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Cold sore
Other namesfever blister,[1] herpes labialis,[1] oral herpes,[2] orolabial herpes[3]
A cold sore on the lower lip. Note the blisters in a group marked by an arrow.
SpecialtyInfectious disease
SymptomsBurning pain followed by small blisters or sores[1]
ComplicationsHerpes encephalitis, herpetic whitlow[4]
Usual onset< 20 years old[1]
DurationHeals within 10 days[1]
CausesTypically herpes simplex virus type 1 (direct contact)[1][5]
Diagnostic methodUsually based on symptoms[1]
Differential diagnosisHerpangina, aphthous stomatitis, impetigo, mononucleosis[6]
PreventionAvoiding exposure, antiviral medication[7][8]
TreatmentZinc oxide, anesthetic, or antiviral cream,[1] antivirals by mouth[7]
PrognosisGood[1]
Frequency2.5 per 1,000 affected per year[1]

A cold sore[a] is a type of herpes infection caused by the herpes simplex virus that affects primarily the lip.[1] Symptoms typically include a burning pain followed by small blisters or sores.[1] The first attack may also be accompanied by fever, sore throat, and enlarged lymph nodes.[1][9] The rash usually heals within ten days, but the virus remains dormant in the trigeminal ganglion.[1] The virus may periodically reactivate to create another outbreak of sores in the mouth or lip.[1]

The cause is usually herpes simplex virus type 1 (HSV-1) and occasionally herpes simplex virus type 2 (HSV-2).[1] The infection is typically spread between people by direct non-sexual contact.[5] Attacks can be triggered by sunlight, fever, psychological stress, or a menstrual period.[1][9] Direct contact with the genitals can result in genital herpes.[1] Diagnosis is usually based on symptoms but can be confirmed with specific testing.[1][9]

Prevention includes avoiding kissing or using the personal items of a person who is infected.[8] A zinc oxide, anesthetic, or antiviral cream appears to decrease the duration of symptoms by a small amount.[1] Antiviral medications may also decrease the frequency of outbreaks.[1][7]

About 2.5 per 1000 people are affected with outbreaks in any given year.[1] After one episode about 33% of people develop subsequent episodes.[1] Onset often occurs in those less than 20 years old and 80% develop antibodies for the virus by this age.[1] In those with recurrent outbreaks, these typically happen less than three times a year.[10] The frequency of outbreaks generally decreases over time.[1]

Terminology

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The term labia means "lip" in Latin.[11] Herpes labialis does not refer to the labia of the vulva, though the origin of the word is the same. The colloquial terms for this condition ("cold sore" and "fever blister") come from the fact that herpes labialis is often triggered by fever, for example, as may occur during an upper respiratory tract infection (i.e. a cold).[12] When the viral infection affects both face and mouth, the broader term orofacial herpes is sometimes used, whereas herpetic stomatitis describes infection of the mouth specifically; stomatitis is derived from the Greek word stoma, which means "mouth".[13]

Signs and symptoms

[edit]
Herpes labialis spread over the entire circumference of the lips.

Herpes infections usually show no symptoms;[1] when symptoms do appear they typically resolve within two weeks.[14] The main symptom of oral infection is inflammation of the mucosa of the cheek and gums—known as acute herpetic gingivostomatitis—which occurs within 5–10 days of infection. Other symptoms may also develop, including headache, nausea, dizziness and painful ulcers—sometimes confused with canker sores—fever, and sore throat.[14]

Primary HSV infection in adolescents frequently manifests as severe pharyngitis with lesions developing on the cheek and gums. Some individuals develop difficulty in swallowing (dysphagia) and swollen lymph nodes (lymphadenopathy).[14] Primary HSV infections in adults often results in pharyngitis similar to that observed in glandular fever (infectious mononucleosis), but gingivostomatitis is less likely.[15][16]

Recurrent oral infection is more common with HSV-1 infections than with HSV-2. Symptoms typically progress in a series of eight stages:

  1. Latent (weeks to months incident-free): The remission period; After initial infection, the viruses move to sensory nerve ganglia (trigeminal ganglion),[1] where they reside as lifelong, latent viruses. Asymptomatic shedding of contagious virus particles can occur during this stage.
  2. Prodromal (day 0–1): Symptoms often precede a recurrence. Symptoms typically begin with tingling (itching) and reddening of the skin around the infected site. This stage can last from a few days to a few hours preceding the physical manifestation of an infection and is the best time to start treatment.
  3. Inflammation (day 1): Virus begins reproducing and infecting cells at the end of the nerve. The healthy cells react to the invasion with swelling and redness displayed as symptoms of infection.
  4. Pre-sore (day 2–3): This stage is defined by the appearance of tiny, hard, inflamed papules and vesicles that may itch and are painfully sensitive to touch. In time, these fluid-filled blisters form a cluster on the lip (labial) tissue, the area between the lip and skin (vermilion border), and can occur on the nose, chin, and cheeks.[17]
  5. Open lesion (day 4): This is the most painful and contagious of the stages. All the tiny vesicles break open and merge to create one big, open, weeping ulcer. Fluids are slowly discharged from blood vessels and inflamed tissue. This watery discharge is teeming with active viral particles and is highly contagious. Depending on the severity, one may develop a fever and swollen lymph glands under the jaw.[18]
  6. Crusting (day 5–8): A honey/golden crust starts to form from the syrupy exudate. This yellowish or brown crust or scab is not made of active virus but from blood serum containing useful proteins such as immunoglobulins. This appears as the healing process begins. The sore is still painful at this stage, but more painful is the constant cracking of the scab as with movement or stretching of the lips, as in smiling or eating. Virus-filled fluid will still ooze out of the sore through any cracks.
  7. Healing (day 9–14): New skin begins to form underneath the scab as the virus retreats into latency. A series of scabs will form over the sore (called Meier Complex), each one smaller than the last. During this phase irritation, itching, and some pain are common.
  8. Post-scab (12–14 days): A reddish area may linger at the site of viral infection as the destroyed cells are regenerated. Virus shedding can still occur during this stage.

