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Category	Prescription Drug	Strength	Quantity	Cost
Sexual Health (Herpes)	Acyclovir (herpes pills) Denavir (cold sores) Famvir (herpes) Valtrex (herpes) Zovirax (herpes cream)	200 mg 1% 125 mg 500 mg 5%	30 tablets 1 tube 30 tablets 30 tablets 1 tube	$45 $72 $168 $236 $164

Acyclovir (pills, genital herpes, shingles, chickenpox)

Acyclovir is used to treat herpes infections of the skin, lip and genitals; herpes zoster (shingles); and chickenpox. It does not cure herpes infections but decreases pain and itching and promotes healing. Oral Acyclovir decreases the frequency and severity of recurrent sores, but it is used only by people with severe herpes infections because of possible adverse side effects.

Denavir (cold sores, topical medication)

Denavir is a topical antiviral medication used for recurrent cold sores (herpes labialis) on the lips and face in otherwise healthy adult patients. Denavir topical may also be used for other purposes. Apply Denavir to your cold sore every two hours during the daytime for four days using your finger or a cotton swab.

Famvir (genital herpes, cold sores, shingles)

Famvir is an oral medication for both the treatment and the suppression of recurrent genital herpes. It is also used for herpes simplex virus infections (cold sores) and herpes zoster (shingles).

Valtrex (genital herpes, cold sores, shingles)

Valtrex is indicated for the treatment of herpes zoster (shingles), for the treatment or suppression of genital herpes in immunocompetent individuals, for the suppression of recurrent genital herpes in HIV infected individuals and is also used for the treatment of cold sores (herpes labialis).

Zovirax (topical cream, genital herpes, shingles, chickenpox)

Topical Zovirax treats herpes infections of the skin, lip and genitals; herpes zoster (shingles); and chickenpox. Zovirax cream does not cure herpes infections but decreases pain and itching and promotes healing.

A cold sore is a recurrent herpes infection. After primary infection in the oral region, the virus travels through nearby nerves and establishes a dormant infection in a nerve-center (ganglion). It may stay dormant forever or, in approximately one-third of people, the virus will occasionally replicate and travel down the nerve again to the body surface, where it begins to grow in skin cells. This means that the blisters in a cold sore will contain the same virus which originally infected the person. In the immunocompetent person, the cold sore will remain demarcated and will crust over in a few days. Most patients will feel tingling and numbness a day or two before the eruption of the cold sore.

What is genital herpes?

Genital herpes is a common disease worldwide, and it is estimated that 45 million people in the US are afflicted. Most genital herpes infections are caused by a type 2 simplex virus but, about 10% of the time, type 1 may infect the genital tract of both men and women. A new infection is often asymptomatic, which means that an individual may acquire genital herpes without knowing it. The presence of specific antibodies to herpes simplex in serum indicates that a patient has been infected with the virus and studies have shown that only 30% of all adults that have herpes antibodies have a history of genital herpes.

Once the primary infection has occurred, the virus will travel up the nerve cell and establish a dormant infection in the sacral ganglia from where it may re-emerge, sometimes causing blisters in the genital area, and sometimes just being excreted without causing symptoms (asymptomatic shedding). Both the virus present in the blister and shedded virus are contagious. Transmission of the virus most commonly results from sexual contact with an asymptomatic, infected partner.

Herpes Overview

Herpes simplex virus (HSV) infections occur worldwide and can only be transmitted between humans. There are two subtypes of HSV. HSV-1 is commonly associated with oral infection (herpes labialis or cold sores), whereas HSV-2 is associated with genital infection (herpes genitalium or genital herpes). Although HSV-1 and HSV-2 are usually transmitted by different routes and involve different areas of the body, there is an overlap in their distribution, characteristics and clinical manifestations. For example, 10% of oral infections are caused by HSV-2, whereas 10% of genital infections are caused by HSV-1.

Primary infection refers to the first time an individual is infected with any type of HSV. This primary event may or may not be accompanied by clinical symptoms and the individual may be unaware of the infection. The primary infection can be accompanied by blisters, ulcers, or red inflamed areas (lesions), which may occur at a variety of body sites including the eye and the internal and external areas of the mouth or genitals.

