Herpes Simplex Virus (HSV) is 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]
Possibly may cause dry socket, auto-immunity, ...
 

Ocular
 HSV, a neurotropic virus, has been considered the major cause of infectious corneal blindness in the world. Due to treatment and hygiene the advanced World does not experience a large amount of cases, so may not be as apparent, as in the developing World. [45] [61]   In order to understand the implications, this leading coronal infectious virus causes an estimated >1.5 million cases of blindness per yr. [44] In the case of eye infection, the HSV travels from the nerve termini in the cornea along the trigeminal nerve to the trigeminal ganglia in the brain (Axonal_Transport). [45] [61] During reactivation, the HSV travels in the anterograde direction back to the eye to cause recurrent corneal disease which can lead to scaring and loss of sight. [61] In HSV-1, both Th1 and Th2 responses are implicated in the 
development of Herpes Stromal Keratitis (HSK). HSK is the major cause of ocular diseases in developing countries, ranging in severity from blepharitis, conjuctivitis and dendritic keratitis to disciform stromal edema and necrotizing stromal keratitis. [75] HSK is defined by the presence of polymorphonuclear and mononuclear cells with neutrophils being the most abundant infiltrating cells. These cell types may be involved in the IR in concordance with CD4+ T-cells. [75](IR)
 

Epideomology of HSV related to Ocular Herpes Infection:
 

Primary Infection Recurrence
Highest risk of primary infection
            from age 6 mo. to 5 -10 yrs
                    70% kids infected by age 5 yrs
                    90% of these are subclinical
                    70% immune to HSV by age 15-25 yrs
                    90% immune to HSV by age 60 yrs
 occurs in 25% of HSV infections
                 33% recurs once or more per yr
                 67% recurs once or more per 2 yrs
                 after 1st recurrence: 50% risk of recurrence
                 after 2nd recurrence: 75% risk of recurrence
                 after 3rd recurrence: 100% risk of recurrence
                 Males recur 50% more than females
                                                                                                                                                              [44]
Factors Initiating Recurrence:
 
            Sunlight
            Mild trauma
            Extreme heat or cold
            Fever
            Steroids (topical or systemic)
            Infectious disease (systemic or  ocular 
            Poor general health
            Surgery
            Epilation
            Immunosuppressive agents
            Menstruation
            Psychiatric disturbances
            Climate may be a factor
                                                                                                                                      [44]
Encephalitis
HSV infection of the central nervous system is a significant cause of morbidity and often mortality following encephalitis herpetica. Meningismus occurs in approximately 10%-15% of patients with primary genital HSV infections. Rarely, recurrent meningitis may be seen with recurrent genital herpes. [77] Virus can spread to the brain during primary or recurrent HSV infection The temporal lobes are principally involved. [79]


 

Dry socket
A possible association between reactivation of HSV-1 after extraction of lower third molars may be a cause of dry socket (DS). Higher prevalences of DS were associated with increased levels of HSV-1 antibodies, against gB, gC, gD, ICP4 and ICP6, after tooth extraction. In these studies there was increased incidence of HSV-1 reactivation when the root apex was in closer proximity to the mandibular canal. [76]

Auto Immunity

 To add to its repertoire of ill affects, HSV has been implicated in Autoimmune hepatitis. As in most autoimmune diseases, the etiology is unknown. Autoimmune hepatitis is characterized by hypergammaglobulinemia, female predominance, auto-antibodies and a good response to immunosuppression (based on specific autoantibodies and clinical characteristics).   The association of autoimmune hepatitis with a viral etiology is most prominent in autoimmune hepatitis type 2 which is characterized by liver/kidney microsomal (LKM-1) autoantibodies against cytochrome P-450 II D6. Depending on the geographical origin of the patients, which allows for several subgroups to be distinguished, a specific proportion of patients with autoimmune hepatitis type 2 is associated with hepatitis C virus infection, however, the HCV-negative population of patients with autoimmune hepatitis type 2 seems to have a relation with herpes simplex virus (HSV-1) infection. Since the B-cell epitope of cytochrome P-450 II D6, the major LKM-1 antigen, shares sequence homology with the IE-175 protein of HSV-1. The HCV-negative population of autoimmune hepatitis type 2, HLA-DR3 and C4-AQ0 alleles are significantly increased. [46] To associate, in the Immune_responsesection it was found that HLA-DR is a major (MHC) class II antigens associated with the CD4+ 
Immune_response. [16]

      Epidemiology / Pathogenesis / Mode_of_Infection / Immune_Response / Immune_Evasion /
       Pathologies / Treatment / Genetics / Vaccines / Photos / References / Links / HSV Home