Shingles may have additional symptoms, depending on the dermatome involved. The trigeminal nerve is the most commonly involved nerve, of which the ophthalmic division is the most commonly involved branch. When the virus is reactivated in this nerve branch it is termed "zoster ophthalmicus". The skin of the forehead, upper eyelid and orbit of the eye may be involved. Zoster ophthalmicus occurs in approximately 10% to 25% of cases. In some people, symptoms may include conjunctivitis, keratitis, uveitis, and optic nerve that can sometimes cause chronic ocular inflammation, loss of vision, and debilitating pain.

"Shingles oticus", also known as Ramsay Hunt syndrome type II, involves the ear. It is thought to result from the virus spreading from the facial nerve to the vestibulocochlear nerve. Symptoms include hearing loss and vertigo (rotational dizziness).

Shingles may occur in the mouth if the maxillary or mandibular division of the trigeminal nerve is affected, in which the rash may appear on the mucous membrane of the upper jaw (usually the palate, sometimes the gums of the upper teeth) or the lower jaw (tongue or gums of the lower teeth) respectively. Oral involvement may occur alone or in combination with a rash on the skin over the cutaneous distribution of the same trigeminal branch. As with shingles of the skin, the lesions tend to only involve one side, distinguishing it from other oral blistering conditions. In the mouth, shingles appears initially as 1–4 mm opaque blisters (vesicles), which break down quickly to leave ulcers that heal within 10–14 days. The prodromal pain (before the rash) may be confused with toothache. Sometimes this leads to unnecessary dental treatment. Post herpetic neuralgia uncommonly is associated with shingles in the mouth. Unusual complications may occur with intra-oral shingles that are not seen elsewhere. Due to the close relationship of blood vessels to nerves, the virus can spread to involve the blood vessels and compromise the blood supply, sometimes causing ischemic necrosis. Therefore, oral involvement rarely causes complications such as osteonecrosis, tooth loss, periodontitis (gum disease), pulp calcification, pulp necrosis, periapical lesions and tooth developmental anomalies.

The earliest symptoms of shingles, which include headache, fever, and malaise, are nonspecific, and may result in an incorrect diagnosis. These symptoms are commonly followed by sensations of burning pain, itching, hyperesthesia (oversensitivity), or paresthesia ("pins and needles": tingling, pricking, or numbness). Pain can be mild to extreme in the affected dermatome, with sensations that are often described as stinging, tingling, aching, numbing or throbbing, and can be interspersed with quick stabs of agonizing pain.

Shingles in children is often painless, but people are more likely to get shingles as they age, and the disease tends to be more severe.

In most cases after one to two days, but sometimes as long as three weeks, the initial phase is followed by the appearance of the characteristic skin rash. The pain and rash most commonly occurs on the torso, but can appear on the face, eyes or other parts of the body. At first the rash appears similar to the first appearance of hives; however, unlike hives, shingles causes skin changes limited to a dermatome, normally resulting in a stripe or belt-like pattern that is limited to one side of the body and does not cross the midline. "Zoster sine herpete" ("zoster without herpes") describes a person who has all of the symptoms of shingles except this characteristic rash.

Later the rash becomes vesicular, forming small blisters filled with a serous exudate, as the fever and general malaise continue. The painful vesicles eventually become cloudy or darkened as they fill with blood, and crust over within seven to ten days; usually the crusts fall off and the skin heals, but sometimes, after severe blistering, scarring and discolored skin remain.

Neonatal herpes simplex is a HSV infection in an infant. It is a rare but serious condition, usually caused by vertical transmission of HSV-1 or -2) from mother to newborn. During immunodeficiency, herpes simplex can cause unusual lesions in the skin. One of the most striking is the appearance of clean linear erosions in skin creases, with the appearance of a knife cut. Herpetic sycosis is a recurrent or initial herpes simplex infection affecting primarily the hair follicles. Eczema herpeticum is an infection with herpesvirus in patients with chronic atopic dermatitis may result in spread of herpes simples throughout the eczematous areas.

