There are two types of herpes simplex virus, type 1 (HSV-1) and type 2 (HSV-2). HSV-1 more commonly causes infections around the mouth while HSV-2 more commonly causes genital infections. They are transmitted by direct contact with body fluids or lesions of an infected individual. Transmission may still occur when symptoms are not present. Genital herpes is classified as a sexually transmitted infection. It may be spread to an infant during childbirth. After infection, the viruses are transported along sensory nerves to the nerve cell bodies, where they reside lifelong. Causes of recurrence may include: decreased immune function, stress, and sunlight exposure. Oral and genital herpes is usually diagnosed based on the presenting symptoms. The diagnosis may be confirmed by viral culture or detecting herpes DNA in fluid from blisters. Testing the blood for antibodies against the virus can confirm a previous infection but will be negative in new infections.
Cullins explains that the first, or initial, outbreak is usually the worst, and “over time when you have recurrent episodes, you may not have systemic symptoms” or frequent symptoms. But everyone’s body and immune system reacts to the virus differently; while some people may never have many outbreaks, other people may be more chronically symptomatic. The National Institutes of Health indicate that infrequent outbreaks, around one or two per year, are not uncommon.
HSV-2 is commonly referred to as genital herpes because it usually causes cold sores to erupt around the genitalia. In fact, genital herpes is the No. 1 cause of genital ulcers worldwide, according to the Centers for Disease Control and Prevention (CDC), and affects up to 1 in 3 adults (although most who are infected don’t even know it). (5) Both types of herpes viruses are highly contagious, and both can cause cold sores in either area of the body (or sometimes both).
There are two types of herpes simplex viruses (HSV), they are termed HSV-1 and HSV-2. These two viruses have distinctly different DNA, and both cause oral and genital lesions. However, HSV-1 causes about 80% of all oral lesions and only about 20% of genital lesions while HSV-2 causes the reverse (about 80% genital and 20% oral). Studies also suggest that in adolescents, up to 40% of genital herpes is caused by HSV-1 because of reported increased oral/genital contact (transmission by oral sex).
Until the 1980s serological tests for antibodies to HSV were rarely useful to diagnosis and not routinely used in clinical practice. The older IgM serologic assay could not differentiate between antibodies generated in response to HSV-1 or HSV-2 infection. However, a glycoprotein G-specific (IgG) HSV test introduced in the 1980s is more than 98% specific at discriminating HSV-1 from HSV-2.
If you have herpes, you should talk to your sex partner(s) and let him or her know that you do and the risk involved. Using condoms may help lower this risk but it will not get rid of the risk completely. Having sores or other symptoms of herpes can increase your risk of spreading the disease. Even if you do not have any symptoms, you can still infect your sex partners.
Only a health care provider can diagnose herpes by performing a physical exam and tests. A blood test can tell if you are infected with oral or genital herpes — even if you don't have symptoms. Health care providers can also confirm herpes infection by testing fluids taken from the sores. If you think you have herpes sores, get them checked out as soon as possible. Your local Planned Parenthood health center, many other health centers that test for sexually transmitted diseases, private health care providers, and health departments offer herpes tests and herpes treatments.
Following active infection, herpes viruses establish a latent infection in sensory and autonomic ganglia of the nervous system. The double-stranded DNA of the virus is incorporated into the cell physiology by infection of the nucleus of a nerve's cell body. HSV latency is static; no virus is produced; and is controlled by a number of viral genes, including latency-associated transcript.