Herpes simplex virus(redirected from Herpes simplex I virus)
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Unlike cellular organisms, viruses do not contain all the biochemical mechanisms for their own replication; they replicate by using the biochemical mechanisms of a host cell to synthesize and assemble their separate components. (Some do contain or produce essential enzymes when there is no cellular enzyme that will serve.) When a complete virus particle (virion) comes in contact with a host cell, only the viral nucleic acid and, in some viruses, a few enzymes are injected into the host cell.
Within the host cell the genetic material of a DNA virus is replicated and transcribed into messenger RNA by host cell enzymes, and proteins coded for by viral genes are synthesized by host cell ribosomes. These are the proteins that form the capsid (protein coat); there may also be a few enzymes or regulatory proteins involved in assembling the capsid around newly synthesized viral nucleic acid, in controlling the biochemical mechanisms of the host cell, and in lysing the host cell when new virions have been assembled. Some of these may already have been present within the initial virus, and others may be coded for by the viral genome for production within the host cell.
Because host cells do not have the ability to replicate “viral RNA” but are able to transcribe messenger RNA, RNA viruses must contain enzymes to produce genetic material for new virions. For certain viruses the RNA is replicated by a viral enzyme (transcriptase) contained in the virion, or produced by the host cell using the viral RNA as a messenger. In other viruses a reverse transcriptase contained in the virion transcribes the genetic message on the viral RNA into DNA, which is then replicated by the host cell. Reverse transcriptase is actually a combination of two enzymes: a polymerase that assembles the new DNA copy and an RNase that degrades the source RNA.
In viruses that have membranes, membrane-bound viral proteins are synthesized by the host cell and move, like host cell membrane proteins, to the cell surface. When these proteins assemble to form the capsid, part of the host cell membrane is pinched off to form the envelope of the virion.
Some viruses have only a few genes coding for capsid proteins. Other more complex ones may have a few hundred genes. But no virus has the thousands of genes required by even the simplest cells. Although in general viruses “steal” their lipid envelope from the host cell, virtually all of them produce “envelope proteins” that penetrate the envelope and serve as receptors. Some envelope proteins facilitate viral entry into the cell, and others have directly pathogenic effects.
Some viruses do not produce rapid lysis of host cells, but rather remain latent for long periods in the host before the appearance of clinical symptoms. This carrier state can take any of several different forms. The term latency is used to denote the interval from infection to clinical manifestations. In the lentiviruses, it was formerly mistakenly believed that virus was inactive during this period. The true situation is that lentiviruses are rapidly replicating and spawning dozens of quasi-species until a particularly effective one overruns the ability of the host's immune system to defeat it. Other viruses, however, such as the herpesviruses, actually enter a time known as “viral latency,” when little or no replication is taking place until further replication is initiated by a specific trigger. For many years all forms of latency were thought to be identical, but now it has been discovered that there are different types with basic and important distinctions.
In viral latency, most of the host cells may be protected from infection by immune mechanisms involving antibodies to the viral particles or interferon. Cell-mediated immunity is essential, especially in dealing with infected host cells. Cytotoxic lymphocytes may also act as antigen-presenting cells to better coordinate the immune response. Containment of virus in mucosal tissues is far more complex, involving follicular dendritic cells and Langerhans cells.
Some enveloped RNA viruses can be produced in infected cells that continue growing and dividing without being killed. This probably involves some sort of intracellular regulation of viral growth. It is also possible for the DNA of some viruses to be incorporated into the host cell DNA, producing a carrier state. These are almost always retroviruses, which are called proviruses before and after integration of viral DNA into the host genome.
Few viruses produce toxins, although viral infections of bacteria can cause previously innocuous bacteria to become much more pathogenic and toxic. Other viral proteins, such as some of the human immunodeficiency virus, appear to be actively toxic, but those are the exception, not the rule.
However, viruses are highly antigenic. Mechanisms of pathologic injury to cells include cell lysis; induction of cell proliferation (as in certain warts and molluscum contagiosum); formation of giant cells, syncytia, or intracellular inclusion bodies caused by the virus; and perhaps most importantly, symptoms caused by the host's immune response, such as inflammation or the deposition of antigen-antibody complexes in tissues.
Because viral reproduction is almost completely carried out by host cell mechanisms, there are few points in the process where stopping viral reproduction will not also kill host cells. For this reason there are no chemotherapeutic agents for most viral diseases. acyclovir is an antiviral that requires viral proteins to become active. Some viral infections can be prevented by vaccination (active immunization), and others can be treated by passive immunization with immune globulin, although this has been shown to be effective against only a few dozen viruses.
her·pes sim·plex(hĕrpēz simpleks)
Synonym(s): herpes facialis, herpes febrilis, herpes labialis, Simplexvirus.