The recurrent infection is thus often called herpes simplex labialis. Rare reinfections occur inside the mouth (intraoral HSV stomatitis) affecting the gums, alveolar ridge, hard palate, and the back of the tongue, possibly accompanied by herpes labialis.[14]

A lesion caused by herpes simplex can occur in the corner of the mouth and be mistaken for angular cheilitis of another cause. Sometimes termed "angular herpes simplex".[19] A cold sore at the corner of the mouth behaves similarly to elsewhere on the lips. Rather than utilizing antifungal creams, angular herpes simplex is treated in the same way as a cold sore, with topical antiviral drugs.[20]

Causes

[edit]

Herpes labialis infection occurs when the herpes simplex virus comes into contact with oral mucosal tissue or abraded skin of the mouth.[17] Infection by the type 1 strain of herpes simplex virus (HSV-1) is most common; however, cases of oral infection by the type 2 strain are increasing.[14]

Oral HSV-2 shedding is rare, and "usually noted in the context of first episode genital herpes."[21] In general, both types can cause oral or genital herpes.[22][23][24]

Cold sores are the result of the virus reactivating in the body. Once HSV-1 has entered the body, it never leaves. The virus moves from the mouth to remain latent in the central nervous system. In approximately one-third of people, the virus can "wake up" or reactivate to cause disease. When reactivation occurs, the virus travels down the nerves to the skin where it may cause blisters (cold sores) around the lips or mouth area.[25]

In case of Herpes zoster the nose can be affected.[26]

Cold sore outbreaks may be influenced by stress, menstruation, sunlight,[27] sunburn, fever, dehydration, or local skin trauma.[28] Surgical procedures such as dental or neural surgery, lip tattooing, or dermabrasion are also common triggers. HSV-1 can in rare cases be transmitted to newborn babies by family members or hospital staff who have cold sores; this can cause a severe disease called neonatal herpes simplex.

People can transfer the virus from their cold sores to other areas of the body, such as the eye, skin, or fingers; this is called autoinoculation. Eye infection, in the form of conjunctivitis or keratitis, can happen when the eyes are rubbed after touching the lesion. Finger infection (herpetic whitlow) can occur when a child with cold sores or primary HSV-1 infection sucks his fingers.[29][30]

Blood tests for herpes may differentiate between type 1 and type 2. When a person is not experiencing any symptoms, a blood test alone does not reveal the site of infection. Genital herpes infections occurred with almost equal frequency as type 1 or 2 in younger adults when samples were taken from genital lesions. Herpes in the mouth is more likely to be caused by type 1, but (see above) also can be type 2. The only way to know for certain if a positive blood test for herpes is due to infection of the mouth, genitals, or elsewhere, is to sample from lesions.[31][32] This is not possible if the affected individual is asymptomatic. The body's immune system typically fights the virus.[33]

Prevention

[edit]

Primary infection

[edit]

The likelihood of the infection can be reduced through avoidance of touching an area with active infection, avoiding contact sports during active infection, and frequent hand washing, use of mouth rinsing (anti-viral, anti-bacterial) products.[34][35][36][1] During active infection (outbreaks with oral lesions) avoid oral-to-oral kissing and oral-genital sex without protection.[34][35][1][37] HSV1 can be transmitted to uninfected partners through oral sex, resulting in genital lesions.[1][34][35] Healthcare workers working with patients who have active lesions are advised to use gloves, eye protection, and mouth protection during physical, mucosal, and bronchoscopic procedures and examinations.[35]

Recurrent infection

[edit]

In some cases, sun exposure can lead to HSV-1 reactivation, therefore use of zinc-based sunscreen or topical and oral therapeutics such as acyclovir and valacyclovir may prove helpful.[38][39][1][35] Other triggers for recurrent herpetic infection includes fever, common cold, fatigue, emotional stress, trauma, sideropenia, oral cancer therapy, immunosuppression, chemotherapy, oral and facial surgery, menstruation, and epidural morphine, and upset GI.[39] Surgical procedures like nerve root decompression, facial dermabrasion, and ablative laser resurfacing can increase risks of reactivation by 50–70%.[35]

Treatment

[edit]

Despite no cure or vaccine for the virus, a human body's immune system and specific antibodies typically fight the virus.[33] Treatment options include no treatment, topical creams (indifferent, antiviral, and anaesthetic), and oral antiviral medications. Indifferent topical creams include zinc oxide and glycerin cream, which can have itching and burning sensation as side effects and docosanol.[40][1] Docosanol, a saturated fatty alcohol, was approved by the United States Food and Drug Administration for herpes labialis in adults with properly functioning immune systems. It is comparable in effectiveness to prescription topical antiviral agents. Due to docosanol's mechanism of action, there is little risk of drug resistance.[40] Antivirals creams include acyclovir and penciclovir, which can speed healing by as much as 10%.[41][1] Oral antivirals include acyclovir, valaciclovir, and famciclovir.[1] Famciclovir or valacyclovir, taken in pill form, can be effective using a single day, high-dose application and is more cost effective and convenient than the traditional treatment of lower doses for 5–7 days.[42] Anaesthetic creams include lidocaine and prilocaine which has shown reduction in duration of subjective symptoms and eruptions.[1]

