Microbiology · MU Sofia

97. Family Herpesviridae – Herpes Simplex Virus (HSV-1, HSV-2) & Varicella Zoster Virus (VZV)

Covers the general features of the Herpesviridae family, then HSV-1 and HSV-2 in terms of types, pathogenesis, clinical disease forms, diagnosis and antiviral treatment. Goes on to varicella-zoster virus, covering chickenpox and shingles, their clinical course, diagnosis, treatment and vaccination. Ends with a table comparing HSV and VZV on disease, latency, rash pattern and vaccines.

Inside: 5 sections · 7 labelled pictures · 3 tables · 14 flashcards · 4 min

Topic 97 of 113 in the MU Sofia syllabus for Microbiology (Dental Medicine, Year 2). The free AceMed note covers it in 5 sections, about 341 words (4 min of reading), with 14 flashcards.

In this note

  1. Family Herpesviridae – Herpes Simplex Virus (HSV-1, HSV-2) & Varicella Zoster Virus (VZV)
  2. I. Family Herpesviridae – General Features
  3. II. Herpes Simplex Virus (HSV)
  4. III. Varicella Zoster Virus (VZV)
  5. Comparison Table: HSV vs VZV

I. Family Herpesviridae – General Features

  • Large, enveloped viruses, with double-stranded linear DNA genome.
  • Icosahedral capsid, surrounded by tegument proteins and lipid envelope with glycoproteins.
  • Replicate in the nucleus.
  • Unique property: ability to establish latency in host cells and reactivate under stress or immunosuppression.
  • Human herpesviruses: HSV-1, HSV-2, VZV, CMV, EBV, HHV-6, HHV-7, HHV-8.

II. Herpes Simplex Virus (HSV)

A. Types

  • HSV-1: primarily oral, facial infections.
  • HSV-2: primarily genital infections.

B. Pathogenesis

  • Entry via mucosa or abraded skin → local replication.
  • Infects sensory nerve endings → retrograde transport to sensory ganglia (trigeminal for HSV-1, sacral for HSV-2).
  • Latent infection in ganglia → reactivated by stress, fever, UV light, immunosuppression.

C. Clinical Features

D. Diagnosis

  • Tzanck smear: multinucleated giant cells, Cowdry type A inclusions.
  • PCR: preferred (especially CSF for encephalitis).
  • Direct fluorescent antibody, viral culture.
  • Serology: IgG for past infection.

E. Treatment

  • Acyclovir, valacyclovir, famciclovir (inhibit viral DNA polymerase).
  • Early initiation in encephalitis critical.
  • Lifelong latent infection persists.

III. Varicella Zoster Virus (VZV)

A. Overview

  • Also called HHV-3
  • Causes primary infection (chickenpox) and reactivation (shingles/Herpes zoster)

B. Pathogenesis

  • Entry via respiratory droplets → replication in nasopharynx and lymph nodes.
  • Viremia → disseminates to skin → chickenpox (varicella).
  • Virus becomes latent in dorsal root or cranial nerve ganglia.
  • Reactivation → travels down nerve → dermatomal rash (zoster).

C. Clinical Features

1. Varicella (Chickenpox)

  • Fever, malaise, vesicular rash: "dew drop on a rose petal" → macule → papule → vesicle → crust.
  • Rash appears in crops: lesions in different stages.
  • Complications: pneumonia, cerebellar ataxia, superinfection (S. aureus).

2. Herpes Zoster (Shingles)

  • Reactivation in elderly or immunocompromised.
  • Painful, unilateral vesicular rash in dermatomal distribution.
  • May lead to post-herpetic neuralgia.
  • Herpes zoster ophthalmicus if trigeminal (V1) involved → can threaten vision.

D. Diagnosis

  • Tzanck smear (shared with HSV): multinucleated giant cells.
  • PCR from lesion fluid = gold standard.
  • Direct fluorescent antibody.

E. Treatment

  • Acyclovir, valacyclovir, famciclovir (oral for zoster; IV in severe varicella).
  • Pain management for post-herpetic neuralgia.

F. Prevention

  • Live attenuated vaccine:
  • Varicella vaccine for children (12–15 months, booster at 4–6 years)
  • Zoster vaccine (recombinant, inactivated) for ≥50 yrs
  • VZIG (varicella-zoster immune globulin) for post-exposure in high-risk patients (e.g., pregnant, immunocompromised)

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