Herpetic keratoconjunctivitis, a primary infection, typically presents as swelling of the conjunctiva and eyelids (blepharoconjunctivitis), accompanied by small white itchy lesions on the surface of the cornea.

Herpetic sycosis is a recurrent or initial herpes simplex infection affecting primarily the hair follicle.

Herpes infections usually show no symptoms; when symptoms do appear they typically resolve within two weeks. 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.

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). Primary HSV infections in adults often results in pharyngitis similar to that observed in glandular fever (infectious mononucleosis), but gingivostomatitis is less likely.

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), 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.

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.

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, however, is the constant cracking of the scab as one moves or stretches their 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".

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". 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.

The term "labia" means "lip". Herpes labialis does not refer to the labia of the genitals, though the origin of the word is the same. When the viral infection affects both face and mouth, the broader term "orofacial herpes" is used, whereas the term "herpetic stomatitis" is used to specifically describe infection of the mouth; "stomatitis" is derived from the Greek word stoma that means "mouth".

HSV infection causes several distinct medical disorders. Common infection of the skin or mucosa may affect the face and mouth (orofacial herpes), genitalia (genital herpes), or hands (herpetic whitlow). More serious disorders occur when the virus infects and damages the eye (herpes keratitis), or invades the central nervous system, damaging the brain (herpes encephalitis). People with immature or suppressed immune systems, such as newborns, transplant recipients, or people with AIDS, are prone to severe complications from HSV infections. HSV infection has also been associated with cognitive deficits of bipolar disorder, and Alzheimer's disease, although this is often dependent on the genetics of the infected person.

In all cases, HSV is never removed from the body by the immune system. Following a primary infection, the virus enters the nerves at the site of primary infection, migrates to the cell body of the neuron, and becomes latent in the ganglion. As a result of primary infection, the body produces antibodies to the particular type of HSV involved, preventing a subsequent infection of that type at a different site. In HSV-1-infected individuals, seroconversion after an oral infection prevents additional HSV-1 infections such as whitlow, genital herpes, and herpes of the eye. Prior HSV-1 seroconversion seems to reduce the symptoms of a later HSV-2 infection, although HSV-2 can still be contracted.

Many people infected with HSV-2 display no physical symptoms—individuals with no symptoms are described as asymptomatic or as having subclinical herpes.

People with herpes esophagitis experience pain with eating and trouble swallowing. Other symptoms can include food impaction, hiccups, weight loss, fever, and on rare occasions upper gastrointestinal bleeding as noted in the image above and tracheoesophageal fistula. Frequently one can see herpetiform lesions in the mouth and lips.

Anterior uveitis develops in 40–50% of cases with HZO within 2 weeks of onset of the skin rashes. Typical HZO keratitis at least mild iritis, especially if Hutchinson's sign is positive for the presence of vescicles upon the tip of the nose.

Features:

This non-granulomatous iridocyclitis is associated with:

- Small keratic precipitates

- Mild aqueous flare

- Occasionally haemorrhagic hypopion.

HZO uveitis is associated with complications such as iris atrophy and secondary glaucoma are not uncommon. Complicated cataract may develop in the late stages of the disease.

In males, the lesions occur on the glans penis, shaft of the penis or other parts of the genital region, on the inner thigh, buttocks, or anus. In females, lesions appear on or near the pubis, clitoris or other parts of the vulva, buttocks or anus.

Other common symptoms include pain, itching, and burning. Less frequent, yet still common, symptoms include discharge from the penis or vagina, fever, headache, muscle pain (myalgia), swollen and enlarged lymph nodes and malaise. Women often experience additional symptoms that include painful urination (dysuria) and cervicitis. Herpetic proctitis (inflammation of the anus and rectum) is common for individuals participating in anal intercourse.

