Viral Diseases – Infection Types, Immune Response, Transmission & Control

Housekeeping / Session Logistics

  • Session ran without a break; target finish time 09{:}50
  • Students encouraged to use chat for questions; host periodically checked and adjusted entry permissions
  • Next two teaching blocks:
    • Tutorials on infection categories next week
    • Full Immune-System module in two weeks (will revisit many of today’s diagrams)

Recap of Previous Lecture (Structure & Classification)

  • Viruses are obligate intracellular parasites; replicate only by hijacking host cell machinery
  • Basic components: nucleic acid core, capsid, (sometimes) lipid envelope with glycoprotein spikes
  • Enveloped vs. naked particles ⇒ impacts survival on surfaces & susceptibility to disinfectants

How Viruses Cause Disease

  • Enter host cell → shut down normal function or induce lysis ⇒ cell death
  • Damage scale (thousands → millions of cells) produces signs & symptoms
  • Symptom categories correlate with infection style (acute, persistent, latent, etc.)

Definitions of Infection Types

  • Acute (lytic)
    • Rapid onset, short duration, self-limiting
    • Canonical example: common cold; runny nose, sore throat resolve in ≈ 1 week
  • Subclinical
    • Few or vague symptoms ("off-colour", mild fever, small lymph-node swellings)
    • Patient rarely seeks care; diagnosis often retrospective via antibodies
    • Shares overlap with "asymptomatic" but patient may feel something
  • Persistent categories
    1. Latent – dormant inside cells, flare when immunity drops
    2. Slow – continuous pathological process, new neuro/organ signs later
    3. Chronic (carrier) – constant low-level viraemia/shedding without symptoms
    4. Oncogenic transformation – viral genes drive uncontrolled mitosis

Antibody Primer

  • Antibody (Ig) schematic: Y-shaped; binding sites at arm tips engage antigenic epitopes
  • Titer (TITER) = concentration of specific antibodies in serum (clinical immunity gauge)

Subclinical-Example Focus: Rubella & CMV in Pregnancy

  • Rubella (German measles) usually mild/subclinical in adults but teratogenic in 1st trimester
  • CMV behaves similarly; no licensed vaccine yet
  • Diagnostic principle: plot IgM vs. IgG over time

    \text{Exposure}\;\xrightarrow{≈7\text{ days}}\uparrow IgM\; (peaks≈3 wks)\;\rightarrow0,\quad
    \uparrow IgG\; \text{persists months–life}
  • Detection of high maternal IgM or rising IgG during pregnancy ⇒ timing of infection deduced

Latent Infections

  • Hallmark: Primary acute episode, long dormancy, episodic reactivation
  • Viral genome hides mainly in neurons (immune-privileged)
  • Reactivation triggers: stress, UV exposure, concurrent illness, age-related immunity drop
  • Key examples & nursing implications:
    • HSV-1 → recurrent cold sores (perioral vesicles)
    • VZV (Varicella-Zoster) → chickenpox in childhood, shingles in elders or hospitalised patients
    • Dermatomal blistering "stripe"; risk of post-herpetic neuralgia & ophthalmic involvement
    • EBV latency in B-cells; possible later malignancies
    • HIV persists within T-cells & macrophages

Slow Viral Infections

  • Gradual pathogenic build-up; new symptoms differ from acute phase
  • Classic: Subacute Sclerosing Panencephalitis (SSPE)
    • Onset 6{-}8 yrs post-measles
    • Progressive neurodegeneration → vegetative state → fatal (~2 yrs course)
    • Emphasises measles vaccination value

Chronic / Carrier State

  • Continuous low-grade replication; virus detectable in blood/faeces
  • Patient asymptomatic yet infectious
  • Hepatitis B paradigm:
    • Acute episode ± jaundice
    • Transition probability: 90\% if infected in infancy, 10\% in adults
    • Chronic carriers risk cirrhosis & hepatocellular carcinoma

Viral Oncogenesis

  • Viral insertion/mutation of host DNA → dysregulated cell division (neoplasia → carcinoma)
  • Confirmed links:
    • HTLV-1 → Adult T-cell leukaemia
    • HPV (types 16/18 etc.) → cervical & anogenital cancers (basis for HPV vaccine)
    • HHV-8 → Kaposi’s sarcoma (noted in AIDS)
    • HBV/HCV → hepatocellular carcinoma
    • EBV → Burkitt lymphoma, nasopharyngeal carcinoma

Innate & Adaptive Immune Response to Viruses

  • Initial viraemia spreads via blood & lymph
  • Infected cells secrete interferon → nearby cells heighten antiviral state + recruit immunity
  • Cell-mediated (T-cell) response crucial because virus is intracellular
    • Cytotoxic T-cells (CTLs) destroy infected host cells
  • Humoral (B-cell) arm produces neutralising antibodies for extracellular virions
  • Outcome: clearance + formation of memory T & B cells (future protection)
  • Clinical correlate: Fever, myalgia, lymphadenopathy driven by cytokines, not virus itself

