Herpes Simplex Virus: Transmission and Transmissibility

What is Herpes Infection?

Herpes Simplex Virus (HSV) invades the body through skin and mucous membranes. Then virus invade the nervous system, establishes latent (dormant) infection in nerve cell ganglia nearest to the original site of infection. HSV is a chronic infection, with periods of asymptomatic viral shedding and unpredictable recurrences of blister-like lesions.

There are two types of HSV: Herpes simplex virus type 1 (HSV-1) and Herpes simplex virus type 2 (HSV-2).

HSV-1 is usually the cause of oral infection. Initial oral infection with HSV-1 may cause gingivostomatitis (mainly in children) and herpetic pharyngitis (mainly in adolescents and adults). Recurrent infection causes herpes labialis (or cold sores) [9]. HSV-1 infects about 80% of the U.S. population and usually appears on the lips in cold sores.

Most cases of genital herpes are caused by HSV-2. Genital herpes is a sexually transmitted disease.

While genital HSV can be a frustrating and painful condition, in general the virus is less a medical problem than a social problem. For most people genital herpes is no more dangerous than cold sores.

Many people with genital herpes don't know they have it, and are unaware they may be spreading virus to others. Many have no symptoms or mistake their symptoms for something else, such as jock itch, insect bites, hemorrhoids, yeast infections, razor burn, or allergies.

Difference between HSV-1 and HSV-2

The main difference between the two types of herpes virus is in where they typically establish latency (lie dormant) in the body -- their "site of preference."

  • HSV-1 usually establishes latency in the trigeminal ganglion, a collection of nerve cells near the ear. Reactivating from there, HSV-1 causes viral shedding and outbreaks on lips, nose, oral mucosa, and sometimes other parts of the face.
  • HSV-2 usually establishes latency in the sacral ganglion at the base of the spine. Reactivating from there, HSV-2 causes viral shedding and outbreaks on genital area, buttocks, and rarely other body parts below the waist.

Nevertheless, either type can infect both oral and genital areas. Genital herpes can be caused by both HSV-1 and HSV-2. And signs and symptoms of initial genital herpes caused by HSV-1 or HSV-2 are indistinguishable. However, subsequent recurrences are more frequent with HSV-2.

Oral HSV-2 although possible, occurs very rarely.

How to distinguish between HSV-1 and HSV- 2?

Either type of herpes virus can invade both oral genital areas of the body. Only serologic tests for herpes antibodies to viral glycoprotein G allow to definitely distinguish between HSV-1 and HSV- 2.

HSV-1 reactivates more frequently in the oral than in the genital area. Similarly, for HSV-2, reactivation in the genital area is 8 to 10 times more frequent than oral reactivation.

HSV-2 strains shut off host cellular protein synthesis more rapidly and more completely than do HSV-1 strains[14].

HSV-1 is the most common cause of sporadic, viral encephalitis. HSV-2 is the most common cause of recurrent, benign lymphocytic meningitis.

First-episode manifestation

Primary oral infection with HSV-1 usually causes gingivostomatitis (mainly in children) and herpetic pharyngitis (mainly in adolescents and adults).

Primary genital herpes can be caused by both HSV-1 and HSV-2. Signs and symptoms of the first genital herpes episode caused by both HSV-1 and HSV-2 are indistinguishable. However, recurrences are more frequent with HSV-2. The clinical courses of first-episode genital herpes among patients with HSV-1 and HSV-2 infections are identical. However, the 12-month recurrence rates among patients with first episode are 90% for HSV-2 and 55% for HSV-1 infection[15].

Transmission & Transmissibility

Herpes virus is spread only through direct contact of broken (abraded) skin and mucous membranes with the contagious area (an infected person's herpes lesions, mucosal surfaces, genital or oral secretions). Mucous membranes of the mouth and genital area are the most vulnerable sites.

Broken areas of skin and intact mucous membranes permit entry of the virus ("inoculation") and initiation of its replication in cells of the epidermis and dermis.