After 2–3 weeks, existing lesions progress into ulcers and then crust and heal, although lesions on mucosal surfaces may never form crusts. In rare cases, involvement of the sacral region of the spinal cord can cause acute urinary retention and one-sided symptoms and signs of myeloradiculitis (a combination of myelitis and radiculitis): pain, sensory loss, abnormal sensations (paresthesia) and rash. Historically, this has been termed Elsberg syndrome, although this entity is not clearly defined.

Herpes gladiatorum is characterized by a rash with clusters of sometimes painful fluid-filled blisters, often on the neck, chest, face, stomach, and legs. The infection is often accompanied by lymphadenopathy (enlargement of the lymph nodes), fever, sore throat, and headache. Often, the accompanying symptoms are much more of an inconvenience than the actual skin blisters and rash.

Each blister contains infectious virus particles (virions). Close contact, particularly abrasive contact as found in contact sports, causes the infected blisters to burst and pass the infection along. Autoinoculation (self-infection) can occur through self-contact, leading to infection at multiple sites on the body.

Herpes gladiatorum symptoms may last up to a few weeks, and if they occur during the first outbreak, they can be more pronounced. In recurrences of the ailment, symptoms are milder, even if lesions still tend to occur. With recurrent infections scabs may form at 3 days yet the lesions are still considered infectious up til 6.4 days after starting oral antiviral medications. Healing takes place without leaving scars. It is possible that the condition evolves asymptomatically and sores are never present.

Herpes gladiatorum is one of the most infectious of herpes-caused diseases, and is transmissible by skin-to-skin contact. The disease was first described in the 1960s in the "New England Journal of Medicine". It is caused by contagious infection with human herpes simplex virus type 1 (HSV-1), which more commonly causes oral herpes (cold sores). Another strain, HSV-2 usually causes genital herpes, although the strains are very similar and either can cause herpes in any location.

While the disease is commonly passed through normal human contact, it is strongly associated with contact sports—outbreaks in sporting clubs being relatively common.

Other names for the disease are herpes rugbiorum or "scrumpox" (after rugby football), "wrestler's herpes" or "mat pox" (after wrestling). In one of the largest outbreaks ever among high-school wrestlers at a four-week intensive training camp, HSV was identified in 60 of 175 wrestlers. Lesions were on the head in 73 percent of the wrestlers, the extremities in 42 percent, and the trunk in 28 percent. Physical symptoms sometimes recur in the skin. Previous adolescent HSV-1 seroconversion would preclude most herpes gladiatorum, but being that stress and trauma are recognized triggers, such a person would be likely to infect others.

Any potential ocular involvement should be assessed by an ophthalmologist as complications such as episcleritis and uveitis may occur.

Neonatal herpes manifests itself in three forms: skin, eyes, and mouth herpes (SEM) sometimes referred to as "localized", disseminated herpes (DIS), and central nervous system herpes(CNS).

- SEM herpes is characterized by external lesions but no internal organ involvement. Lesions are likely to appear on trauma sites such as the attachment site of fetal scalp electrodes, forceps or vacuum extractors that are used during delivery, in the margin of the eyes, the nasopharynx, and in areas associated with trauma or surgery (including circumcision).

- DIS herpes affects internal organs, particularly the liver.

- CNS herpes is an infection of the nervous system and the brain that can lead to encephalitis. Infants with CNS herpes present with seizures, tremors, lethargy, and irritability, they feed poorly, have unstable temperatures, and their fontanelle (soft spot of the skull) may bulge.

CNS herpes is associated with highest morbidity, and DIS herpes has a higher mortality rate. These categories are not mutually exclusive and there is often overlap of two or more types. SEM herpes has the best prognosis of the three, however, if left untreated it may progress to disseminated or CNS herpes with its attendant increases in mortality and morbidity.

Death from neonatal HSV disease in the U.S. is currently decreasing; The current death rate is about 25%, down from as high as 85% in untreated cases just a few decades ago. Other complications from neonatal herpes include prematurity with approximately 50% of cases having a gestation of 38 weeks or less, and a concurrent sepsis in approximately one quarter of cases that further clouds speedy diagnosis.

