Varicella zoster virus (VZV) has a high level of infectivity and has a worldwide prevalence. Shingles is a re-activation of latent VZV infection: zoster can only occur in someone who has previously had chickenpox (varicella).

Shingles has no relationship to season and does not occur in epidemics. There is, however, a strong relationship with increasing age. The incidence rate of shingles ranges from 1.2 to 3.4 per 1,000 person‐years among younger healthy individuals, increasing to 3.9–11.8 per 1,000 person‐years among those older than 65 years, and incidence rates worldwide are similar.

This relationship with age has been demonstrated in many countries, and is attributed to the fact that cellular immunity declines as people grow older.

Another important risk factor is immunosuppression. Other risk factors include psychological stress. According to a study in North Carolina, "black subjects were significantly less likely to develop zoster than were white subjects." It is unclear whether the risk is different by gender. Other potential risk factors include mechanical trauma and exposure to immunotoxins.

There is no strong evidence for a genetic link or a link to family history. A 2008 study showed that people with close relatives who had had shingles were twice as likely to develop it themselves, but a 2010 study found no such link.

Adults with latent VZV infection who are exposed intermittently to children with chickenpox receive an immune boost. This periodic boost to the immune system helps to prevent shingles in older adults. When routine chickenpox vaccination was introduced in the United States, there was concern that, because older adults would no longer receive this natural periodic boost, there would be an increase in the incidence of shingles.

Multiple studies and surveillance data, at least when viewed superficially, demonstrate no consistent trends in incidence in the U.S. since the chickenpox vaccination program began in 1995. However, upon closer inspection, the two studies that showed no increase in shingles incidence were conducted among populations where varicella vaccination was not as yet widespread in the community. A later study by Patel "et al." concluded that since the introduction of the chickenpox vaccine, hospitalization costs for complications of shingles increased by more than $700 million annually for those over age 60. Another study by Yih "et al". reported that as varicella vaccine coverage in children increased, the incidence of varicella decreased, and the occurrence of shingles among adults increased by 90%. The results of a further study by Yawn "et al". showed a 28% increase in shingles incidence from 1996 to 2001. It is likely that incidence rate will change in the future, due to the aging of the population, changes in therapy for malignant and autoimmune diseases, and changes in chickenpox vaccination rates; a wide adoption of zoster vaccination could dramatically reduce the incidence rate.

In one study, it was estimated that 26% of those who contract shingles eventually present complications. Postherpetic neuralgia arises in approximately 20% of people with shingles. A study of 1994 California data found hospitalization rates of 2.1 per 100,000 person-years, rising to 9.3 per 100,000 person-years for ages 60 and up. An earlier Connecticut study found a higher hospitalization rate; the difference may be due to the prevalence of HIV in the earlier study, or to the introduction of antivirals in California before 1994.

The duration of the visible blistering caused by varicella zoster virus varies in children usually from 4 to 7 days, and the appearance of new blisters begins to subside after the fifth day. Chickenpox infection is milder in young children, and symptomatic treatment, with sodium bicarbonate baths or antihistamine medication may ease itching. It is recommended to keep new infants from birth up to age 6 months away from an infected person for 10 to 21 days because their immune systems are not developed enough to handle the stress it can bring on. Paracetamol (acetaminophen) is widely used to reduce fever. Aspirin, or products containing aspirin, should not be given to children with chickenpox, as it can cause Reye's Syndrome.

In adults, the disease is more severe, though the incidence is much less common. Infection in adults is associated with greater morbidity and mortality due to pneumonia (either direct viral pneumonia or secondary bacterial pneumonia), bronchitis (either viral bronchitis or secondary bacterial bronchitis), hepatitis, and encephalitis. In particular, up to 10% of pregnant women with chickenpox develop pneumonia, the severity of which increases with onset later in gestation. In England and Wales, 75% of deaths due to chickenpox are in adults. Inflammation of the brain, or encephalitis, can occur in immunocompromised individuals, although the risk is higher with herpes zoster. Necrotizing fasciitis is also a rare complication.

Varicella can be lethal to adults with impaired immunity. The number of people in this high-risk group has increased, due to the HIV epidemic and the increased use of immunosuppressive therapies. Varicella is a particular problem in hospitals, when there are patients with immune systems weakened by drugs (e.g., high-dose steroids) or HIV.