HSV can be transmitted through the following activities:

  • Penile-vaginal intercourse
  • Anal intercourse
  • Oral-genital sexual contact
  • Any mucous membrane to mucous membrane contact (e.g. kissing)
  • Any other sexual body-to-body contact (with or without penetration)
  • Sharing sex objects

The herpes virus is quite fragile. HSV does not survive outside the body for more than about 10 seconds, and although it can survive for slightly longer in warm, moist conditions, it dies very quickly once exposed to the air. Transmission through inanimate objects such as toilet seats is unlikely. Precautions include not sharing towels, underwear, or other objects that come into contact with genital lesions.

Note: Humans are the only natural reservoir for transmission of HSV [7]. This virus is not transmitted to humans by animals.

Genital herpes is not hereditary. The virus has no effect on fertility and is not transmitted via men's sperm or women's ova.

It is more common for oral HSV-1 to be transmitted to the genitals through oral sex, than it is for HSV-2 to be transmitted to the mouth. If a person has oral herpes (cold sores), and performs oral sex on the partner, it is possible for that person to transmit the virus to the genitals from this action, and vice versa.

If you already have certain HSV type then acquisition of another type of HSV is more difficult (though certainly possible). This is because either type, contracted orally or genitally, causes the body to produce antibodies, some of which are active against both HSV-1 and HSV-2. This acquired immune response gives some limited protection if the body encounters a second type. When a person with a prior HSV infection does contract the second type, the first episode tends to be less severe than when no prior antibodies are present.

Almost all HSV-2 is encountered after childhood, when people become sexually active. Those who have a prior infection with HSV-1 have an acquired immune response that lowers (though doesn't eliminate) the risk of acquiring HSV-2. According to the research [10], previous oral HSV-1 infection reduces the acquisition of subsequent HSV-2 infection by 40%.

Prior oral HSV-1 infection lowers the risk of acquiring genital HSV-1 infection even further. Studies show that genital HSV-1 infections almost always occur in people who have no prior infection with HSV of either type [11]. In the absence of prior oral infection, however, HSV-1 spreads easily to the genital area, usually through oral sex. In some countries, such as Japan and parts of Great Britain, genital HSV-1 is as common as genital HSV-2, or more common.

If you have genital HSV-1 and your partner has genital HSV-2 and you have unprotected sex, there is a small but real risk that you will get HSV-2, resulting in more outbreaks and more shedding. There are documented cases where a person acquires HSV-2 after a prior genital HSV-1 infection. It doesn't happen often, but it does happen. However, it's very unlikely that your partner will get genital HSV-1 from you. It's possible, but very unusual.

If your partner has genital HSV-2 and you perform oral sex on him or her, there is a very low risk that you will get oral HSV-2. According to one study, almost 100% of recognizable HSV-2 infection is genital (Nahmias, Scandinavian Journal of Infectious Diseases Supplement, 1990). One reason is that most adults are already infected with HSV-1 orally, which provides some immunity against infection with HSV-2. Another reason is that oral HSV-2 rarely reactivates, so even if an infection does exist, no one knows [1].

If you acquire genital HSV-1 through oral sex, you can spread the virus to a partner through genital sex. But probably it is not as easily as it was spread through oral sex. The main reason is that the virus reactivates and sheds less often outside its site of preference. Only about 25% of people with genital HSV- 1 shed virus at all in the absence of symptoms, while 55% of people with HSV-2 do [13]. However, transmission of genital HSV-1 during asymptomatic shedding has been well documented. In other words, genital HSV-1 can be spread through genital sex, even when there are no symptoms.

Viral shedding
The medical terminology for the virus being released from the surface of the skin is called viral shedding. Viral shedding can occur with symptoms (symptomatic herpes) and without symptoms (asymptomatic herpes). You may (if you have classic herpes lesions) or may not be aware that viral shedding is occurring. The virus cannot be spread when it is inactive (in the nerve cell). There is no simple way to know if the herpes virus is active when there are no symptoms. In fact, studies have shown that most people get HSV from sexual contact during times of asymptomatic viral shedding.