Treatment recommendations vary on the severity of the symptoms and chronicity of the infection. Treatment with oral antivirals such as acyclovir in children within 72 hours of illness onset has shown to shorten duration of fever, odynophagia, and lesions, and to reduce viral shedding.[35][1] For patient with mild to moderate symptoms, local anaesthetic such as lidocaine for pain without antiviral may be sufficient. However, those with occasional severe recurrences of lesions may use oral antivirals.[1][35] Patients with severe cases such as those with frequent recurrences of lesions, presence of disfiguring lesions, and serious systematic complications may need chronic suppressive therapy on top of the antiviral therapies.[35][1]

Mouth-rinse with combinations of ethanol and essential oils against herpes as therapeutic method is recommended by the German Society of Hospital Hygiene.[43] Further research into virucidal effects of essential oils exists.[44][45]

Epidemiology

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Herpes labialis is common throughout the world. A large survey of young adults on six continents reported that 33% of males and 28% of females had herpes labialis on two or more occasions during the year before the study. The lifetime prevalence in the United States of America is estimated at 20–45% of the adult population. Lifetime prevalence in France was reported by one study as 32% in males and 42% in females. In Germany, the prevalence was reported at 32% in people aged between 35 and 44 years, and 20% in those aged 65–74. In Jordan, another study reported a lifetime prevalence of 26%.[46]

Research

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Main article: Herpes simplex research

Research has gone into vaccines and drugs for both prevention and treatment of herpes infections.[47][48][49][50][51][52]

Notes

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References

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[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Cold sore

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from Grokipedia
A cold sore, also known as a fever blister or herpes labialis, is a common viral infection that causes small, painful, fluid-filled blisters typically on the border of the lips (the edge where the lip meets the skin, on the upper or lower lip), at the corners of the mouth (mouth angles), and sometimes spreading to under the nose, cheeks, or chin; less commonly, they appear inside the mouth on the mucosa or around the , , or . These blisters usually appear in clusters and result from reactivation of the type 1 (HSV-1), which remains dormant in nerve cells after initial infection. The infection is highly contagious and affects an estimated 64% of people under the age of 50 worldwide, often acquired during childhood through non-sexual contact. The primary cause of cold sores is HSV-1, though HSV-2 (typically associated with ) can occasionally be responsible. Initial infection may be asymptomatic or cause flu-like symptoms, but subsequent outbreaks are triggered by factors such as stress, illness, sunlight exposure, or weakened immunity. Transmission occurs via direct contact with infected saliva, skin, or mucous membranes, especially during active outbreaks when blisters are present, but the virus can also spread asymptomatically. Once infected, the virus cannot be eliminated from the body and may lead to recurrent episodes throughout life. Symptoms typically begin with a tingling, itching, or burning sensation in the affected area, followed by redness and the formation of blisters within 1-2 days. The blisters then burst, ooze, and form a yellowish crust before healing, with the entire process lasting 7-10 days in most cases, though it can extend to 2-4 weeks without intervention. Complications are rare but may include secondary bacterial infections, spread to the eyes (herpetic keratitis), or more frequent outbreaks in immunocompromised individuals. There is no cure for cold sores, but antiviral medications such as acyclovir, valacyclovir, or can reduce outbreak severity, duration, and frequency if started early. Over-the-counter creams, pain relievers, and home remedies like ice or lip balms provide symptomatic relief, while preventive measures include avoiding triggers, using daily , and abstaining from close contact during outbreaks. is usually clinical based on appearance, though lab tests like PCR can confirm HSV in atypical cases.

Overview and Terminology

Definition

A cold sore, also known as herpes labialis, is a recurrent, self-limiting vesicular eruption that typically appears on or around the lips and is caused by infection with type 1 (HSV-1), though type 2 (HSV-2) can occasionally be responsible. These lesions consist of small, fluid-filled blisters that cluster together, often preceded by a prodromal phase, and they generally resolve without scarring within 7 to 10 days. Unlike other manifestations of oral herpes, such as intraoral ulcers or gingivostomatitis, cold sores are distinguished by their external labial location and the characteristic prodromal tingling, itching, or burning sensation that signals impending outbreak. This specificity aids in clinical recognition and differentiates them from similar conditions like or . The condition has been recognized as a distinct entity since ancient times, with descriptions of recurring lip sores appearing in the writings of around 400 BCE, though its infectious nature remained unknown until the . Formal virological definition emerged following the isolation of HSV in 1919 and the serological distinction of HSV-1 from HSV-2 in the 1960s, establishing cold sores as a primary manifestation of HSV-1 reactivation from latency in the .

