Herpes simplex virus

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any member of a unique class of infectious agents, which were originally distinguished by their smallness (hence, they were described as “filtrable” because of their ability to pass through fine ceramic filters that blocked all cells, including bacteria) and their inability to replicate outside of and without assistance of a living host cell. Because these properties are shared by certain bacteria (rickettsiae, chlamydiae), viruses are now characterized by their simple organization and their unique mode of replication. A virus consists of genetic material, which may be either DNA or RNA, and is surrounded by a protein coat and, in some viruses, by a membranous envelope.

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.
Comparison of shapes and sizes of viruses.
attenuated virus one whose pathogenicity has been reduced by serial animal passage or other means.
B19 virus a species belonging to the genus Erythrovirus that binds to the erythrocyte P blood group antigen and is the cause of erythema infectiosum. In patients with hemolytic anemia or sickle cell disease it causes aplastic crisis; it can also cause acute arthritis. Fetal infection can cause hydrops fetalis and spontaneous abortion or death in utero. Persistent infection in immunocompromised patients can lead to chronic bone marrow failure. Called also human parvovirus B19.
bacterial virus one that is capable of producing transmissible lysis of bacteria; see also bacteriophage.
coryza virus rhinovirus.
Coxsackie virus coxsackievirus.
defective virus one that cannot be completely replicated or cannot form a protein coat; in some cases replication can proceed if missing gene functions are supplied by other viruses; see also helper virus.
dengue virus a flavivirus, existing as four antigenically related but distinct types (designated 1, 2, 3, and 4), that causes both the classic and hemorrhagic forms of dengue.
DNA virus a virus whose genome consists of DNA.
Ebola virus an RNA virus almost identical to the Marburg virus but serologically distinct; it causes a disease similar to that caused by the Marburg virus.
encephalomyocarditis virus an enterovirus that causes mild aseptic meningitis and encephalomyocarditis.
enteric v's enterovirus.
enteric orphan v's orphan viruses isolated from the intestinal tract of humans and other animals.
Epstein-Barr virus (EBV) a herpeslike virus that causes infectious mononucleosis and is associated with Burkitt's lymphoma and nasopharyngeal carcinoma; see also epstein-barr virus.
fixed virus a virus whose virulence and incubation period have been stabilized by serial passage and have remained fixed during further transmission, as opposed to a street virus.
helper virus one that aids in the development of a defective virus by supplying or restoring the activity of the viral gene or enabling it to form a protein coat.
hepatitis A virus (HAV) any virus of the genus Hepatovirus that causes hepatitis a. This has the most rapid onset of the hepatitis viruses affecting humans; transmission is easier than for the hepatitis B and C viruses, but infection generally does not persist. While infection with this virus alone is usually not life-threatening, coincident infection with hepatitis C virus is generally rapidly fatal.
hepatitis B virus (HBV) a species of genus Orthohepadnavirus that causes hepatitis b.
hepatitis C virus a species of genus Hepacivirus that causes hepatitis c; its latency period may last 30 years or more.
hepatitis D virus (HDV) (hepatitis delta virus) an unclassified defective RNA virus, thought of as a parasite of the hepatitis B virus and transmitted in the same manner; it requires enzymes and other assistance from HBV to replicate. This virus magnifies the pathogenicity of hepatitis B virus many times and is the etiologic agent of hepatitis d.
hepatitis E virus an enterically transmitted calicivirus that causes hepatitis e.
hepatitis G virus (HGV) a parenterally transmitted flavivirus originally isolated from a patient with chronic hepatitis; most infections are benign, and it is uncertain what role, if any, HGV plays in the etiology of liver disease.
hepatotropic virus a virus that primarily affects the liver, such as the hepatitis viruses.
herpes virus herpesvirus.
herpes simplex virus former name for any virus that causes herpes simplex, now called human herpesviruses; see herpesvirus.
human immunodeficiency virus (HIV) either of two species of lentiviruses that cause acquired immunodeficiency syndrome (AIDS). HIV-1 is found around the world and HIV-2 is found primarily in West Africa. Progression of HIV-2 infection to AIDS is generally slower and less extreme than that of HIV-1. The virus is believed to induce permanent infection and has a propensity toward a subset of T lymphocytes called the CD4 cells. The infected cells become dysfunctional and eventually the host's immune system is overwhelmed or exhausted; death ensues, usually as a result of infection. The virus is not transmitted through casual contact; the most common routes of transmission are through sexual intercourse, direct exposure to contaminated blood, and transplacental transmission from mother to fetus.
Human immunodeficiency virus: retrovirus particle. From Copstead, 1995.
human T-cell leukemia virus (human T-cell lymphotropic virus) former names for human T-lymphotropic virus.