Secondary bacterial infection of skin lesions, manifesting as impetigo, cellulitis, and erysipelas, is the most common complication in healthy children. Disseminated primary varicella infection usually seen in the immunocompromised may have high morbidity. Ninety percent of cases of varicella pneumonia occur in the adult population. Rarer complications of disseminated chickenpox include myocarditis, hepatitis, and glomerulonephritis.

Hemorrhagic complications are more common in the immunocompromised or immunosuppressed populations, although healthy children and adults have been affected. Five major clinical syndromes have been described: febrile purpura, malignant chickenpox with purpura, postinfectious purpura, purpura fulminans, and anaphylactoid purpura. These syndromes have variable courses, with febrile purpura being the most benign of the syndromes and having an uncomplicated outcome. In contrast, malignant chickenpox with purpura is a grave clinical condition that has a mortality rate of greater than 70%. The cause of these hemorrhagic chickenpox syndromes is not known.

The rash and pain usually subside within three to five weeks, but about one in five people develop a painful condition called postherpetic neuralgia, which is often difficult to manage. In some people, shingles can reactivate presenting as "zoster sine herpete": pain radiating along the path of a single spinal nerve (a "dermatomal distribution"), but without an accompanying rash. This condition may involve complications that affect several levels of the nervous system and cause many cranial neuropathies, polyneuritis, myelitis, or aseptic meningitis. Other serious effects that may occur in some cases include partial facial paralysis (usually temporary), ear damage, or encephalitis. During pregnancy, first infections with VZV, causing chickenpox, may lead to infection of the fetus and complications in the newborn, but chronic infection or reactivation in shingles are not associated with fetal infection.

There is a slightly increased risk of developing cancer after a shingles infection. However, the mechanism is unclear and mortality from cancer did not appear to increase as a direct result of the presence of the virus. Instead, the increased risk may result from the immune suppression that allows the reactivation of the virus.

Although shingles typically resolves within 3–5 weeks, certain complications may arise:

- Secondary bacterial infection

- Motor involvement, including weakness especially in "motor herpes zoster"

- Eye involvement: trigeminal nerve involvement (as seen in herpes ophthalmicus) should be treated early and aggressively as it may lead to blindness. Involvement of the tip of the nose in the zoster rash is a strong predictor of herpes ophthalmicus.

- Postherpetic neuralgia, a condition of chronic pain following shingles

Developing countries are more severely affected by TORCH syndrome.

After a chickenpox infection, the virus remains dormant in the body's nerve tissues. The immune system keeps the virus at bay, but later in life, usually in an adult, it can be reactivated and cause a different form of the viral infection called shingles (also known as herpes zoster).

The United States Advisory Committee on Immunization Practices (ACIP) suggests that every adult over the age of 60 years get the "herpes zoster" vaccine.

Shingles affects one in five adults infected with chickenpox as children, especially those who are immune-suppressed, particularly from cancer, HIV, or other conditions. Stress can bring on shingles as well, although scientists are still researching the connection. Shingles are most commonly found in adults over the age of 60 who were diagnosed with chickenpox when they were under the age of 1.

Many viral infections of the central nervous system occur in seasonal peaks or as epidemics, whereas others, such as herpes simplex encephalitis, are sporadic. In endemic areas it is mostly a disease of children, but as the disease spreads to new regions, or nonimmune travelers visit endemic regions, nonimmune adults are also affected.

Following active infection, herpes viruses establish a latent infection in sensory and autonomic ganglia of the nervous system. The double-stranded DNA of the virus is incorporated into the cell physiology by infection of the nucleus of a nerve's cell body. HSV latency is static; no virus is produced; and is controlled by a number of viral genes, including latency-associated transcript.

Many HSV-infected people experience recurrence within the first year of infection. Prodrome precedes development of lesions. Prodromal symptoms include tingling (paresthesia), itching, and pain where lumbosacral nerves innervate the skin. Prodrome may occur as long as several days or as short as a few hours before lesions develop. Beginning antiviral treatment when prodrome is experienced can reduce the appearance and duration of lesions in some individuals. During recurrence, fewer lesions are likely to develop and are less painful and heal faster (within 5–10 days without antiviral treatment) than those occurring during the primary infection. Subsequent outbreaks tend to be periodic or episodic, occurring on average four or five times a year when not using antiviral therapy.

