: Infected cells undergo programmed cell death (apoptosis), preventing viral spread.
  5. Interferons (IFNs): These cytokines are produced by infected cells and activate antiviral responses in neighboring cells. There are two types: Type I IFNs (IFN-α, IFN-β, etc.) and Type II IFN (IFN-γ).

Acquired Immunity

Viral antigens trigger humoral and cellular immune responses. Free viral particles are phagocytosed, processed, and presented to T helper cells, which activate B cells. B cells differentiate into plasma cells that produce antibodies. Antibodies neutralize viruses by blocking absorption, opsonizing them for phagocytosis, and activating complement. Cellular immunity involves cytotoxic T cells that kill infected cells presenting viral antigens on MHC-I molecules.

Bacterial Infection

Bacteria cause disease through:

  1. Toxin production
  2. Enzyme production
  3. Intracellular invasion

Toxin Production

Exotoxins: Proteins produced by bacteria, classified as protoplasmic (released upon bacterial death) or extracellular (released during bacterial life).

Endotoxins: Lipopolysaccharides found in the cell wall of Gram-negative bacteria, released upon lysis.

Enzyme Production

Bacteria produce enzymes that damage tissues and facilitate spread. Examples include hyaluronidase, fibrinolytic enzymes, collagenases, elastases, and proteolytic enzymes.

Intracellular Invasion

Some bacteria (e.g., Mycobacterium tuberculosis, Brucella abortus, Salmonella) invade and multiply within cells, evading host defenses.

Defense Against Bacteria

Innate Immunity

Includes physical barriers, chemical substances (e.g., lysozyme, complement), sentinel cells (macrophages, dendritic cells), and inflammation.

Acquired Immunity

Macrophages and dendritic cells present bacterial antigens to T helper cells, which activate B cells to produce antibodies. Antibodies neutralize toxins, opsonize bacteria, and activate complement. Cellular immunity involves cytotoxic T cells.

Bacteria have evolved mechanisms to evade host defenses, such as resistance to lysosomal enzymes, inhibition of phagolysosome maturation, and antigenic variation.