Etymology and nomenclature

The term "cold sore" emerged in the as a compound of "cold" and "sore," with its earliest recorded use dating to in , reflecting the observed tendency of the lesions to recur during colds, fevers, or cold weather. Earlier references to the condition appear in historical texts, such as 16th-century literature alluding to blisters, and even further back to ancient descriptions of "fever blisters" or "herpetic fever blisters." In medical nomenclature, "cold sore" is synonymous with herpes labialis—Latin for "herpes of the lip"—oral herpes, and fever blister, terms that emphasize the location and recurrent nature of the eruption. The root word "" originates from the herpēs, meaning "to creep," coined by around the 5th century BCE to describe the spreading, serpentine pattern of skin lesions. Advances in during the refined this terminology; the was first isolated in 1919, and by the 1960s, researchers distinguished HSV-1 (primarily causing oral infections like cold sores) from HSV-2, leading to more precise, virus-specific naming conventions. A common lay misconception confuses cold sores with canker sores (aphthous ulcers), which are non-contagious, non-viral ulcers inside the mouth, unlike the viral, externally visible cold sores.

Clinical Presentation

Signs and symptoms

Cold sores, primarily caused by herpes simplex virus type 1 (HSV-1), present with characteristic local and sometimes systemic symptoms during outbreaks. The initial prodromal phase typically involves itching, burning, or tingling sensations at the site, often around the or , occurring 1-2 days before visible lesions emerge. The vesicular stage follows, featuring clusters of small, fluid-filled blisters (usually 1-3 mm in diameter, forming groups up to 2-10 mm) primarily on the lip border (the edge where the lip meets the skin, on the upper or lower lip), at the lip corners (mouth angles), and sometimes spreading to under the nose, on the cheeks, or chin; less commonly inside the mouth on the mucosa. These blisters form on an erythematous base, accompanied by mild pain and swelling. These blisters rupture within 2-4 days, leading to shallow ulceration and subsequent crusting or scabbing, with the full outbreak resolving in 7-10 days. Associated local symptoms include tenderness and regional , particularly in the ; systemic effects such as fever are rare in recurrent episodes but more common in primary infections. Primary infections tend to be more severe, often manifesting as extensive gingivostomatitis with painful oral ulcers, , , and muscle aches, whereas recurrent infections are generally milder and confined to the perioral area. Outbreaks vary in frequency, typically occurring 1-2 times per year, though some individuals may experience more frequent recurrences, and can be triggered by factors like emotional stress, ultraviolet light exposure, or concurrent illness.

Complications and differential diagnosis

Although cold sores typically resolve without long-term effects, rare complications can arise, particularly if the infection spreads or becomes superinfected. Secondary bacterial infections may occur when open sores are colonized by bacteria such as Staphylococcus aureus, leading to cellulitis or impetiginization of the lesions. In severe cases, HSV infection can lead to herpes encephalitis, a life-threatening condition primarily affecting neonates or immunocompromised individuals, with mortality exceeding 70% if untreated. Ocular involvement, such as herpes simplex keratitis, can develop from autoinoculation when virus from lip lesions contacts the eye, potentially causing corneal ulcers and vision impairment if not promptly treated. Individuals with weakened immune systems face heightened risks of more extensive or chronic manifestations. In patients with , particularly those with counts below 100 cells/mm³, cold sores can progress to large, deep, non-healing ulcerations that are painful and prone to secondary infections. Solid organ transplant recipients on immunosuppressive therapy are susceptible to disseminated (HSV) infections, including visceral involvement beyond mucocutaneous sites. Post-2020 studies have identified potential associations between infection or and HSV reactivation, with some evidence suggesting exacerbated oral herpes episodes in affected individuals due to immune dysregulation. In pediatric populations, particularly toddlers, primary HSV-1 infections can lead to severe complications such as extensive gingivostomatitis with widespread mouth sores, swollen gums, fever, and reduced fluid intake. Eczema herpeticum, a disseminated HSV infection occurring in children with atopic dermatitis, is a rare but serious complication characterized by widespread blistering, pain, and flu-like symptoms, potentially requiring hospitalization. For guidance on when to seek medical attention in pediatric cases, including severe, widespread, or prolonged outbreaks, refer to the Diagnosis and Management section. Differentiating cold sores from similar perioral conditions is essential for appropriate management. Angular cheilitis, often due to fungal (Candida) or bacterial causes, presents with fissured, inflamed corners of the mouth without vesicles, unlike the clustered blisters of HSV. Impetigo, a superficial staphylococcal or streptococcal infection, features honey-crusted erosions rather than the vesicular-crusting progression of cold sores, and is a common mimic in children. Aphthous ulcers, which are non-viral and typically intraoral, lack the external lip location and recurrent clustering seen in herpes labialis. Allergic contact dermatitis may mimic irritation with erythema and scaling but usually involves broader exposure to irritants like lip balms and does not form vesicles. Key diagnostic clues for confirming cold sores include the recurrent nature of lesions at the of the lips, prodromal tingling, and grouped vesicles on an erythematous base. Laboratory confirmation can be achieved via Tzanck smear, which reveals multinucleated giant cells, or (PCR) testing for HSV DNA, offering high sensitivity for differentiation from mimics.