human T-lymphotropic virus (HTLV) either of two related species of retroviruses that have an affinity for the helper cell type of T lymphocytes. HTLV-1 causes chronic infection and is associated with adult T-cell leukemia and a type of myelopathy. HTLV-2 has been isolated from an atypical variant of hairy cell leukemia and from patients with other hematological disorders, but no clear association with disease has been established.
influenza virus any of a group of orthomyxoviruses that cause influenza; there are at least three serotypes or species (A, B, and C). Serotype A viruses are subject to major antigenic changes (antigenic shifts) as well as minor gradual antigenic changes (antigenic drift) and cause widespread epidemics and pandemics. Serotypes B and C are chiefly associated with sporadic epidemics.
influenza A virus (influenza B virus) (influenza C virus) species in the genera Influenzavirus A, Influenzavirus B, and Influenzavirus C; see influenza virus.
La Crosse virus a virus of the California serogroup of the genus Bunyavirus, the etiologic agent of La Crosse encephalitis.
latent virus one that ordinarily occurs in a noninfective state and is demonstrable by indirect methods that activate it.
lytic virus one that is replicated in the host cell and causes death and lysis of the cell.
maedi/visna virus a lentivirus that is the etiologic agent of a type of pneumonia in sheep.
Marburg virus an RNA virus occurring in Africa, transmitted by insect bites, and causing marburg virus disease.
masked virus latent virus.
measles virus a paramyxovirus that is the cause of measles.
mumps virus a paramyxovirus that causes mumps and sometimes tenderness and swelling of the testes, pancreas, ovaries, or other organs.
Norwalk virus a calicivirus that is common cause of epidemics of acute gastroenteritis, with diarrhea and vomiting that last 24 to 48 hours.
oncogenic v's an epidemiologic class of viruses that are acquired by close contact or injection and cause usually persistent infection; they may induce cell transformation and malignancy.
orphan v's viruses isolated in tissue culture, but not found specifically associated with any disease.
parainfluenza virus any of various paramyxoviruses that cause upper respiratory tract disease of varying severity.
poliomyelitis virus see poliovirus.
pox virus poxvirus.
rabies virus an RNA virus of the rhabdovirus group that causes rabies.
respiratory syncytial virus (RSV) any of a genus of single-stranded paramyxoviruses; the name is derived from the type of disease produced (respiratory infection) and the microscopic appearance of the viruses in cell cultures. RSV can cause a wide variety of respiratory disorders ranging from a mild cold to serious or even fatal disease of the lung in the very young and very old. It regularly produces an outbreak of infection each winter and virtually disappears in the summer months. The most severe infections in children are in the very young, especially those who are preterm, immunologically compromised, or suffering from a congenital heart defect or preexisting lung disorder. Adults at risk for infection include parents and others who are repeatedly exposed to young children, for example, pediatric nurses and day care attendants. The course of infection tends to be milder in adults than in children and about 15 per cent of affected adults have no symptoms. In the very elderly these infections may have the same degree of seriousness and clinical manifestations as in the very young.
RNA virus a virus whose genome consists of RNA.
rubella virus a togavirus that is the etiologic agent of rubella.
satellite virus a strain of virus unable to replicate except in the presence of helper virus; considered to be deficient in coding for capsid formation.
simian-human immunodeficiency virus a chimeric, engineered virus with the envelope of human immunodeficiency virus and the cytoplasm and nucleus of simian immunodeficiency virus; it is used in animal models because it is a better mimic of HIV than SIV is.
simian immunodeficiency virus (SIV) a lentivirus closely related to human immunodeficiency virus that causes inapparent infection in African green monkeys and a disease resembling acquired immunodeficiency syndrome in macaques and chimpanzees.
slow virus any virus that remains latent for long periods in the infected host before the appearance of clinical symptoms.
smallpox virus variola virus.
street virus virus from a naturally infected animal, as opposed to a laboratory-adapted strain of the virus.
vaccinia virus a species of orthopoxvirus that does not occur in nature and has been propagated for many years only in the laboratory for use as an active vaccine against smallpox. The present virus is derived from the original one used by Jenner, obtained from the lesions of cowpox, but the origin of the original virus remains unclear.
varicella-zoster virus former name for human herpesvirus 3; see herpesvirus.
variola virus the virtually extinct orthopoxvirus that is the etiologic agent of smallpox. No natural infection has occurred since 1977, and no reservoir of the virus now exists.
West Nile virus a virus of the genus Flavivirus, the cause of West Nile encephalitis; it is transmitted by Culex mosquitoes, with wild birds serving as the reservoir. It was originally endemic in Africa, Asia, and Europe, but recently spread to North America.
wild-type virus street virus.
Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing, and Allied Health, Seventh Edition. © 2003 by Saunders, an imprint of Elsevier, Inc. All rights reserved.