When Herpes virus is most likely to be transmitted
Herpes virus is most likely to be transmitted from moment the prodromal symptoms are noticed until the area is completely healed and the skin looks normal again. Sexual contact (oral, vaginal, or anal) is very risky during this time.

Likelihood of HSV transmission
Let's say you have an infected male and an uninfected female. If they avoid sex during outbreaks, don't use condoms regularly, and don't take antiviral therapy every day, the risk of transmission is about 10% per year. But if you add condoms, it reduces transmission by about 50%, if he takes valacyclovir (Valtrex®) 500 mg once a day, he can reduce transmission also by about 50%. So you can see that the numbers get very low! If it is a woman infected with HSV 2 having sex with an uninfected male, given the circumstances listed above again, then the transmission rate is about 4% prior to the interventions of condoms and Valtrex®.

Asymptomatic shedding and transmission

Individuals who reactivate the virus without visible symptoms still release the virus in the oral or genital tract. Asymptomatic viral shedders are at risk of unknowingly spreading the virus to partners.

Virus type
Researchers have found that people with HSV-2 genital herpes tend to have more shedding than those with HSV-1 genital herpes. The rate of asymptomatic shedding from the genital area for HSV-1 is approximately 5% of the time when the person has no symptoms. Typically in the first year of infection with genital HSV-2, one will shed about 6-10% of those days when there are no symptoms. This of course will decrease over time as well.

Duration of infection
The rate of shedding decreases over time. People with new infections are more likely to shed the virus than those with an infection more than a year old.

Frequency of recurrences
Rate of asymptomatic shedding of HSV also related to frequency of recurrences of genital herpes. People with frequent recurrences may shed the virus more often, but this is still an area being studied. About 50% of asymptomatic shedding events occur more than 7 days before or after a herpes outbreak.

Why Herpes virus is not curable?

Neural tissue transport of herpes simplex virus results in life-long latent infection. HSV remain in the body for life, hidden in a dormant state inside nerve cells.

The virus escapes the usual immune response by penetrating nerve fibres. As the immune system moves in to control the infection, the virus conceals itself within nerve cells. The virus is carried to the nerve "cell body" in a swelling called a ganglion located close to the spinal cord. When it reaches the cell body, the viral DNA is added alongside the nerve cell's own DNA in the nucleus. It remains there, hidden within the nerve cell and in an inactive state, for the lifetime of the infected individual.

Retrograde transport through adjacent neural tissue to sensory ganglia leads to lifelong latent infection. Once reactivated, the virus is transported by the neuron back to the epithelium, where more replication occurs, and another outbreak ensues.

Genital Herpes symptoms

Symptoms of genital herpes can vary in appearance and intensity. Some people have no symptoms or such mild symptoms that they don't suspect they have an infection. For others, the first episode of herpes (primary infection) can cause one or more very painful lesions to erupt on the skin.

Genital herpes lesions usually appear within 2 to 10 days after being exposed to the virus, and can last from two to four weeks. First to appear are small red bumps, which develop into blisters. Then the blisters become open sores, which later dry up, crust over, and heal without leaving a scar. Symptoms experienced during lesion formation include: swollen lymph glands, headaches, fever or general malaise, pain, muscle aches.

After the initial outbreak, the virus moves away from the skin surface and travels along the nerve pathways to nerve roots at the base of the spine and goes into an inactive phase. The virus may reactivate and lesions reappear at the same site as the original infection, but usually are much less severe. If the infection is caused by HSV-1, the (first year) recurrence rate is 50%. The HSV-2 recurrence rate during first year is 80-90%.

Frequency of outbreaks

Researchers don't know why recurrences happen, or why their frequency and severity vary.