Etiology and Pathophysiology

Causative agents

Cold sores, or herpes labialis, are primarily caused by , a double-stranded belonging to the Alphaherpesvirinae subfamily of the family. This establishes lifelong latency in sensory neurons, particularly within the , following initial infection. HSV-1 is highly prevalent worldwide, with seroprevalence estimates indicating that approximately 64% of people under 50 years of age are infected globally, based on 2025 data. The viral structure of HSV-1 consists of an enveloped icosahedral capsid surrounding a linear double-stranded DNA genome of about 152 kilobase pairs (kbp), which encodes roughly 80 genes responsible for replication, assembly, and host interaction. These genes enable the virus to undergo lytic replication in epithelial cells while maintaining latent reservoirs in neurons. Although HSV-1 is the dominant agent, herpes simplex virus type 2 (HSV-2)—typically responsible for genital herpes—can occasionally cause oral lesions, often resulting from oral-genital transmission. HSV-2 shares a similar genomic and structural profile with HSV-1 but exhibits distinct tropism preferences. It is essential to differentiate these agents from varicella-zoster virus (VZV), another member of the Alphaherpesvirinae subfamily, which causes chickenpox during primary infection and shingles upon reactivation but does not produce cold sores.

Viral lifecycle and reactivation

The herpes simplex virus type 1 (HSV-1) initiates primary infection by attaching to and fusing with the plasma membrane of epithelial cells in the oral mucosa or skin, primarily via receptors such as nectin-1 and herpesvirus entry mediator (HVEM). Following fusion, the viral capsid is transported along microtubules to the nuclear pore, where the double-stranded DNA genome is injected into the nucleus to commence the lytic replication cycle. This cycle unfolds in sequential gene expression phases: immediate-early (α) genes, including ICP0 and ICP4, are transcribed first using host RNA polymerase II, establishing a permissive environment by counteracting cellular defenses and activating subsequent transcription; early (β) genes then encode enzymes for viral DNA replication, such as the helicase-primase complex (UL5-UL8-UL52) and DNA polymerase (UL30); finally, late (γ) genes produce structural proteins for capsid assembly, envelopment, and maturation. Newly assembled nucleocapsids acquire a primary envelope by budding through the inner nuclear membrane, followed by de-envelopment in the perinuclear space and secondary envelopment at trans-Golgi or endosomal membranes, culminating in virion release via exocytosis and cell lysis. During primary infection, lytic replication predominantly occurs in mucosal epithelial cells, leading to local spread and in some cases, while a of virions invades sensory nerve terminals at the infection site. These virions are transported retrogradely via dynein motors along axons to the trigeminal or other sensory ganglia, evading immune detection to establish latency. In the neuronal nuclei, the viral genome circularizes and persists as an extrachromosomal , maintained without lytic replication through epigenetic silencing via formation on viral promoters. The latency-associated transcript (LAT) locus is actively transcribed, producing non-coding RNAs that promote neuronal survival by inhibiting , modulating structure, and suppressing lytic , thus ensuring long-term genome persistence. Reactivation from latency is precipitated by environmental or physiological stimuli, including UV radiation, hormonal changes, or stress, which alter neuronal signaling or dynamics to derepress the viral genome. This leads to within the , followed by anterograde of new virions via motors back to the peripheral , distinguishing recurrent infections—which originate from ganglionic reservoirs and produce milder, localized outbreaks—from primary infections driven by mucosal lytic spread.

Transmission and Prevention

Modes of transmission

Cold sores, caused by herpes simplex virus type 1 (HSV-1), are primarily transmitted through direct contact with infected or mucosal secretions from an individual harboring the virus. This occurs via activities such as kissing or sharing utensils, , or razors, with transmission involving contact with mucous membranes or abraded skin. The risk is highest during periods of active lesions, when vesicular fluid contains high concentrations of virus, typically ranging from 10^6 to 10^8 virions per milliliter. HSV-1 can also spread through asymptomatic , where the virus is released from the without visible symptoms or lesions. Studies indicate that subclinical shedding occurs in a notable proportion of seropositive individuals, with recent estimating rates around 3-5% of days for oral sites in those with genital HSV-1, though higher episodic shedding is common in oral infections overall. Vertical transmission of HSV-1 from to child is rare, primarily occurring during delivery if the mother has a primary genital near term, with low risk (less than 1%) associated with recurrent infections. In children, HSV-1 leading to cold sores is often acquired in through non-sexual contact, such as close familial interactions involving exchange. Following exposure, the for HSV-1 infection typically ranges from 2 to 12 days before symptoms manifest.

Preventive measures

Preventing cold sores, caused by type 1 (HSV-1), involves strategies to avoid initial acquisition and minimize recurrences in infected individuals. Primary prevention emphasizes reducing transmission risks, while measures for recurrent cases target triggers and viral reactivation. Behavioral practices are key to limiting spread. Individuals with active outbreaks should avoid direct contact, such as kissing or , and refrain from sharing items like , utensils, or towels that may harbor the . Regular hand , especially after touching the face or sores, further reduces transmission risk. Additionally, applying broad-spectrum or with SPF 30 or higher can prevent (UV) light from triggering recurrences, as UV exposure is a known activator of latent HSV-1. For primary prevention in sexual contexts, disclosing HSV-1 to partners is recommended to facilitate informed decisions. use during oral-genital contact offers partial protection, though efficacy is limited due to potential skin-to-skin transmission beyond covered areas. from sexual activity during outbreaks provides the highest safeguard. In those with frequent recurrences (six or more per year), daily suppressive antiviral therapy is advised. Valacyclovir at 500 mg once daily reduces outbreak frequency by 70-80% and decreases , thereby lowering transmission risk. This approach is supported by clinical guidelines for immunocompetent adults. Lifestyle modifications can help manage triggers for recurrences. Stress reduction techniques, such as or adequate sleep, may lessen outbreak frequency, as emotional and physical stress can reactivate the . Supporting immune function through a balanced diet rich in vitamins (e.g., C and E) and regular exercise is also beneficial, though evidence for specific supplements is limited. During active outbreaks, avoiding acidic, salty, or spicy foods is recommended to prevent irritation of open blisters, which can cause stinging, burning, or prolong healing. Some studies suggest that high-arginine foods, such as nuts and chocolate, may promote viral replication and worsen outbreaks in susceptible individuals, though evidence varies and not all sources agree on strong dietary triggers. Processed foods, refined carbohydrates, and excess sugar may indirectly affect immune function, potentially increasing recurrence risk, but individual triggers vary and direct evidence linking diet to outbreaks is limited. These dietary considerations complement management strategies outlined in the Diagnosis and Management section. Public health efforts include educating individuals about asymptomatic shedding, which occurs in the majority of infected individuals (at least 70% shed monthly) and accounts for most transmissions without visible sores. Awareness campaigns promote consistent preventive behaviors to curb unwitting spread.

