Genital Herpes

I have infected 45 million Americans and will infect 1 million more Americans each year. Who am I?

Herpes, from the ancient Greek meaning to creep or crawl, is the name of a family of viruses of which herpes simplex virus 1 and herpes simplex virus 2 (HSV-1 and HSV-2) are the most serious human pathogens. HSV-1 is normally associated with orofacial infections and encephalitis, whereas HSV-2 usually causes genital infections and can be transmitted from infected mothers to neonates. Both viruses establish latent infections in sensory neurons and, upon reactivation, cause lesions at or near point of entry into the body.

While HSV-1 and HSV-2 are different viruses, under a microscope, HSV-1 and 2 are virtually identical, sharing approximately 50% of their DNA and are treated similarly.

HSV-1 and HSV-2 contain a large double-stranded DNA molecule. HSV is gram negative, consists of 162 capsomers and replication takes place within the nuclei of eukaryotic cells. The HSV virion has four parts: an electrondense core containing viral DNA; an icosapentahedral capsid; a tegument-an amorphous layer of proteins that surround the capsid; and an envelope. HSV-1 and HSV-2 encode at least 84 different polypeptides. Each protein does many things, hence HSV genes can encode several hundred different functions. To initiate infection, HSV attaches to at least three different classes of cell-surface receptor and fuses its envelope with the plasma membrane. The capsid, minus its envelope, is transported to the nuclear pore, through which it releases viral DNA into the nucleus. HSV replicates by three rounds of transcription that yield: alpha (immediate early) proteins that mainly regulate viral replication; beta (early) proteins that synthesise and package DNA; and gamma (late) proteins, most of which are virion proteins. Of the 84 known polypeptides, at least 47 are not needed for viral replication in cultured cells. These 47 genes are not completely dispensable. Some complement cellular genes that are not expressed in terminally differentiated cells; others alter cellular metabolism to ensure high virus yields. Mutant viruses lacking these genes cannot survive in nature.

The symptoms of genital herpes vary widely form person to person. Some people have severe symptoms (such as many painful sores), while others have mild symptoms. When symptoms of a first episode of genital herpes occure, they show up two to ten days after having sex with an infected person. These signs can last from two to three weeks. The early symptoms can include an itching or burning sensation; pain in the legs, buttocks, or genital area; vaginal discharge; or a feeling of pressure in the abdominal region.

Within a few days, sores (also called lesions) appear at the site of infection. Lesions can also occur on the cervix in women or in the urinary passage in men. These small red bumps may develop into blisters or painful open sores. Over a period of days, the sores become crusted and then heal without scarring. Other symptoms of a first episode of genital herpes can include fever, headache, muscle aches, painful or difficult urination, vaginal discharge, and swollen glands in the groin area.

Anyone infected with either virus can experience flare-ups. In people who have healthy immune systems, a herpes flare-up usually lasts a few weeks. In people with compromised immune systems the herpes sores can last for longer than a month. In a very small number of cases, herpes can spread to other organs, including the eyes, the throat, the lungs, and the brain.

HSV-1 and HSV-2 look identical under the microscope, and either type can infect the mouth or genitals. Most commonly, however, HSV-1 occurs above the waist, and HSV-2 occurs below the waist. Both HSV-1 and HSV-2 live in nerve cells, usually under the skin. Neither virus is always active. They often