The causes of reactivation are uncertain, but several potential triggers have been documented. A 2009 study showed the protein VP16 plays a key role in reactivation of the dormant virus. Changes in the immune system during menstruation may play a role in HSV-1 reactivation. Concurrent infections, such as viral upper respiratory tract infection or other febrile diseases, can cause outbreaks. Reactivation due to other infections is the likely source of the historic terms 'cold sore' and 'fever blister'.

Other identified triggers include local injury to the face, lips, eyes, or mouth; trauma; surgery; radiotherapy; and exposure to wind, ultraviolet light, or sunlight.

The frequency and severity of recurrent outbreaks vary greatly between people. Some individuals' outbreaks can be quite debilitating, with large, painful lesions persisting for several weeks, while others experience only minor itching or burning for a few days. Some evidence indicates genetics play a role in the frequency of cold sore outbreaks. An area of human chromosome 21 that includes six genes has been linked to frequent oral herpes outbreaks. An immunity to the virus is built over time. Most infected individuals experience fewer outbreaks and outbreak symptoms often become less severe. After several years, some people become perpetually asymptomatic and no longer experience outbreaks, though they may still be contagious to others. Immunocompromised individuals may experience longer, more frequent, and more severe episodes. Antiviral medication has been proven to shorten the frequency and duration of outbreaks. Outbreaks may occur at the original site of the infection or in proximity to nerve endings that reach out from the infected ganglia. In the case of a genital infection, sores can appear at the original site of infection or near the base of the spine, the buttocks, or the back of the thighs.

HSV-2-infected individuals are at higher risk for acquiring HIV when practicing unprotected sex with HIV-positive persons, in particular during an outbreak with active lesions.

As with almost all sexually transmitted infections, women are more susceptible to acquiring genital HSV-2 than men. On an annual basis, without the use of antivirals or condoms, the transmission risk of HSV-2 from infected male to female is about 8–11%.

This is believed to be due to the increased exposure of mucosal tissue to potential infection sites. Transmission risk from infected female to male is around 4–5% annually. Suppressive antiviral therapy reduces these risks by 50%. Antivirals also help prevent the development of symptomatic HSV in infection scenarios, meaning the infected partner will be seropositive but symptom-free by about 50%. Condom use also reduces the transmission risk significantly. Condom use is much more effective at preventing male-to-female transmission than "vice versa". Previous HSV-1 infection may reduce the risk for acquisition of HSV-2 infection among women by a factor of three, although the one study that states this has a small sample size of 14 transmissions out of 214 couples.

However, asymptomatic carriers of the HSV-2 virus are still contagious. In many infections, the first symptom people will have of their own infections is the horizontal transmission to a sexual partner or the vertical transmission of neonatal herpes to a newborn at term. Since most asymptomatic individuals are unaware of their infection, they are considered at high risk for spreading HSV.

In October 2011, the anti-HIV drug tenofovir, when used topically in a microbicidal vaginal gel, was reported to reduce herpes virus sexual transmission by 51%.

Meningitis is a very common in children. Newborns can develop herpes virus infections through contact with infected secretions in the birth canal. Other viral infections are acquired by breathing air contaminated with virus-containing droplets exhaled by an infected person. Arbovirus infections are acquired from bites by infected insects (called epidemic encephalitis). Viral central nervous system infections in newborns and infants usually begin with fever. The inability of infants to communicate directly makes it difficult to understand their symptoms. Newborns may have no other symptoms and may initially not otherwise appear ill. Infants older than a month or so typically become irritable and fussy and refuse to eat. Vomiting is common. Sometimes the soft spot on top of a newborn's head (fontanelle) bulges, indicating an increase in pressure on the brain. Because irritation of the meninges is worsened by movement, an infant with meningitis may cry more, rather than calm down, when picked up and rocked. Some infants develop a strange, high-pitched cry. Infants with encephalitis often have seizures or other abnormal movements. Infants with severe encephalitis may become lethargic and comatose and then die. To make the diagnosis of meningitis or the diagnosis of encephalitis, doctors do a spinal tap (lumbar puncture) to obtain cerebrospinal fluid (CSF) for laboratory analysis in children.

TORCH syndrome can be prevented by treating an infected pregnant person, thereby preventing the infection from affecting the fetus.

