Herpes simplex viruses are everywhere. They are host-adapted pathogens that result in various disease states. The virus has types: HSV-1 (herpes simplex virus type 1) and HSV-2 (herpes simplex virus type 2). Both viruses are closely related, yet vary in epidemiology. Traditionally, HSV-1 is associated with or facial disease, while herpes simplex 2 is associated with disease in the genitalia; but, lesion location isn’t essentially indicative of the viral type.
Up to 80% of herpes infections do not present with symptoms (asymptomatic). Symptomatic infections can be categorized by significant recurrence and morbidity. In immunocompromised hosts, the infections can result in life-threatening complications.
The prevalence of herpes infection globally has risen over the past several decades, which makes it a huge public health concern. Fast recognition of herpes infection and early therapy initiation are of highest importance in the disease’s management.
Pathophysiology: Herpes simplex 2
HSV (both type 1 and type 2) belongs to Herpesviridae (herpesvirus family) and the Alphaherpesvirinae subfamily. It’s a double-stranded DNA virus which is characterized by the distinctive biological properties such as:
Neurovirulence (the ability to invade and reproduce in the nervous system)
Latency (the latent infection’s establishment and maintenance in nerve cell ganglia near the site of infection): In orofacial herpes infections, trigeminal ganglia are most frequently involved, while, the sacral ganglia are involved in genital herpes infection.
Reactivation: The reactivation and duplication of latent herpes, always in the site provided by the ganglia wherein latency was established, can be triggered by different stimuli (e.g., trauma, fever, emotional stress, menstruation, sunlight), causing covert or overt recurring infection and shedding of the virus. In immunocompetent people who are at the same risk of getting HSV-1 and HSV-2 genitally and orally, HSV-1 reactivates more often in the oral area rather than the genital. Similarly, HSV-2 reactivates 8 to 10 times more frequently in the genital area than in the orolabia. Reactivation is more severe and common in immunocompromised people.
Dissemination of HSV infection can take place in individuals with impaired T-cell immunity, like in organ transplant recipients as well as in people with AIDS.
HSV is globally distributed. Humans are the mere natural reservoirs, and vectors are not involved in the spread. Endemicity is simply maintained in the majority of human communities due to latent infection, episodic reactivation, and asymptomatic virus shedding.
HSV is spread by direct skin-to-skin contact, and infection takes place via the virus’ inoculation into prone mucosal surfaces (e.g., conjunctiva, cervix, oropharynx) or through tiny skin cracks. The virus is readily idled at room temperature as well as by drying; therefore, fomitic and aerosol spread are uncommon.
Frequency of Herpes in the United States
HSV is global, and most people show a few evidence of herpes infection. HSV-1 is typically acquired during childhood by direct contact with virus-containing oral secretions. The HSV-2 presence can be utilized as an indirect sexual activity measure in a few cases. Seroprevalence rates don’t reflect how many of the infected person has or will have symptomatic herpes episodic recurrence.
Seroprevalence: HSV-1 antibodies increase with age beginning in childhood and relate with race, cultural group, and socioeconomic status. By age 30, 80% of people in low socioeconomic status and 50% in higher socioeconomic status are positive. Antibodies to HSV-2 start to develop at puberty, linking with the sexual activity degree. The lifetime seroprevalence can be 20% to 80%.