Diagnosis and Management

Diagnostic approaches

Diagnosis of cold sores, also known as herpes labialis caused primarily by type 1 (HSV-1), typically begins with clinical evaluation based on patient history and characteristic appearance, such as clustered vesicles on an erythematous base around the or , which is reliable for recurrent cases due to their distinctive progression from to ulceration and crusting. In recurrent episodes, clinical diagnosis alone suffices in most immunocompetent individuals without the need for further testing, as the presentation is often . Laboratory confirmation is pursued when clinical features are atypical or in specific scenarios, with viral culture historically considered the gold standard but limited by its low sensitivity (around 50% for vesicular lesions, lower for crusted ones) and slow turnaround time of 2-5 days. (PCR) testing of lesion swabs has become the preferred method due to its high sensitivity (90-100% for detecting HSV DNA in active lesions) and rapid results, often within hours, making it particularly useful for timely in first episodes or suspected complications. Serologic testing detects antibodies to HSV, with type-specific IgG assays indicating past exposure (sensitivity 80-98%) and persistence lifelong, while IgM tests for acute are unreliable due to cross-reactivity with other viruses and lack of type specificity, and thus not recommended. The Tzanck smear, a rapid cytologic examination of scrapings stained with Wright-Giemsa, reveals multinucleated giant cells suggestive of herpetic but cannot differentiate HSV from varicella-zoster virus (VZV) and has variable sensitivity (60-70%), limiting its utility to quick bedside confirmation in resource-poor settings. Advanced techniques, such as on lesion biopsies or next-generation sequencing, are reserved for atypical presentations, such as in immunocompromised patients where dissemination may occur, offering high specificity for HSV identification but requiring specialized facilities. Testing is indicated for first-episode infections to confirm HSV etiology and type, in immunocompromised individuals with severe or prolonged symptoms to guide management, or when differentials like bacterial or aphthous ulcers are suspected, though routine testing is unnecessary for typical recurrent cold sores.

Treatment options

Treatment of cold sores, or herpes labialis caused by type 1 (HSV-1), primarily involves antiviral medications to reduce outbreak duration and severity when initiated early, ideally at the prodromal stage. Oral antivirals are more effective than topical formulations for shortening healing time by approximately 1 day if started within 72 hours of symptom onset. Recommended options include acyclovir at 400 mg orally three times daily for 7-10 days or 200 mg five times daily for 7-10 days, valacyclovir at 2 grams orally twice daily for 1 day, and at 1,500 mg orally as a single dose. Topical acyclovir 5% cream applied five times daily for 4 days can provide modest benefit but is less efficacious than . Other topical antiviral options include penciclovir 1% cream (e.g., Denavir), applied every two hours while awake for up to four days, which may offer similar benefits to acyclovir cream where available. Symptomatic relief focuses on alleviating , , and discomfort without interfering with . Over-the-counter analgesics such as ibuprofen or acetaminophen can reduce and swelling associated with lesions. Docosanol 10% cream (Abreva), a top over-the-counter option, applied five times daily at the first sign of tingling or symptoms, may shorten healing time by about 12 hours by inhibiting viral fusion to host cells. In some regions, over-the-counter creams containing acyclovir (e.g., Zovirax) or penciclovir (e.g., Denavir) are available as additional topical treatments. Corticosteroids should be avoided, as they may prolong and delay resolution. For young children, such as toddlers around 2 years old, medical attention should be sought if the cold sore is severe, widespread, very painful, lasts more than 10 days, or is associated with mouth sores or swollen gums (gingivostomatitis), reduced drinking or eating, fever, or weakened immunity. In such cases, a doctor may prescribe oral acyclovir or assess for complications. It is always advisable to consult a pharmacist or doctor before initiating any treatment, especially for first outbreaks or extensive sores on the cheeks. Diagnosis should be confirmed to differentiate from mimicking conditions like impetigo or eczema herpeticum. For individuals with frequent or severe recurrent episodes (six or more per year), long-term suppressive therapy with oral antivirals is recommended to reduce outbreak frequency and duration. Acyclovir 400 mg twice daily has been shown to decrease clinical recurrences by 53% and culture-positive episodes by 71% over 4 months, with similar efficacy maintained long-term up to 10 years without significant adverse effects. Valacyclovir 500 mg once or twice daily or famciclovir 250 mg twice daily offer comparable suppression. Self-care measures complement pharmacological treatments by promoting comfort and preventing secondary . Applying wrapped in a cloth to the for 10-15 minutes several times daily can soothe pain and reduce swelling. supplements (1,000-3,000 mg daily) have mixed evidence; while some studies suggest they may inhibit HSV replication by competing with , randomized trials show no significant benefit for treating active sores, though higher doses might reduce recurrence frequency in susceptible individuals. Recent reviews as of 2025 find insufficient evidence to recommend supplements for preventing or treating cold sores. During outbreaks, avoiding acidic, salty, or spicy foods is advisable, as they can irritate open blisters, causing stinging, burning, or prolonging healing. High-arginine foods such as nuts, peanuts, and chocolate may promote viral replication in some individuals according to certain studies and expert recommendations, though evidence varies and not all sources agree on their role as strong triggers. Processed foods, refined carbohydrates, and excess sugar may indirectly impair immune function, potentially worsening outbreaks. Individual dietary triggers vary, and overall evidence linking specific diets directly to triggering or exacerbating outbreaks remains limited. Emerging therapies aim to enhance pain relief and accelerate healing beyond traditional antivirals. or applied to lesions can reduce pain and promote faster crust sloughing, with one study demonstrating improved healing rates when combined with antivirals. Updated guidelines as of 2024 emphasize initiating any intervention as early as possible to maximize efficacy, particularly for immunocompetent patients.