Once HSV has infected an individual it will remain in the body for life, hidden in a dormant state inside nerve cells. In the majority of infected people, the virus remains dormant for life, whereas in approximately a third of infected individuals, the virus wakes up (reactivates) and replicates. In the presence of an intact immune system, such reactivation may be without symptoms or it may exhibit with an eruption of blisters around the mouth or in the genital region including the buttocks. Blisters are typically grouped in a 1 cm diameter circle with some redness, crusting and occasionally ulceration. Individuals who reactivate the virus without obvious clinical symptoms still make copies of it in the oral or genital tract. This phenomenon is called viral shedding and viral shedders are at risk of unknowingly spreading the virus to partners through the sharing of utensils, kissing or sexual intercourse.

What is a Herpes Simplex Virus (HSV)?

HSV is a large, double stranded DNA virus. All the programming of the virus’ ability to infect someone is contained in the DNA. The DNA is packaged in a diamond shaped protein structure, called an icosahedron. The virus also has an overcoat or envelope, which is necessary for the docking procedure when the virus infects a cell. In other words, an HSV particle without the envelope is not infectious, since it cannot dock with and enter the cell.

How does HSV enter the body?

The virus gains entry into the body, not through intact skin, but through mucous membranes, such as those in the oral region, vagina, tip of the penis or the eye. The virus will first replicate (make copies of itself) inside surface cells at these sites, eventually killing the infected surface cells. In a person with normal immunity, the immune system is quickly mobilized to contain the primary infection.

However, before this happens, the virus gains entry to the nerve cell end-plates (structures that help us to feel things like pain and temperature) present at the skin surface. The end-plates connect to the more deeply located nerve cell body through an elongated nerve fiber or axon. This cell in turn is connected to serially coupled layers of internal nerve cells, which eventually lead to a ganglion, a collection of nerve cell bodies just like a node in an electricity grid. Through such intricate connections, the nerve cells eventually lead into and communicate with the central nervous system or the brain. The axons are protected by myelin blankets, just like the insulating material around electrical wires, but the endings are bare, as are the nodes where one nerve cell extension connects with the next (synapse). It is thought that the virus sheds its envelope as soon as it has entered the nerve and uses the axon as a conduit, hiding from immune system attack, as if it were inside a Trojan Horse.

HSV has specifically chosen the nerve cell body and ultimately the ganglion (HSV-1 resides in the trigeminal ganglion; HSV-2 resides in the sacral ganglia) as a site where it remains dormant. It is from these locations that the virus may reactivate from its dormant state to the respective innervated (nerve-cell-serviced) body areas. This is why dormant virus from the trigeminal ganglion (oral or facial area) reactivate in the oral or facial region, whereas dormant virus from the sacral ganglion (lower back/spine area) reactivate to the genital area or the buttock.

What is latency?

Within a day of infection, the naked virus arrives at the nerve cell nucleus, and it injects its genetic material (DNA). It then resides in the nerve cell nucleus in a dormant (latent) form. According to most researchers, virus replication will not occur at this stage and no new virus particles will be formed. The precise molecular mechanism for this event (establishment and maintenance of latency) is unknown, but reflects an interplay between viral and nerve cell factors. However, other researchers argue that a low level of replication must occur in order to keep the virus machine well oiled. This could be compared to car maintenance. For proper functioning, it is not a good idea to leave a car in the garage for years, but to drive it at least occasionally. If this were the case for HSV, it would likely result in low level viral shedding at the peripheral skin site.

Why does HSV recur?

It is important, from the virus survival point of view, to be able to fire-up and begin to replicate should circumstances become uncomfortable inside the neuron (the infected person suffers a trauma, acquires a severe disease, becomes immunocompromised or dies). We do not understand why stress and sunshine, for example, tend to trigger HSV reactivation. When this happens, new virus particles are created and transported back to the skin and mucous membranes through the neuronal highway. They then begin to replicate in the surface cells, creating a blister in the form of a cold sore or genital herpes. The surface cells balloon up and become filled with fluid. This fluid contains millions of infectious viral particles. We believe the infected nerve cells usually survive during this reactivation process. We also think that HSV particles not only travel down to the skin and mucous membranes, but may also travel in the opposite direction leading them closer to the brain. Some researchers suggest that healthy immunocompetent people may, in fact, harbor dormant virus inside the brain.

Disclaimer

This drug information is for your information purposes only. It is not intended that this information covers all uses, directions, drug interactions, precautions, or adverse effects of your medication. This is only general information, and should not be relied on for any purpose. It should not be construed as containing specific instructions for any particular patient. We disclaim all responsibility for the accuracy and reliability of this information, and/or any consequences arising from the use of this information, including damage or adverse consequences to persons or property, however such damages or consequences arise. No warranty, either expressed or implied, is made in regards to this information.