Viral Pathogenesis and Immunity Quiz

Viral Pathogenesis

• Viruses enter the body by inhalation, ingestion, contact (urogenital system), skin (injections, blood transfusion), insect or animal bites.
• Viruses replicate at the primary site of entry; some cause local infections, others spread to distant organs via the blood (viremia) or other means (e.g., nerves), resulting in systemic or deep viral infections.

Differences Between Local and Systemic Viral Infections

• Local Infections: Example: common cold (rhinovirus). Pathogenesis is at the portal of entry, incubation period is relatively short, viremia is absent, immunity is usually short, and secretory IgA plays a significant role.
• Systemic Infections: Example: Measles. Pathogenesis is at distant sites, incubation period is relatively long, viremia is present, immunity is usually long-lasting, and secretory IgA plays a less significant role.

Immunity to Viruses

• Innate Immunity (NK cells): Cytotoxic killing of virally infected cells occurs early in the infection process.
• Type I Interferon: Virally infected cells produce IFN-α and IFN-β, inhibiting viral replication, inducing an antiviral state, activating NK cells, and increasing MHC I expression for improved viral peptide presentation.

B-Specific Immunity (Humoral Response)

• Antibodies: Crucial for defense before and after viral entry.
• Antibody Functions: Neutralizing antibodies prevent viral attachment and entry, opsonizing antibodies enhance phagocytosis, and complement activation enhances phagocytosis.
• Secretory IgA: Important for neutralizing viruses entering the mucosa, while circulating IgM and IgG defend against viruses circulating in the bloodstream before reaching their target cells.

B-Specific Immunity (T Cell Response)

• Cytotoxic T Cells (Tc Cells): The primary mechanism of specific immunity against established viral infections; they kill infected cells.
• Helper T Cells (Th Cells): Support the immune response by releasing cytokines. Th1 cytokines, especially IL-2 and IFN-γ, are crucial for Tc cell proliferation, activation, and NK cell activation.

Fate of Viral Infections

• Inapparent/Subclinical: Infection with no noticeable signs or symptoms.
• Apparent (Disease): Infection with clinical signs and symptoms (local or systemic).
• Persistent/Chronic: Virus continuously present, often with minimal clinical symptoms (e.g., chronic hepatitis B).
• Latent: Virus persists in a dormant form, intermittently flaring up to produce disease (e.g., herpes viruses).
• Slow Virus Infections: Long incubation periods (months or years) caused by conventional viruses (e.g., variant measles viruses causing subacute sclerosing panencephalitis (SSPE)) or unconventional agents (prions).

Viral Zoonosis

• Viral transmission from animals to humans. Examples include rabies, influenza A viruses, and various viral hemorrhagic fevers (yellow fever, dengue fever, Rift Valley fever, Ebola and Marburg viruses).

Classification of Viruses

• A (Symptomatology): Old classification based on the diseases produced (tropism - e.g., neurotropic viruses, enteroviruses).
• B (Families, Genera, Species): Classification based on nucleic acid type (DNA or RNA), virus size, symmetry, presence/absence of envelope, and replication strategy. This is a more modern and structured approach.
• Baltimore Classification Scheme: A system used to organize viruses based on their genome structure and the method they use for mRNA production.

Diagnosis of Viral Infections

• Direct Methods: Direct detection of viruses or their components (e.g., using PCR or antigen detection). Isolation of viruses.
• Indirect Methods: Using serological tests (measuring antibodies) or skin tests to diagnose viral infection.

Test your knowledge on the pathogenesis of viral infections and the differences between local and systemic infections. This quiz covers key concepts including routes of entry, the role of immunity, and the dynamics of viral replication. Understand the mechanisms underlying viral infections and the body's immune response.