Supportive Care & Pharmacotherapy

  • Rest, hydration, balanced nutrition; minimise physical stress to optimise immunity
  • Paracetamol (acetaminophen) ↓ pain & fever but may prolong viraemia; benefits often outweigh
  • Antivirals limited because targeting replication risks damaging host DNA/RNA
    • Nucleoside analogues (e.g., AZT = Zidovudine for HIV; Acyclovir for HSV/VZV)
    • Reverse-transcriptase / protease / integrase inhibitors in HIV regimen
    • Interferon-α once trialled broadly; modest efficacy, notable side-effects

Immune-Evasion Strategies

  • Shielding inside host cells; “stealth” if infected cell lacks distress signals
  • Antigenic drift/shift – e.g., Influenza alters surface hemagglutinin/neuraminidase yearly
  • Latency – viral quiescence (herpes family)
  • Direct immunosuppression – HIV destroys CD4^+ T-cells

Shedding, Survival & Epidemics

  • Peak infectivity usually during prodrome – prior to obvious illness (drives outbreaks)
  • Environmental survival varies:
    • Enveloped virions short-lived; naked capsids hardier
    • Temperature, UV light, humidity all influential
    • Selected data:
    • RSV: 6 h on countertops; 40 min on cloth; 20 min on skin
    • HBV: up to 7 days dried blood
    • HEV: months
    • Coronaviruses remain viable ≤9 days on surfaces at room-T; rapid loss above 27^{\circ}\text{C} or with 70\% ethanol (≤1 min)

Transmission Routes & Examples

  1. Airborne / Aerosol – influenza, SARS-CoV-2; hardest to control
  2. Fecal–Oral – hepatitis A, rotavirus, norovirus, enteroviruses (e.g., polio)
    • Rotavirus major cause of paediatric dehydration; vaccine now available
    • Norovirus: prolonged shedding post-symptoms; repeated infections common
  3. Body Fluids & Direct Contact – blood, semen, saliva, breast milk
    • HBV, HCV, HIV, HSV, CMV; transplant transmission
  4. Vector-Borne (Arboviruses) – mosquitoes & ticks
    • Australian examples: Ross River, Murray Valley encephalitis, Barmah Forest, dengue
    • Outbreak requires virus source + competent mosquito species + suitable climate
  5. Vertical (Mother → Child)
    • Placental, perinatal, or breastfeeding transfer
    • High maternal–infant HBV transmission (≈90\%) without prophylaxis
    • Management: maternal antivirals/IgG, neonatal vaccination, possible C-section for active genital HSV

Teratogenic Viruses

  • Rubella & CMV cause congenital heart, CNS, ocular defects
  • CMV = leading viral cause of congenital anomalies in Australia (no vaccine)

Inactivation & Environmental Control

  • Physical: heat, UV light, drying
  • Chemical: alcohols, bleach, strong alkalis → disrupt envelopes/capsids
  • Note: some agents (e.g., chlorhexidine) poor against certain viruses
  • Hospital protocols: surface cleaning, hand hygiene, PPE, vector eradication

Laboratory Diagnosis

  1. Molecular – PCR/RT-PCR amplifies viral RNA/DNA (gold standard for SARS-CoV-2)
  2. Antigen detection – immunofluorescence, ELISA, rapid lateral-flow tests
  3. Serology – IgM (recent) vs IgG (past) titres; useful for prenatal screening
  4. Culture – growth in cell lines; expensive, slow, not always feasible

Summary of Antiviral Agents (conceptual)

  • Target unique viral enzymes or replication steps to spare host
  • Limited spectrum & potential toxicity
  • Main classes/exemplars:
    • Nucleoside analogues: Acyclovir (HSV/VZV), Ganciclovir (CMV), Ribavirin (RSV, HCV)
    • Reverse-Transcriptase Inhibitors: AZT, Tenofovir
    • Protease/Integrase Inhibitors: HIV therapy
    • Neuraminidase Inhibitors: Oseltamivir for influenza
    • Interferons: adjunct for HBV/HCV, variable success

Nursing & Public-Health Points

  • Hospitalised and elderly patients are immunocompromised ⇒ watch for latent reactivations (e.g., shingles)
  • Enforce standard & transmission-based precautions (airborne, droplet, contact)
  • Educate patients: hand hygiene, vaccination schedules (MMR, HPV, HBV, Rotavirus, Influenza)
  • Outbreak control: early identification, isolation, environmental decontamination, vector management
  • Supportive care optimisation: monitor hydration, nutrition, analgesia, antipyretic balance
  • Tutorial next week: case studies on infection categories & antibody graphs
  • Immune System block (week after): deeper dive into cytokines, T-cell activation pathways, memory formation
  • Pharmacology (Year 2): detailed mechanisms & side-effects of antiviral drug classes
  • Epidemiology unit: modelling prodromal shedding & herd immunity thresholds R_0