Herpes esophagitis is a viral infection of the esophagus caused by "Herpes simplex virus" (HSV).

While the disease most often occurs in immunocompromised patients, including post-chemotherapy, immunosuppression with organ transplants and in AIDS, herpes esophagitis can also occur in immunocompetent individuals.

Genital herpes can be spread by viral shedding prior to and following the visual signs of symptoms.

This classic herpetic lesion consists of a linear branching corneal ulcer (dendritic ulcer). During eye exam the defect is examined after staining with fluorescein dye. The underlying cornea has minimal inflammation.

Patients with epithelial keratitis complain of foreign-body sensation, light sensitivity, redness and blurred vision.

Focal or diffuse reduction in corneal sensation develops following recurrent epithelial keratitis.

In immune deficient patients or with the use of corticosteroids the ulcer may become large and in these cases it is called geographic ulcer.

Recurrent herpes of the eye is caused by reactivation of the virus in a latently infected sensory ganglion, transport of the virus down the nerve axon to sensory nerve endings, and subsequent infection of ocular surface.

The following classification of herpes simplex keratitis is important for understanding this disease:

The early (prodromal) symptoms in adolescents and adults are nausea, loss of appetite, aching muscles, and headache. This is followed by the characteristic rash or oral sores, malaise, and a low-grade fever that signal the presence of the disease. Oral manifestations of the disease (enanthem) not uncommonly may precede the external rash (exanthem). In children the illness is not usually preceded by prodromal symptoms, and the first sign is the rash or the spots in the oral cavity. The rash begins as small red dots on the face, scalp, torso, upper arms and legs; progressing over 10–12 hours to small bumps, blisters and pustules; followed by umbilication and the formation of scabs.

At the blister stage, intense itching is usually present. Blisters may also occur on the palms, soles, and genital area. Commonly, visible evidence of the disease develops in the oral cavity and tonsil areas in the form of small ulcers which can be painful or itchy or both; this enanthem (internal rash) can precede the exanthem (external rash) by 1 to 3 days or can be concurrent. These symptoms of chickenpox appear 10 to 21 days after exposure to a contagious person. Adults may have a more widespread rash and longer fever, and they are more likely to experience complications, such as varicella pneumonia.

Because watery nasal discharge containing live virus usually precedes both exanthem (external rash) and enanthem (oral ulcers) by 1 to 2 days, the infected person actually becomes contagious one to two days before recognition of the disease. Contagiousness persists until all vesicular lesions have become dry crusts (scabs), which usually entails four or five days, by which time nasal shedding of live virus ceases.

The condition usually resolves by itself within a couple of weeks. The rash may, however, last for up to one month. Chickenpox is contagious starting from one to two days before the appearance of the rash and lasts until the lesions have crusted.

Chickenpox is rarely fatal, although it is generally more severe in adult men than in women or children. Non-immune pregnant women and those with a suppressed immune system are at highest risk of serious complications. Arterial ischemic stroke (AIS) associated with chickenpox in the previous year accounts for nearly one third of childhood AIS. The most common late complication of chickenpox is shingles (herpes zoster), caused by reactivation of the "varicella zoster" virus decades after the initial, often childhood, chickenpox infection.

Neonatal herpes simplex is a rare but serious condition, usually caused by vertical transmission of herpes simplex virus from mother to newborn. Around 1 in every 3,500 babies in the United States contract the infection.

Most individuals with HSE show a decrease in their level of consciousness and an altered mental state presenting as confusion, and changes in personality. Increased numbers of white blood cells can be found in patient's cerebrospinal fluid, without the presence of pathogenic bacteria and fungi. Patients typically have a fever and may have seizures. The electrical activity of the brain changes as the disease progresses, first showing abnormalities in one temporal lobe of the brain, which spread to the other temporal lobe 7–10 days later. Imaging by CT or MRI shows characteristic changes in the temporal lobes (see Figure). Definite diagnosis requires testing of the cerebrospinal fluid (CSF) by a lumbar puncture (spinal tap) for presence of the virus. The testing takes several days to perform, and patients with suspected Herpes encephalitis should be treated with acyclovir immediately while waiting for test results.

