In very rare cases HSV- 1 can spread spontaneously to the brain, causing herpes encephalitis, a dangerous infection that can lead to death. Like HSV-1, type 2 is usually mild-so mild that two- thirds of infected people don’t even know they have it. For example, most people infected with HSV-1 in the genital area have few, if any, outbreaks after the initial episode, far fewer than is typical with either oral HSV-1 or genital HSV-2. HSV-1 can cause either oral or genital infections, whereas HSV-2 causes predominantly genital herpes. Therefore, HSV-2 seroprevalence can be used as a marker of genital herpes. Disease can be monophasic, recurrent or chronic. Encephalitis is the most serious neurological complication caused by HSV-1. Virus replicates at the portal of entry, usually oral or genital mucosal tissue, leading to infection of sensory nerve endings. Whereas HSV-1 latency is found only in cranial nerve ganglia, HSV-2 becomes latent in lumbrosacral ganglia.
Symptomatic disease is characterized by fever to 104oF, oral lesions, sore throat, fetor oris, anorexia, cervical adenopathy, and mucosal edema. Primary genital herpes caused by HSV-1 are more likely to be symptomatic than are those caused by HSV-2 (130). Herpetic whitlow of a distal phalanx can arise from either HSV-1 or HSV-2. Animal studies suggest that activated macrophages, interferons, and, to a lesser extent, natural killer cells are important in limiting initial HSV infection, whereas humoral immunity and cell-mediated immunity are important in controlling both initial and recurrent infections. HSV-1 is the predominant type implicated in oral lesions, HSV-2 is the predominant type implicated in genital lesions. The virus lies latent and in times of stress/illness they can reactivate and cause cold sores. Also, canker sores have nothing to do with herpes, and are inside the mouth, whereas cold sores are herpetic lesions typically on the corners of the mouth/lips. Members of the group can cause productive lytic infections, in which infectious virus is produced and cells are killed, or nonproductive lytic infections, in which viral DNA persists but complete replication does not occur and cells survive. HSV-1 primary infection occurs mainly in childhood, whereas HSV-2 infection occurs predominantly in sexually active adolescents and young adults. HSV-1 is usually transmitted by an oral route and HSV-2 by a genital route. 7,8 Moreover, patients dually infected with HSV-1 and HSV-2 have fewer recurrences of genital herpes than those infected with HSV-2 alone.2 With either virus type, after a variable prodrome of tenderness, itching, or tingling, lesions develop on the penis, labia minora, labia majora, perineum, mons pubis, or buttocks.
The fact that diseases for which there are effective therapies that can be prevented by changing behavior are still rampant illustrates the complex nature of these diseases and the enormous challenges faced by the medical and public health communities in dealing with them. Herpes simplex virus (HSV) infections, syphilis, and chancroid account for almost all the STDs characterized by genital ulcers in the United States. HSV-2 infections are almost always sexually acquired, whereas HSV-1 infections may be caused by anogenital or orolabial infections. With recent data indicating a link between genital herpes and either strain, a re-evaluation of risk factors for HSV-1/HSV-2 infection and co-infection is needed. Whereas age, sex, race, and level of education independently predicted all three outcomes, lifetime sexual activity as well as use of tobacco products and recreational drugs mainly correlated with HSV-2 infection and HSV-1/HSV-2 co-infection. We specifically hypothesized that risk factors for one HSV strain will differ among those who are co-infected with the other HSV stain compared to those who are not. The symptoms of primary oral infection with HSV-1.
Sexually Transmitted Diseases
Since the type of herpes simplex virus (HSV) infection affects prognosis and subsequent counseling, type-specific testing to distinguish HSV-1 from HSV-2 is always recommended. Herpes simplex viruses (HSV-1, HSV-2; Herpesvirus hominis) produce a variety of infections involving mucocutaneous surfaces, the central nervous system (CNS), and on occasion visceral organs. Either restriction endonuclease analysis or sequencing of viral DNA can be used to distinguish between the two subtypes and among strains of each subtype. There is no cure for Herpes simplex virus infection, and there are currently no vaccines that would prevent the virus from infecting humans. These vaccines contain a harmless or weakened version of the disease-causing virus. Notably, HSV-1 has emerged as a predominant cause of genital disease in the developed world (Roberts et al.