Frequency of herpes outbreaks depends on three factors:

  • Person's immune system. It's also the reason that both HSV-1 and HSV-2 can pose serious challenges for infants, who have a limited immune response.
  • How long a person has had the infection. Over time, recurrences of both HSV- 1 and HSV-2 tend to decrease. It is not clear why a decrease of herpes reactivation occurs over time, but is believed to be due to the buildup of antibodies in the infected persons system.
    Most people diagnosed with HSV-2 affecting the genital area typically have four or five symptomatic recurrences the first year. After the first year, most people have fewer and milder recurrences, lasting a week or less.
  • Site of preference and virus type. Outbreaks are more likely when HSV-1 is oral and HSV-2 is genital.
    While HSV can infect both genital and oral areas, both types cause milder infections when they are away from "home" territory. Outside their site of preference, both type 1 and 2 lose their power. Oral HSV-1 infection recurs more frequently than oral HSV-2, and genital HSV-2 recurs more often than genital HSV-1 [2]. In fact, genital HSV-2 is twice as likely to reactivate and recurs 8-10 times more frequently than genital HSV-1 infection [8]. It is estimated that HSV-1 currently accounts for as many as 30% of all genital herpes cases in the U.S and 2-5% of the recurring outbreaks are associated with the herpes type 1 virus.

HSV-2 infection in the oral area very rarely causes problems. Oral HSV-2 infections are very rare. But even when an infection occurs, recurrent outbreaks are extremely rare. In one study (Lafferty et al., New England Journal of Medicine, 1987), oral HSV-2 recurred an average of 0.01 times a year in newly infected people.

Outbreaks triggers

Some triggers of outbreaks:

  • stress
  • illness
  • poor nutrition
  • menstruation
  • vigorous sex
  • sunlight
  • local physical injury
  • suppression of the immune system

Sources & References:

  • 1. Wald A, Ericsson M, Krantz E, Selke S, Corey L. Oral shedding of herpes simplex virus type 2. Sex Transm Infect. 2004 Aug;80(4):272-6. PubMed
  • 2. Lafferty WE, Coombs RW, Benedetti J, Critchlow C, Corey L. Recurrences after oral and genital herpes simplex virus infection. Influence of site of infection and viral type. N Engl J Med. 1987 Jun 4;316(23):1444-9. PubMed
  • 3. Dr. Edward K. Wagner's Herpes simplex virus Research
  • 4. Genital Herpes: A Hidden Epidemic - Article from the FDA reveals many facts about herpes
  • 5. National Herpes Resource Center A service of the American Social Health Association
  • 6. Genital Herpes - Information from U.S. Centers for Disease Control and Prevention
  • 7. Kimberlin DW. Neonatal Herpes Simplex Infection. Clin Microbiol Rev. 2004 Jan;17(1):1-13. PubMed
  • 8. Dennis L. Kasper, Anthony S. Fauci. Harrison Infectious diseases . McGraw-Hill Professional; 1 edition, 2010
  • 9. Bennett JE, Dolin R, Blaser MJ. Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases. 8th Ed. Philadelphia: Elsevier Saunders; 2014, Chapter 138.
  • 10. Mertz GJ, Benedetti J, Ashley R, Selke SA, Corey L. Risk factors for the sexual transmission of genital herpes. Ann Intern Med. 1992 Feb 1;116(3):197-202. PubMed
  • 11. Corey L, Adams HG, Brown ZA, Holmes KK. Genital herpes simplex virus infections: clinical manifestations, course, and complications. Ann Intern Med. 1983 Jun;98(6):958-72. PubMed
  • 13. Wald A, Zeh J, Selke S, Ashley RL, Corey L. Virologic characteristics of subclinical and symptomatic genital herpes infections. N Engl J Med. 1995 Sep 21;333(12):770-5 PubMed
  • 14. Murphy JA, Duerst RJ, Smith TJ, Morrison LA. Herpes simplex virus type 2 virion host shutoff protein regulates alpha/beta interferon but not adaptive immune responses during primary infection in vivo. J Virol. 2003 Sep;77(17):9337-45. PubMed
  • 15. Engelberg R, Carrell D, Krantz E, et al. Natural history of genital herpes simplex virus type 1 infection. Sex Transm Dis. 2003;30:174-177.

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Created: August 18, 2006
Last updated: February 24, 2016

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