Herpes simplex virus; HSV
Herpes Simplex Virus
|Mean LOS:||6 days|
|Description:||MEDICAL: Minor Skin Disorders With Major CC|
There are two types of herpes simplex virus (HSV), type 1 and type 2. HSV-1 causes infection above the waist, such as “cold sores” that occur on the mouth. This type may occur in the genital area as a result of oral-genital sexual practices. After the initial infection, the virus is dormant, but the patient is a carrier and likely to have recurrent infections. Events that trigger recurrences are sun exposure, fever, menses, stress, and lack of sleep.
HSV-2 causes lesions in the genital area. In the primary episode, multiple, blisterlike, painful vesicles erupt on the vulva, perineum, cervix, tip or shaft of the penis, or perianal area within 3 to 5 days after the initial exposure. The virus then becomes dormant and resides in the nerve ganglia of the affected area. Repeated outbreaks can happen at any time, but most patients have less severe regular recurrences that are more likely to occur during menses, pregnancy, or times of illness and stress. The more severe the primary outbreak, the more frequent the recurring infections. In the United States, 22% of the adult population has HSV-2, and 1.7 million new cases are diagnosed each year.
Active HSV is associated with spontaneous abortion in the first trimester of pregnancy and an increased risk of preterm labor after 20 weeks’ gestation. If a patient has active herpes around the time of the estimated date of delivery, cesarean section is the preferred method of delivery. Infected infants can develop the following signs and symptoms after an incubation period of 2 to 12 days: fever, hypothermia, jaundice, seizures, poor feeding, and vesicular skin lesions.
To cause an infection, HSV needs to come into direct contact with the genitals, mouth, eyes, open sores, or cracks in the skin. HSV-2 is sexually transmitted through contact with an infected person. Pregnant women can transmit the herpes virus to the fetus, especially during a primary outbreak. Transmission can occur when the membranes rupture or during a vaginal delivery, but transplacental transmission is extremely rare. Asymptomatic transmission is very uncommon.
Heritable immune responses could be protective or increase susceptibility.
Gender, ethnic/racial, and life span considerations
Because teenagers are engaging in sexual activity earlier than ever before, they have a higher risk today than in the past of contracting HSV; the number of adolescents with HSV is therefore increasing. Because there is no cure for herpes, recurrent outbreaks of HSV occur over a lifetime. HSV-2 affects one in five men and one in four women and is more prevalent in African Americans and Mexican Americans than in whites.
Global health considerations
HSV is present around the globe, and the global prevalence of HSV infections is increasing.
If the patient has an oral lesion, ask about a sore throat, increased salivation, anorexia, and mouth pain. During a primary episode, the patient may experience flu-like symptoms, such as fever, malaise, and enlarged lymph nodes. If the lesion is not a primary one, the patient usually does not have any systemic complaints but may complain of a tingling, itching, or painful sensation at the site of the lesion. If the patient has a genital lesion, obtain a detailed summary of his or her sexual activity, including number of partners, use of barrier protection and birth control measures, participation in oral or anal intercourse, and previous (if any) history of sexually transmitted infections (STIs). Inquire about any burning with urination, dysuria, dyspareunia, pruritus, fever, chills, headache, and general malaise. On some occasions, the patient may be asymptomatic or have such mild symptoms that the outbreak goes unnoticed.
The most common symptom is the appearance of a herpetic lesion. Inspect the lips and the oral and pharyngeal mucosa for lesions and inflammation. The lesion may appear as a red, swollen vesicle, or if it has ruptured, it is ulcerlike with yellow crusting. Palpation of the lymph nodes in the neck may reveal cervical adenopathy. Take the patient’s temperature. Inspect the genitalia for fluid-filled vesicles, or if the vesicles have ruptured, note an edematous, erythematous oozing ulcer with a yellow center. Examine the cervix by using a speculum and inspect the walls of the vagina. Inspect the patient’s perianal skin and the labia and vulva or penis and foreskin carefully to identify all lesions; note any abnormal discharge.
Ask the patient about sexual practices, partners, and birth control methods. Assess the patient’s knowledge of STIs and their implications. Assess the patient’s ability to cope with having an STI. The diagnosis of an STI can be very upsetting to a woman or man who believes she or he was involved in a monogamous relationship. Tell patients that an outbreak of genital HSV may have had its origins even 20 to 30 years before the outbreak.
|Test||Normal Result||Abnormality With Condition||Explanation|
|Polymerase chain reaction (PCR)||Negative for HSV DNA||Positive for HSV DNA||Demonstrates presence of viruses|
|Viral culture||Negative||Positive for HSV; differentiates between HSV-1 and HSV-2||Demonstrates presence of viruses in an active lesion; cultures are most accurate in the first several days of ulceration|
Other Tests: Serological tests may also be done in the presence of symptoms and a negative culture.