Key measures to prevent outbreaks of the disease are maintaining hygiene standards and using screening to exclude persons with suspicious infections from engaging in contact sports. A skin check performed before practice or competition takes place can identify individuals who should be evaluated, and if necessary treated by a healthcare professional. In certain situations, i.e. participating in wrestling camps, consider placing participants on valacyclovir 1GM daily for the duration of camp. 10-year study has shown 89.5% reduction in outbreaks and probable prevention of contracting the virus. Medication must be started 5 days before participation to ensure proper concentrations exist.

Herpes gladiatorum is only caused by the herpes simplex virus. Shingles, also manifesting as skin rashes with blisters, is caused by a different virus, herpes zoster. Other agents may cause skin infections, for example ringworm is primarily due to the fungal dermatophyte, "T. tonsurans". Impetigo, cellulitis, folliculitis and carbuncles are usually due to "Staphylococcus aureus" or Beta-hemolytic streptococcus bacteria. These less common forms can be potentially more serious. Anti-viral treatments will not have an effect in non-viral cases. Bacterial infections must be treated with antibiotics and fungal infections with anti-fungal medication.

Herpesviral Encephalitis can be treated with high-dose intravenous acyclovir. Without treatment, HSE results in rapid death in approximately 70% of cases; survivors suffer severe neurological damage. When treated, HSE is still fatal in one-third of cases, and causes serious long-term neurological damage in over half of survivors. Twenty percent of treated patients recover with minor damage. Only a small population of survivors (2.5%) regain completely normal brain function. Indeed, many amnesic cases in the scientific literature have etiologies involving HSE. Earlier treatment (within 48 hours of symptom onset) improves the chances of a good recovery. Rarely, treated individuals can have relapse of infection weeks to months later. There is evidence that aberrant inflammation triggered by herpes simplex can result in granulomatous inflammation in the brain, which responds to steroids. While the herpes virus can be spread, encephalitis itself is not infectious. Other viruses can cause similar symptoms of encephalitis, though usually milder (Herpesvirus 6, varicella zoster virus, Epstein-Barr, cytomegalovirus, coxsackievirus, etc.).

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.

Viral encephalitis is a type of encephalitis caused by a virus.

It is unclear if anticonvulsants used in people with viral encephalitis would prevent seizures.

In the United States there are typically between a couple of hundred and a couple of thousand cases a year.

The most common preventative measure against mumps is a vaccination with a mumps vaccine, invented by American microbiologist Maurice Hilleman at Merck. The vaccine may be given separately or as part of the MMR immunization vaccine that also protects against measles and rubella. In the US, MMR is now being supplanted by MMRV, which adds protection against chickenpox (varicella, HHV3). The WHO (World Health Organization) recommends the use of mumps vaccines in all countries with well-functioning childhood vaccination programmes. In the United Kingdom it is routinely given to children at age 13 months with a booster at 3–5 years (preschool) This confers lifelong immunity. The American Academy of Pediatrics recommends the routine administration of MMR vaccine at ages 12–15 months and at 4–6 years. In some locations, the vaccine is given again between four and six years of age, or between 11 and 12 years of age if not previously given. The efficacy of the vaccine depends on the strain of the vaccine, but is usually around 80 percent. The Jeryl Lynn strain is most commonly used in developed countries but has been shown to have reduced efficacy in epidemic situations. The Leningrad-Zagreb strain commonly used in developing countries appears to have superior efficacy in epidemic situations.

Because of the outbreaks within college and university settings, many governments have established vaccination programs to prevent large-scale outbreaks. In Canada, provincial governments and the Public Health Agency of Canada have all participated in awareness campaigns to encourage students ranging from grade one to college and university to get vaccinated.

Some anti-vaccine activists protest against the administration of a vaccine against mumps, claiming that the attenuated vaccine strain is harmful, and/or that the wild disease is beneficial. There is no evidence whatsoever to support the claim that the wild disease is beneficial, or that the MMR vaccine is harmful. Claims have been made that the MMR vaccine is linked to autism and inflammatory bowel disease, including one study by Andrew Wakefield. The paper was discredited and retracted in 2010 and Wakefield was later stripped of his license after his work was found to be an "elaborate fraud". Also, subsequent studies indicate no link between vaccination with the MMR and autism. Since the dangers of the disease are well known, and the dangers of the vaccine are quite minimal, most doctors recommend vaccination.