Epidemiology and Impact

Global prevalence

Cold sores, primarily caused by herpes simplex virus type 1 (HSV-1), affect a significant portion of the global population. According to the World Health Organization's 2025 estimates, approximately 3.8 billion people under the age of 50—representing 64% of this demographic—have worldwide, with most cases manifesting as oral . Seroprevalence is notably higher in low- and lower-middle-income regions, exceeding 90% in many African countries, compared to approximately 38% in children and 64% in adults in high-income settings like the (as of 2022 data). In high-income countries like the , HSV-1 seroprevalence is declining at approximately 1% per year. Among those infected, 20-40% experience recurrent outbreaks of oral herpes, with lifetime in the estimated at about 30%, or one-third of the population. Global trends in HSV-1 have remained relatively stable over recent decades, though geographic variations show higher seroprevalence in densely populated urban areas due to closer contact opportunities, while lower rates are observed in isolated or remote populations with limited interpersonal transmission. Children in developing countries represent a key at-risk group, with approximately 50% acquiring by age 5 through close family or community interactions. This early acquisition contributes to the overall global burden, particularly in resource-limited settings where preventive measures are less accessible.

Societal and psychological effects

Cold sores, caused by type 1 (), carry a degree of despite being primarily transmitted through non-sexual means like kissing or sharing utensils, often leading to and among sufferers. This association with viruses, which are sometimes conflated with sexually transmitted infections, can result in avoidance behaviors; for instance, a national survey found that 71% of cold sore sufferers avoided intimacy with partners during outbreaks, while a Canadian survey indicated that 50% reported negative self-image and limitations in social life. The psychological toll of recurrent cold sores includes heightened anxiety and depressive symptoms, particularly among frequent sufferers, as emotional distress can both trigger outbreaks and exacerbate feelings of shame or isolation. Initial diagnosis often provokes strong reactions such as , , or depression, though these typically diminish within six months as individuals adjust to the condition's manageability. Recent studies highlight HSV-1's potential links to broader burdens, including associations with increased depression risk modulated by genetic factors, underscoring the need for support in management. Economically, cold sores impose substantial costs through healthcare expenditures and productivity losses, with the global cold sore treatment market valued at approximately $1.02 billion in 2024, driven largely by over-the-counter and prescription antivirals. , recurrent outbreaks contribute to and reduced work efficiency, compounding the financial strain on individuals and healthcare systems, though precise annual figures for oral HSV-1 remain understudied compared to . Cultural misconceptions perpetuate misinformation about cold sores, such as the myth that home remedies like or can cure them, when in reality, these only provide symptomatic relief without addressing the underlying viral reactivation. Another common belief is that oral cold sores are entirely distinct from and pose no transmission risk, ignoring that HSV-1 can cause genital infections via oral-genital contact in up to 50% of cases. Public health challenges include significant underreporting of cold sores, as up to 90% of HSV-1 infections are or mild, leading many to self-treat with over-the-counter products rather than seek medical evaluation, which hinders accurate tracking. Stigma further discourages disclosure and testing, contributing to gaps in ; awareness campaigns are essential to educate on transmission, reduce , and promote early intervention.