her·pes sim·plex

a variety of infections caused by herpesvirus types 1 and 2; type 1 infections are marked most commonly by the eruption of one or more groups of vesicles on the vermilion border of the lips or at the external nares, type 2 by such lesions on the genitalia; both types often are recrudescent and reappear during other febrile illnesses or even physiologic states such as menstruation. The viruses frequently become latent and may not be expressed for years.
Farlex Partner Medical Dictionary © Farlex 2012

her·pes sim·plex

(hĕrpēz simpleks)
A variety of infections caused by herpesvirus types 1 and 2; type 1 infections are marked most commonly by the eruption of one or more groups of vesicles on the vermilion border of the lips or at the external nares, type 2 by such lesions on the genitalia; both types often are recrudescent and reappear during other febrile illnesses or even physiologic states such as menstruation.
Synonym(s): herpes facialis, herpes febrilis, herpes labialis, Simplexvirus.
Medical Dictionary for the Health Professions and Nursing © Farlex 2012

Herpes simplex virus; HSV

A very common sexually transmitted infection; Type-2 HSV causes genital herpes and type-1 HSV usually causes cold sores but also can cause genital herpes; congenital HSV can be transmitted to the fetus during birth if the mother has an active infection.
Gale Encyclopedia of Medicine. Copyright 2008 The Gale Group, Inc. All rights reserved.

Herpes Simplex Virus

DRG Category:606
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.

Genetic considerations

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.

Physical examination

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.

Diagnostic highlights

TestNormal ResultAbnormality With ConditionExplanation
Polymerase chain reaction (PCR)Negative for HSV DNAPositive for HSV DNADemonstrates presence of viruses
Viral cultureNegativePositive for HSV; differentiates between HSV-1 and HSV-2Demonstrates 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


Anxiety related to a knowledge deficit of cause, treatment, and prevention of HSV


Anxiety control; Coping; Social interaction skills; Acceptance: Health status; Symptom control behavior


Anxiety 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.

Pharmacologic highlights

Medication or Drug ClassDosageDescriptionRationale
AntiviralDepends on the drug and if the outbreak is primary or recurrentPenciclovir (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).

Documentation guidelines

  • 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.

Diseases and Disorders, © 2011 Farlex and Partners

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?

A. Cold sores contain the HSV-1 virus, which is the herpes simplex virus . While your boyfriend has cold sores, he should wash his hands often, especially after touching his face. He shouldn't share cups and eating utensils with others since he is very contagious. You should not kiss him or touch the cold sores either, in order not to be infected.

More discussions about Herpes simplex virus
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References in periodicals archive ?
(a) Sera from individuals working at monkey forests in SE Asia [19, 20] were tested by ELISA as described [21, 22] against HSV1 (dark blue), HSV2 (light blue), BV (red), HVP2 (orange), squirrel monkey herpesvirus (light green), and spider monkey herpesvirus (dark green) antigens.
Interestingly, infiltration of [CD4.sup.+] and [CD8.sup.+] T cells was also increased by IVIG at day 7 pi (Figures 2(e) and 2(f)) and ~40% of infiltrating [CD8.sup.+] T cells were HSV1 specific as determined by tetramer staining at day 21 pi (Figures 3(d) and 3(e); representative FACS plot shown in Supplementary Figure 1 available online at https://doi.org/10.1155/2017/5238402).
We initially hypothesized that the treatment with N2a tumor cells transduced with HSV1 (M002) encoding murine IL12 will demonstrate enhanced antitumor activity compared to M002 alone (or serve as more efficient vaccination vehicle than virus alone).
In particular, as emerging from the review below, a growing interest is devoted to investigating the effects of H1N1 in PD (Section 4.1), of HSV1 in AD (Section 4.2), and of retroviruses in ALS (Section 4.3).
Result of cross-reactivity tests Pathogen CMV/FAM Internal control Cy5 Parvovirus B19 - + TTV - + HPV - + EBV - + HBV - + HSV1 - + HSV2 - + TTV: Transfusion transmitted virus; HPV: Human papillomavirus; EBV: Epstein-Barr virus; HBV: Hepatitis B virus; HSV: Herpes simplex virus TABLE 6.
Viradux Research, Ltd is a provider of anti-herpetic treatment solutions targeted at the rapid resolution of symptoms related to HSV1 and HSV2 infections.
Os virus mais comuns sao os Papovavirus (que provocam as verrugas) e herpes simples (HSV1 e HSV2), ocorrendo frequentemente em dentistas, enfermeiros e patologistas (2,3,6,18).
After confirming HSV1 infection, the replication of HSV-1 was inhibited using three siRNA molecules against the UL 39 gene from HSV-1 (si-UL 39-1, si-UL 39-2, si-UL39-3).
Herpetic gingivostomatitis is caused by herpes simplex virus-1 (HSV1) and communicated through personal contact, e.g., transmission via the saliva of the mother.
Virological tests ([micro]mmunoglobulin M-IgM and immunoglobulin G -IgG for Coxsackievirus, Adenovirus, herpes simplex virus 1- HSV1, varicella-zoster virus--VZV) were negative, except for IgG, which was positive for adenovirus and HSV 1.
By freezing in -80[degrees]C and thawing for three times, HSV1 particles were released.