Herpesviral encephalitis is encephalitis due to herpes simplex virus.

Herpes simplex encephalitis (HSE) is a viral infection of the human central nervous system. It is estimated to affect at least 1 in 500,000 individuals per year and some studies suggest an incidence rate of 5.9 cases per 100,000 live births. The majority of cases of herpes encephalitis are caused by herpes simplex virus-1 (HSV-1), the same virus that causes cold sores. 57% of American adults are infected with HSV-1, which is spread through droplets, casual contact, and sometimes sexual contact, though most infected people never have cold sores. About 10% of cases of herpes encephalitis are due to HSV-2, which is typically spread through sexual contact. About 1 in 3 cases of HSE result from primary HSV-1 infection, predominantly occurring in individuals under the age of 18; 2 in 3 cases occur in seropositive persons, few of whom have history of recurrent orofacial herpes. Approximately 50% of individuals who develop HSE are over 50 years of age.

Chickenpox, also known as varicella, is a highly contagious disease caused by the initial infection with varicella zoster virus (VZV). The disease results in a characteristic skin rash that forms small, itchy blisters, which eventually scab over. It usually starts on the chest, back, and face then spreads to the rest of the body. Other symptoms may include fever, tiredness, and headaches. Symptoms usually last five to seven days. Complications may occasionally include pneumonia, inflammation of the brain, and bacterial skin infections. The disease is often more severe in adults than in children. Symptoms begin 10 to 21 days after exposure to the virus.

Chickenpox is an airborne disease which spreads easily through the coughs and sneezes of an infected person. It may be spread from one to two days before the rash appears until all lesions have crusted over. It may also spread through contact with the blisters. Those with shingles may spread chickenpox to those who are not immune through contact with the blisters. The disease can usually be diagnosed based on the presenting symptom; however, in unusual cases it may be confirmed by polymerase chain reaction (PCR) testing of the blister fluid or scabs. Testing for antibodies may be done to determine if a person is or is not immune. People usually only get chickenpox once. Although reinfections by the virus occur, these reinfections usually do not cause any symptoms.

The varicella vaccine has resulted in a decrease in the number of cases and complications from the disease. It protects about 70 to 90 percent of people from disease with a greater benefit for severe disease. Routine immunization of children is recommended in many countries. Immunization within three days of exposure may improve outcomes in children. Treatment of those infected may include calamine lotion to help with itching, keeping the fingernails short to decrease injury from scratching, and the use of paracetamol (acetaminophen) to help with fevers. For those at increased risk of complications antiviral medication such as aciclovir are recommended.

Chickenpox occurs in all parts of the world. In 2013 there were 140 million cases of chickenpox and herpes zoster worldwide. Before routine immunization the number of cases occurring each year was similar to the number of people born. Since immunization the number of infections in the United States has decreased nearly 90%. In 2015 chickenpox resulted in 6,400 deaths globally – down from 8,900 in 1990. Death occurs in about 1 per 60,000 cases. Chickenpox was not separated from smallpox until the late 19th century. In 1888 its connection to shingles was determined. The first documented use of the term "chicken pox" was in 1658. Various explanations have been suggested for the use of "chicken" in the name, one being the relative mildness of the disease.

Characteristics of a viral infection can include pain, swelling, redness, impaired function, fever, drowsiness, confusion and convulsions.

The most common diseases caused by chronic viral infections are subacute-sclerosing panencephalitis, progressive multifocal leukoencephalopathy, retrovirus disease and spongiform encephalopathies.

Though caused by different infections, the signs and symptoms of TORCH syndrome are consistent. They include hepatosplenomegaly (enlargement of the liver and spleen), fever, lethargy, difficulty feeding, anemia, petechiae, purpurae, jaundice, and chorioretinitis. The specific infection may cause additional symptoms.

TORCH syndrome may develop before birth, causing stillbirth, in the neonatal period, or later in life.