Herpes simplex Virus

Herpes simplex Virus (HSV)
There are two distinct herpes simplex viruses: type 1 and type 2 (HSV-1, HSV-2) Their genomes are similar in organization. However, they can be distinguished by sequence analysis or by restriction enzyme analysis of viral DNA. The two viruses cross-react serologically, but some unique proteins exist for each type.
Table 3. Comparison of Herpes Simplex Virus Type 1 and Type 2.


Characteristics HSV-1 HSV-2
Biochemical    
  Viral DNA base composition (G + C) 67% 69%
  Buoyant density of DNA (g/cm3)
  1.726 1.728
  Buoyant density of virions (g/cm3)
  1.271 1.267
  Homology between viral DNAs ~50% ~50%
Biologic    
  Animal vectors or reservoirs None None
  Site of latency Trigeminal ganglia Sacral ganglia
Epidemiologic    
  Age of primary infection Young children Young adults
  Transmission Contact (often saliva) Sexual
Clinical    
  Primary infection:    
    Gingivostomatitis + -
    Pharyngotonsillitis + -
    Keratoconjunctivitis + -
    Neonatal infections ± +
  Recurrent infection:    
    Cold sores, fever blisters + -
    Keratitis + -
  Primary or recurrent infection:    
    Cutaneous herpes    
       Skin above the waist + ±
       Skin below the waist ± +
       Hands or arms + +
    Herpetic whitlow + +
    Eczema herpeticum + -
    Genital herpes ± +
    Herpes encephalitis + -
    Herpes meningitis ± +

Diagnosis of HSV Infections
- Cytopathology
A rapid cytologic method is to stain scrapings obtained from the base of a vesicle (eg, with Giemsa s stain); the presence of multinucleated giant cells indicates that herpesvirus (HSV-1 or HSV-2) and contain Cow dry type An inclusion bodies Formation , In the course of viral multiplication within cells, virus-specific structures called inclusion bodies may be produced. They become far larger than the individual virus particle and often have an affinity for acid dyes (eg, eosin). They may be situated in the nucleus (herpesvirus), in the cytoplasm (poxvirus), or in both (measles virus). In many viral infections, the inclusion bodies are the site of development of the virions (the viral factories). Variations in the appearance of inclusion material depend largely upon the tissue fixative used. The presence of inclusion bodies may be of considerable diagnostic aid. The intracytoplasmic inclusion in nerve cells—the Negri body—is pathognomonic for rabies.
- Quantitation of Viruses
The cells can also be stained with specific antibodies in an immunofluorescence test and it is also possible to detect viral DNA by in situ hybridization. Type-specific antibodies can distinguish between HSV-1 and HSV-2.
- Polymerase Chain Reaction (PCR)
PCR assays can be used to detect virus and are sensitive and specific. PCR amplification of viral DNA .
- Serology
Antibodies appear in 4–7 days after infection and reach a peak in 2–4 weeks. They persist with minor fluctuations for the life of the host.
Treatment, Prevention, & Control
Several antiviral drugs have proved effective against HSV infections, including acyclovir, valacyclovir, and vidarabine. Acyclovir is currently the standard therapy. All are inhibitors of viral DNA synthesis. Acyclovir, a nucleoside analog.
Vaccine
Recombinant HSV-2 glycoprotein ( that found in viral envelope ) can be used .