The WHO, the American Academy of Pediatrics, the Advisory Committee on Immunization Practices of the Centers for Disease Control and Prevention, the American Academy of Family Physicians, the British Medical Association and the Royal Pharmaceutical Society of Great Britain currently recommend routine vaccination of children against mumps. The British Medical Association and Royal Pharmaceutical Society of Great Britain had previously recommended against general mumps vaccination, changing that recommendation in 1987.

Before the introduction of the mumps vaccine, the mumps virus was the leading cause of viral meningoencephalitis in the United States. However, encephalitis occurs rarely (less than two per 100,000). In one of the largest studies in the literature, the most common symptoms of mumps meningoencephalitis were found to be fever (97 percent), vomiting (94 percent) and headache (88.8 percent). The mumps vaccine was introduced into the United States in December 1967: since its introduction there has been a steady decrease in the incidence of mumps and mumps virus infection. There were 151,209 cases of mumps reported in 1968. From 2001 to 2008, the case average was only 265 per year, excluding an outbreak of less than 6000 cases in 2006 attributed largely to university contagion in young adults.

The most common causes of viral meningitis in the United States are non-polio enteroviruses. The viruses that cause meningitis are typically acquired from sick contacts. However, in most cases, people infected with viruses that may cause meningitis do not actually develop meningitis.

Viruses that can cause meningitis include:

Although for a long time, the cause of Mollaret's meningitis was not known, recent work has associated this problem with herpes simplex viruses, which cause cold sores, occular herpes as well as genital herpes.

Cases of Mollaret's resulting from varicella zoster virus infection, diagnosed by polymerase chain reaction (PCR), have been documented. In these cases, PCR for herpes simplex was negative.

Some patients also report frequent shingles outbreaks. Varicella zoster virus, which causes chickenpox and shingles is part of the herpes family, and is sometimes called "herpes zoster virus". CNS epidermoid cysts can give rise to Mollaret's meningitis especially with surgical manipulation of cyst contents.

A familial association, where more than one family member had Mollaret's, has been documented.

Babies can also become infected by their mothers during birth. Some infectious agents may be transmitted to the embryo or fetus in the uterus, while passing through the birth canal, or even shortly after birth. The distinction is important because when transmission is primarily during or after birth, medical intervention can help prevent infections in the infant.

During birth, babies are exposed to maternal blood, body fluids, and to the maternal genital tract without the placental barrier intervening. Because of this, blood-borne microorganisms (hepatitis B, HIV), organisms associated with sexually transmitted disease (e.g., "Neisseria gonorrhoeae" and "Chlamydia trachomatis"), and normal fauna of the genitourinary tract (e.g., "Candida albicans") are among those commonly seen in infection of newborns.

Types of encephalitis in humans include:

- Arbovirus encephalitis

- La Crosse encephalitis

- Enterovirus

- California encephalitis virus

- Japanese encephalitis

- St. Louis encephalitis

- Eastern equine encephalitis virus

- Western equine encephalitis virus

- Venezuelan equine encephalitis virus

- Murray Valley encephalitis virus

- Tick-borne meningoencephalitis

- Powassan encephalitis

- West Nile virus

- Herpes simplex

- Human herpesvirus 6

- Varicella zoster virus

- Rabies

- HIV

- H5N1 encephalitis

- Nipah virus encephalitis

- Lymphocytic choriomeningitis, which also causes encephalitis

The best prevention against viral pneumonia is vaccination against influenza, adenovirus, chickenpox, herpes zoster, measles, and rubella.

The embryo and fetus have little or no immune function. They depend on the immune function of their mother. Several pathogens can cross the placenta and cause (perinatal) infection. Often, microorganisms that produce minor illness in the mother are very dangerous for the developing embryo or fetus. This can result in spontaneous abortion or major developmental disorders. For many infections, the baby is more at risk at particular stages of pregnancy. Problems related to perinatal infection are not always directly noticeable.

It has been proposed that viral meningitis might lead to inflammatory injury of the vertebral artery wall.

The Meningitis Research Foundation is conducting a study to see if new genomic techniques can the speed, accuracy and cost of diagnosing meningitis in children in the UK. The research team will develop a new method to be used for the diagnosis of meningitis, analysing the genetic material of microorganisms found in CSF (cerebrospinal fluid). The new method will first be developed using CSF samples where the microorganism is known, but then will be applied to CSF samples where the microorganism is unknown (estimated at around 40%) to try and identify a cause.

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.