Research and Future Directions

Ongoing studies

Recent genome-wide association studies (GWAS) have identified host genetic variants influencing susceptibility to infectious diseases, with some exploring links to (HSV) infections that cause cold sores. Additionally, polymorphisms in immune-related genes have been implicated in predisposing individuals to more frequent HSV reactivation and shedding. Ongoing into triggers of HSV-1 reactivation is examining the roles of the gut microbiome and hormonal fluctuations. Post-pandemic updates are informed by long-term cohort studies assessing HSV-1 and HSV-2 dynamics. Prospective cohorts have tracked and co-infection patterns, noting changes in HSV-2 prevalence potentially influenced by COVID-19-related immune alterations. The NIAID's 2023-2028 strategic plan, updated in March 2025, emphasizes ongoing cohort efforts to characterize HSV biology and transmission patterns. Monitoring of antiviral resistance remains a priority, particularly for acyclovir-resistant HSV-1 strains in immunocompromised patients, where resistance rates range from 1% to 5% depending on the and treatment duration. A 2025 study in southern reported elevated resistance in hematologic disorder patients, underscoring the need for surveillance in high-risk groups. Case series from the same year documented atypical presentations of resistant infections in immunocompromised individuals with underlying malignancies, highlighting challenges in clinical management. Animal models continue to provide insights into , with and systems being central to current investigations. Guinea pigs serve as the gold standard for modeling genital and orofacial HSV infections, allowing evaluation of spontaneous reactivation and disease progression akin to humans. Recent studies using models have advanced understanding of stress-induced reactivation mechanisms, such as fur plucking to simulate recurrent lesions. A 2025 review affirmed the utility of these models in dissecting viral latency and immune evasion strategies.

Vaccine and therapeutic developments

Efforts to develop vaccines and advanced therapies for , the cause of cold sores, have intensified in recent years, focusing on both prophylactic and therapeutic strategies to address the virus's latency and recurrence. Prophylactic vaccines aim to prevent initial infection, while therapeutic vaccines target individuals already infected to reduce reactivation and shedding. Despite challenges, several candidates are advancing through clinical and preclinical stages, offering hope for improved management beyond current antiviral treatments like acyclovir. mRNA-based vaccines represent a promising frontier, leveraging technology proven effective against other viruses. Moderna's mRNA-1608, a therapeutic vaccine candidate for HSV-2 (with potential cross-protection against HSV-1), completed enrollment in its phase 1/2 trial in March 2024, evaluating safety, immunogenicity, and proof-of-concept clinical benefit in adults aged 18-55 with recurrent . Preclinical studies in animal models demonstrated an 85-100% reduction in genital disease severity, highlighting the platform's potential to elicit robust immune responses against HSV glycoproteins. As of November 2025, the trial data were presented at IDWeek 2025, showing favorable interim safety and immunogenicity results to inform further development. Subunit vaccines targeting glycoprotein D (gD), a key viral entry protein, have provided critical lessons despite past setbacks. The gD/AS04 adjuvant vaccine showed partial efficacy (around 38%) against HSV-1 and HSV-2 genital disease in women seronegative for both viruses in a phase 3 trial but failed overall in mixed populations, eliciting neutralizing antibodies without sufficient T-cell responses to block latency or recurrence. Subsequent analyses revealed that non-neutralizing antibodies and inadequate cellular immunity contributed to the lack of broad protection, informing newer designs that incorporate multiple glycoproteins (e.g., gC, gD, gE) to enhance and T-cell activation. These insights have shifted focus toward multivalent approaches in current pipelines. Gene editing technologies, particularly CRISPR-Cas9 and meganucleases, are emerging as potential curative therapies by targeting latent HSV DNA in neuronal reservoirs. Preclinical studies in 2025 by Excision BioTherapeutics demonstrated that CRISPR-based EBT-104, delivered via AAV9 vectors, nearly eliminated ocular and reduced latent HSV-1 DNA by over 90% in models of herpetic , a complication of cold sores. Similarly, Cancer Center's 2024 work using engineered HSV with gene drives achieved significant reductions during co-infection, suggesting a "" to disrupt latent genomes. These approaches remain in early preclinical phases, with safety profiles showing minimal off-target effects, but challenges include delivery to sensory neurons and long-term efficacy. Novel antivirals like helicase-primase inhibitors offer alternatives to analogs for suppression in recurrent cases. Pritelivir, developed by AiCuris, inhibits HSV replication by blocking the helicase-primase complex essential for viral DNA unwinding, demonstrating superior efficacy to valacyclovir in reducing genital HSV-2 shedding (from 19% to 2.4% of days) in phase 2 trials. A phase 3 trial completed in October 2025 confirmed 's effectiveness in immunocompromised patients with acyclovir-resistant HSV infections, achieving faster resolution and lower viral loads compared to standard care. This oral agent, active against both HSV-1 and HSV-2, is poised for regulatory approval as a suppressive therapy, addressing resistance issues in up to 5-10% of clinical isolates. Another promising antiviral, Assembly Biosciences' ABI-5366, a next-generation helicase-primase inhibitor, showed a 94% reduction in in a Phase Ib reported in August 2025 and is advancing to Phase II for recurrent . Developing therapeutic vaccines for seropositive individuals poses unique challenges, as the virus establishes lifelong latency in neurons, evading immune surveillance and requiring vaccines to boost site-specific T-cell responses to prevent recurrence. Unlike prophylactic vaccines, therapeutic ones must overcome and preexisting antibodies, with early trials showing only modest reductions (15-50%) in shedding without boosters. Strategies like prime-pull vaccination, which attracts T-cells to mucosal sites, have reduced recurrences in animal models but face hurdles in human translation, including adjuvant optimization and targeting neuronal reservoirs. The National Institutes of Health's Strategic Plan for HSV Research (2023-2028) outlines priorities for accelerating and therapy development, emphasizing fundamental and clinical translation. While no HSV vaccines are currently approved, ongoing pipelines suggest potential breakthroughs, with experts projecting approvals for advanced candidates like mRNA-1608 or by the late 2020s if phase 3 data confirm and .

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