The herpes simplex virus (HSV) was isolated in 1938 by Dodd and others from the mouths of children exhibiting acute symptoms. [3] The HSV has many routes of infection, it is transmitted orally, genitally, oral genitally and by autoinoculation. There are multiple sites of herpes infection related to the body and depending on the strain encountered. Both HSV-1 and HSV-2 may cause any of the related pathologies to be discussed but the difference among them resides in their exact mode of infection. The similarities which are shared among these viruses allows them to exhibit similar clinical manifestations but both strains do have increased prevalence for specific areas of the body. Typically, HSV-1 is correlated with oral and ocular infections while HSV-2 is correlated with genital infections. However, both HSV-1 and HSV-2 are known to cause genital herpes, oral-facial infections (gingivostomatitis, labialis, pharyngitis) cutaneous infections ( whitlow, herpes gladatorlum) ocular infections, neonatal herpes, herpes encephalitis, disseminated infection and erythema multiform. [66](PHOTOS)

        At times, the lesions of primary herpes simplex are referred to as ìfever blisters,î ìcold sores,î and/or ìsun blisters;î when referring to oral herpes. [3] In reference to these lesions, HSV not only causes primary pathology but is associated with recurrent pathology which is usually less severe as a consequence of the Immune response (IR). These HSV lesions are associated with HSV-1 and HSV-2 clinical symptoms; which range from a variety of degrees of burning (itchy) sensation, sore throat, sore mouth, fever, malaise, sore genitals, tingling, lethargy alternating with irritability, flu-like symptoms, and general aches with pains - especially down the back, and the back of the legs when associated with genital herpes. [3][48] The fever usually persists for about 1 week but may continue into the second week.  The mucous membrane is extremely painful, apthus ulcers occur throughout the oral cavity and oral pharynx for Oral Herpes and throughout the genital areas for Genital Herpes. These genital lesions may be found on the vulva, vagina, cervix, urethra, and/or perineum in the female and on the penis and/or rectum in the male. [48] In oral herpes infections the gingiva becomes inflamed and swollen and bleeds readily: while the cervical lymph nodes become enlarged and tender. [3]  The disease lesions localize anteriorally, and generally involves the lips, gingiva, anterior tongue and hard palate. These characteristic vesicles increase risk of secondary infection such as autoinoculation as seen with Herpes Whitlow, Ocular Herpes, cutaneous lesions (neck, foot, Ear), or most commonly oral and genital transfer.

 

HSV Whitlow [37]

HSV-1 neck [38]

Foot  [39]

HSV-1 Ear [38]

 

        During primary infection, Type A inclusion bodies (Lipschutz bodies) can be demonstrated in the nucleus of cells from a herpatic ulcer in active herpes simplex infection. [3] Also, multi-nucleated giant cells are found in the biopsies of the infected area, and each nucleus contains an inclusion body. There is marked intracellular and extracellular edema which is a component of the Immune response. [3] A key factor involved in the intracellular edema is the keratinocytes of the middle and basal layers which are infected and undergo cytolysis, resulting in the formation of an intraepidermal lesion, called the papule stage, which rapidly evolves into an epidermal lesion, filled with yellowish fluid, causing displacement of chromatin. [5] These lesions usually persists for 3-4 days.
 
 

Herpes Labialis

At this stage of the pathogenesis is when HSV virions are in high titers in the vesicular fluid and very contagious. [3] The papule then ruptures to form an ulcer surrounded by an erythematous border and eventually a crust of purulent exudate. [4][3]  The exudates are composed of fibrin and polymorphonuclear leukocytes. [5] The ulcers heal in 7-10 days without scars.

        Following initial infection of cells , the virus replicates at these peripheral sites and then gains access to the distal axonal terminae of sensory nerves and travels by retrograde axonal transport to neuronal cell bodies in sensory ganglia, usually the trigeminal and sacral ganglia, where further replication or latency can occur. [19][24] In some cases the infiltrating virus can infect the spinal cord from the dorsal root ganglia. [24] At the earliest detectable clinical stage of recurrent herpetic vesicle, there is already an intense inflammatory response with a marked dermal mononuclear infiltrate consisting predominantly of macrophages and CD4 T lymphocytes (IR). [4] Most frequently recurrences occur at the primary site of infection. Recurrences can be triggered by numerous environmental stimuli including a common cold, fever, severe sunburn, physical fatigue, emotional disturbance, trauma, gastrointestinal disturbances, menstruation, pregnancy, debilitating illnesses, or food allergy. [3][5]
 

Recurrences-Genital

             Genital herpes usually consists of breakouts or episodes, interspersed with symptom free periods. The first episode is usually the most severe, and can start with tingling, itching, or burning in or around the genitals, and this may be followed by pain on passing urine and an outbreak of sores or blisters on or around the genitals. [48]
 
 
 

Psychological Impact:
 
 

 Major consequences

  ø  Pain and discomfort associated with lesions
  ø  Systemic complications such as urinary retention or aseptic meningitis
  ø  Rare complication of disseminated infection seen almost exclusively in the immuno-compromised host.
  ø  Rare complication of prenatal transmission resulting in potentially life threatening neonatal infection
  ø  Increased risk of Acquiring HIV infection if exposed.
  ø  Neurological damage: meningitis, Ocular and Latently Infected neurons
                                                                                                                                        [24][77]
 

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