HSV-1 & HSV-2

Herpes Simplex Virus 1 & 2 (HSV-1) are closely related (~50% nucleic acid identity and over 70% amino acid identity) of the alpha subgroup.

HSV-1 and HSV-2 initially infect and replicate in mucoepithelial cells and then establish latent infection of the innervating neurons. There are various stages of pathology on mucous membranes and skin; 1) macule (flat, often red discolaration), 2) papule (raised bump like), 3) vesicle (raised skin), 4) pustule (vesicular rash infected with bacterial; puss formation), 5) ulcer and 6) crust.

In latent infection, the virus travels through axons to the nuclei of ganglion where the viral genome circularizes. During a latent infection, a specific RNA is the only detectable viral product synthesized in infected cells (latency associated transcript (LAT) and virus replication does not proceed further. The virus can be reactivated (reversal of latency) due to various stimuli (e.g., stress, sunlight).  LAT and thymidine kinase genes are required for reactivation. During reactivation, the virus travels back down the neuron back up to the skin.

Both types of HSV are capable of infecting the skin at any location on the body. Thus, the virus that usually causes oral herpes (HSV-1) can cause genital herpes as well as herpes on the hands and eye. The virus that causes genital herpes (HSV-2) can also cause oral herpes, although it almost exclusively infects the genital area. HSV-1 may cause genital herpes via self-inoculation from oral lesions, or via oral sex. Herpes infections, no matter where they occur first, have a tendency to recur in more or less the same place. Such recurrences may happen often (for example, several times per year) or only occasionally. You would know that you have herpes if you have an outbreak or if a doctor performs a blood test to tell if you have been infected with it. Most adults have been infected with oral or genital herpes and never know it. See Medicine Net

HSV-1

HSV-1 is usually associated with infections above the waist and is typically spread by oral contact (kissing) or by sharing glasses, tooth brushes and other saliva contaminating items.  Most people infected with HSV-1 are asymptomatic. However, primary infection of the head or genital areas can occur (e.g., gingivostomatitis, herpes labialis, keratitis) and can be very serious in the immuncompromised. The primary infection can be spread as by eczema (condition of the skin). Reactivation of the virus (e.g., recurrent cold sores)  is less severe than primary infection.

Structure: 

Herpes simplex virus type 1 (HSV-1), from the alphaherpes virus subfamily, is an enveloped, nuclear-replicating, and large double-stranded DNA virus. The genome of HSV-1 is an about 152 kb linear double-stranded GC-rich DNA sequence, and contains two unique regions called the long unique region (UL) and the short unique region. The genome of HSV-1 is located within the nucleocapsid, which is surrounded by a group of tegument proteins. The nucleocapsid and tegument proteins are surrounded by a lipid envelope studded with glycoproteins which are important for binding to and entry into new susceptible cells. See Wei

HSV-2

HSV-2 is associated with infections below the waist (e.g., 90% of genital herpes is HSV-2, 10% HSV-1) and is mainly spread by sexual contact or from the mother at birth. HSV-2 has a greater potential to cause viremia and associated systemic flu-like symptoms. As with HSV-1, reactivation is less severe than a primary infection.

Symptoms:

The hallmark symptom of herpes is tingling or a burning sensation before the appearance of the outbreak. The classic sign of herpes is a cluster of blisters on a base of red skin. The blisters look like a drop of water filled with clear liquid. These blisters dry up rapidly and leave a crust or scab that lasts anywhere from a few days to a few weeks, depending on the severity of the infection. See Medicine Net

Transmission

The virus is spread from person to person by kissing, by close contact with herpes lesions, or from saliva even when sores are not present. Infected saliva is a common means of virus transmission. The contagious period is highest when people have active blisters or moist sores. Once the blisters have dried and crusted over (within a few days), the risk of contagion is significantly lessened. HSV can also be spread through personal items that are contaminated with the virus, such as lipstick, utensils, and razors. Despite popular myth, catching herpes (cold sores) from surfaces, towels, or washcloths is a very low risk, since the virus does not usually survive long on dry surfaces. See Medicine Net

Treatment

Most anti-herpes drugs are nucleotide analogues or inhibitors of the viral DNA polymerase. Acyclovir (ACV) is currently the most effective. ACV is activated by the viral thymidine kinase and then used as a substrate by the viral DNA polymerase. It is then incorporated into, and prevents elongation of the viral DNA. Derivatives of ACV which are more stable that may be used include amciclovir and valacyclovir.