Primary nursing diagnosis
DiagnosisAnxiety related to a knowledge deficit of cause, treatment, and prevention of HSV
OutcomesAnxiety control; Coping; Social interaction skills; Acceptance: Health status; Symptom control behavior
InterventionsAnxiety reduction; Coping enhancement; Presence; Teaching: Individual; Counseling; Support group; Medication prescribing
Planning and implementation
Because HSV is not curable, treatment focuses on relieving the symptoms. The drug of choice to treat a primary infection of HSV-1 or HSV-2 is acyclovir.
|Medication or Drug Class||Dosage||Description||Rationale|
|Antiviral||Depends on the drug and if the outbreak is primary or recurrent||Penciclovir (Denavir); acyclovir (Zovirax); valacyclovir (Valtrex); famciclovir (Famvir)||Relieves of symptoms, decreases viral shedding (acyclovir is contraindicated during pregnancy); daily dosage for primary episodes is slightly lower than for recurrent infections; some physicians may order chronic suppressive drug therapy, where acyclovir is taken for up to 6 mo|
Other Drugs: Antipyretics, analgesics, viscous lidocaine
Instruct the patient to take all medication ordered, even if symptoms recede before the medication is used up. For comfort during the outbreak, patients may take prescribed analgesics or use warm soaks with Epsom salts or sitz baths. Lesions can be cleaned with Betadine. Encourage patients to wear loose clothing and cotton underwear and to avoid ointments that contain cortisone and petroleum because they slow healing and promote the growth of the virus. Encourage exercise, good nutrition, and stress reduction to decrease the number of recurrent outbreaks (Box 1).
Inform patients that for persons with HSV-2, the risk of acquiring HIV is likely more than double for persons without HSV-2. Help the patient understand that this is a minor problem with which she or he will be inconvenienced from time to time. Adherence to strict guidelines when active lesions are present allows the patient to have a normal sexual relationship. Healthcare workers with active herpes are prohibited from working with immunosuppressed patients or in a nursery setting because of the complications that result in the neonate if HSV transmission occurs.
Evidence-Based Practice and Health Policy
Tronstein, E., Johnston, C., Huang, M.L., Selke, S., Magaret, A., Warren, T., …Wald, A. (2011). Genital shedding of herpes simplex virus among symptomatic and asymptomatic persons with HSV-2 infection. The Journal of the American Medical Association, 305(14), 1441–1449.
- Investigators conducted a prospective study in which 498 participants were diagnosed with HSV-2 through positive antibody testing. During a median follow-up period of 57 days for each participant, viral shedding occurred whether or not participants had a history of any symptoms and even in the absence of current active lesions.
- A history of symptoms was reported by 82.3% of participants with a median of four recurrences per year (IQR, 2 to 8), and absence of active lesions was reported on 89.6% of the follow-up days (25,664 of a total 33,113 days).
- HSV-2 shedding occurred on 20.1% of the follow-up days (95% CI, 18.3 to 22) among participants who had a history of HSV symptoms compared to 10.2% of the follow-up days (95% CI, 7.7 to 13.6) among participants with no history of symptoms (p < 0.001).
- Appearance, location, and number of lesions; drainage from lesions
- Presence of flu-like symptoms that accompany outbreaks
- Patient’s knowledge of cause, treatment, and prevention of HSV
- Patient’s reaction to the diagnosis of an STI
Discharge and home healthcare guidelines
Be sure the patient understands the correct dosage, route, and time of the medication, as well as the importance of taking all prescribed medication even if the symptoms subside. Review events that trigger outbreaks; emphasize the importance of avoiding contact with the lesion in preventing transmission. Teach the female patient that a potential long-term complication is the development of cervical cancer; yearly Papanicolaou (Pap) tests are critical.Living with Genital Herpes: What Patients Need to Know
- Each patient’s symptoms are different; lesions can resemble blisters, cuts in the skin, or spider bites on the buttocks; flu-like symptoms that accompany lesions also vary, as do the frequency and duration of outbreaks.
- Patients are at the highest risk of transmitting HSV to a partner during the time an active lesion is present until complete healing takes place.
- Condoms are not a safe barrier for transmission if an active lesion is present.
- During the time when active lesions are present, patients should engage in sexual activities that avoid contact with the lesions. Abstinence is encouraged if an active lesion is present.
- When lesions are active, extreme caution needs to be taken to avoid transmission by contact with articles such as towels, washcloths, and razors. Good hand washing with soap and water helps prevent the spread of the virus.
- Patients can prevent self-infection to other areas of the body by not touching the sores and using good hand washing.
- It is a myth that if one person has herpes, so does his or her partner.
- Patients should be aware of prodromal symptoms—tingling, itching, pain, numbness—and should begin pharmacologic treatment earlier to better alleviate symptoms.
- Patients should be aware of events that can trigger a repeated outbreak: pregnancy, menses, stress, fever, infectious illness.
- For more information, patients should contact the Herpes Resource Center Hotline: 1-415-328-7710.
Patient discussion about Herpes simplex virus
Q. Are cold sores contagious? My boyfriend has cold sores on his mouth. Can I catch it from him? If so, how can I prevent catching it?