Microbiology · MU Sofia

99. Family Poxviridae – Variola Virus (Smallpox Virus)

Covers the variola virus that causes smallpox, starting with its general features as a large, brick-shaped DNA virus that replicates in the cytoplasm, then its structure, the two infectious forms (IMV and EEV), and the stages of pathogenesis. It goes on to the clinical course and rash evolution, complications and mortality, diagnosis including the differential from varicella, and prevention through vaccinia vaccination and eradication. It ends with the virus's immune evasion strategies.

Inside: 8 sections · 4 labelled pictures · 15 flashcards · 2 min

Topic 99 of 113 in the MU Sofia syllabus for Microbiology (Medicine, Year 3). The free AceMed note covers it in 8 sections, about 298 words (2 min of reading), with 15 flashcards.

In this note

  1. Family Poxviridae – Variola Virus (Smallpox Virus)
  2. I. General Characteristics
  3. II. Structure and Replication
  4. III. Pathogenesis
  5. IV. Clinical Features – Smallpox (Variola major)
  6. V. Diagnosis
  7. VI. Prevention and Eradication
  8. VII. Immune Evasion

I. General Characteristics

  • Family: Poxviridae | Genus: Orthopoxvirus
  • Variola virus is the causative agent of smallpox, an eradicated but historically devastating disease.
  • Large, brick-shaped, enveloped DNA virus (largest known virus infecting humans).
  • Genome: Linear double-stranded DNA, with terminal hairpin loops.
  • Replicates in the cytoplasm (unique among DNA viruses) using its own transcription and replication machinery.

II. Structure and Replication

  • Viral core contains enzymes for transcription (DNA-dependent RNA polymerase, capping, and poly-A enzymes).
  • Entry via membrane fusion or endocytosis → early transcription and protein synthesis.
  • DNA replication occurs in “viral factories” (cytoplasmic inclusions).
  • Produces two infectious forms:
  • Intracellular mature virus (IMV) – stable, responsible for host-to-host spread.
  • Extracellular enveloped virus (EEV) – responsible for cell-to-cell spread.

III. Pathogenesis

  • Entry through respiratory tract or oropharynx → virus multiplies in lymphoid tissue → primary viremia.
  • Spread to internal organs → secondary viremia seeds the skin → clinical rash.
  • Causes extensive cytopathic effects, leading to tissue necrosis and characteristic scarring.
  • Highly contagious; transmission via respiratory droplets or fomites.

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