Herpes Simplex Virus

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Table of Contents

1. Definition

Herpes Simplex Virus (HSV) is a DNA virus from the herpesvirus family that causes recurrent infections, typically presenting as oral or genital sores, and establishes lifelong latency in nerve cells.

2. Taxonomy

  • Realm: Duplodnaviria
    • Kingdom: Heunggongvirae
      • Phylum: Peploviricota
        • Class: Herviviricetes
          • Order: Herpesvirales
            • Family: Herpesviridae
              • Subfamily: Alphaherpesvirinae
                • Genus: Simplexvirus
                  • Species:
                    • Human herpesvirus 1 (HSV-1)
                    • Human herpesvirus 2 (HSV-2)

3. Structure

The Herpes Simplex Virus (HSV) has a structure consisting of a central double-stranded DNA core surrounded by a nucleocapsid, which is encased in a tegument layer and an outer lipid envelope containing glycoproteins such as glycoprotein G (gG). These glycoproteins are crucial for viral entry into host cells and for distinguishing between HSV-1 and HSV-2 in serological analysis.

4. Pathogenesis

Herpes Simplex Virus (HSV) is a cytolytic virus that causes:

  1. Pathological cellular changes leading to cell damage.
  2. Localized inflammation in affected tissues.

Infections caused by HSV-1/HSV-2 are characterized by:

  • Blister formation on the skin or mucous membranes.
  • Primary or secondary lesions, often painful and recurring.

5. Progression of an infection

5.1. Primary Infection

Herpes Simplex Virus (HSV) spreads through direct contact with infected saliva, mucous membranes, or genital secretions.

  • HSV-1 is primarily transmitted via saliva (~80% of cases).
  • HSV-2 is mainly transmitted through sexual contact (~20% of cases).
    After entering the body, HSV infects epithelial cells and replicates, then spreads via nerves to sensory ganglia where it establishes latency.

5.2. Latency Phase

In this phase, the virus becomes dormant in sensory nerve ganglia (e.g., trigeminal ganglia for oral infections, sacral ganglia for genital infections).

  • No virus replication occurs during latency.
  • The viral genome remains in the host cells as a potential source of reactivation throughout life.

5.3. Reactivation

Reactivation occurs when the dormant virus is triggered by factors such as:

  • Stress or immunosuppression,
  • Fever, UV exposure, hormonal changes, or infections.
    The virus travels along the nerves to the skin or mucous membranes, causing lesions similar to the primary infection.

5.4. Recurrences (Endogenous Relapses)

During recurrence, the virus spreads directly from cell to cell, bypassing antibody defenses. This explains why outbreaks can happen despite an immune response.

  • Symptoms may include tingling sensations, blisters, or sores, typically in the same area as the initial infection.

6. Clinical Manifestations

HSV-1

  • Oral herpes (cold sores)
  • Herpes labialis
  • Herpetic gingivostomatitis
  • Herpetic keratitis
  • Herpetic whitlow
  • Encephalitis
  • Eczema herpeticum
  • Herpetic esophagitis
  • Herpetic pharyngitis

HSV-2

  • Genital herpes
  • Neonatal herpes
  • Herpetic whitlow
  • Aseptic meningitis
  • Proctitis
  • Perianal ulcers
  • Disseminated herpes in immunocompromised patients

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Last edit:
2025-01-12 12:51:10
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