Hubbry Logo
ChickenpoxChickenpoxMain
Open search
Chickenpox
Community hub
Chickenpox
logo
8 pages, 0 posts
0 subscribers
Be the first to start a discussion here.
Be the first to start a discussion here.
Chickenpox
Chickenpox
Chickenpox
View on Wikipedia
from Wikipedia

Chickenpox
Other namesvaricella
A patient presenting with the characteristic blisters of chickenpox
SpecialtyInfectious disease
SymptomsSmall, itchy blisters, headache, loss of appetite, tiredness, fever[1]
Usual onset10–21 days after exposure[2]
Duration5–10 days[1]
CausesVaricella zoster virus[3]
PreventionVaricella vaccine[4]
MedicationCalamine lotion, paracetamol (acetaminophen), aciclovir[5]
Deaths6,400 per year (with shingles)[6]

Chickenpox, also known as varicella (/ˌværɪˈsɛlə/ ⓘ VARR-iss-EL-ə), is a highly contagious disease caused by varicella zoster virus (VZV), a member of the herpesvirus family.[3][7][5] The disease results in a characteristic skin rash that forms small, itchy blisters, which eventually scab over.[1] It usually starts on the chest, back, and face.[1] It then spreads to the rest of the body.[1] The rash and other symptoms, such as fever, tiredness, and headaches, usually last five to seven days.[1] Complications may occasionally include pneumonia, inflammation of the brain, and bacterial skin infections.[8] The disease is usually more severe in adults than in children.[9]

Chickenpox is an airborne disease which easily spreads via human-to-human transmission, typically through the coughs and sneezes of an infected person.[5] The incubation period is 10–21 days, after which the characteristic rash appears.[2] It may be spread from one to two days before the rash appears until all lesions have crusted over.[5] It may also spread through contact with the blisters.[5] Those with shingles may spread chickenpox to those who are not immune through contact with the blisters.[5] The disease can usually be diagnosed based on the presenting symptom;[10] however, in unusual cases it may be confirmed by polymerase chain reaction (PCR) testing of the blister fluid or scabs.[9] Testing for antibodies may be done to determine if a person is immune.[9] People usually only get chickenpox once.[5] Although reinfections by the virus occur, these reinfections usually do not cause any symptoms.[11]

Since its introduction in 1995 in the United States, the varicella vaccine has resulted in a decrease in the number of cases and complications from the disease.[4] It protects about 70–90 percent of people from disease with a greater benefit for severe disease.[9] Routine immunization of children is recommended in many countries.[12] Immunization within three days of exposure may improve outcomes in children.[13] 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.[5] For those at increased risk of complications, antiviral medication such as aciclovir is recommended.[5]

Chickenpox occurs in all parts of the world.[9] In 2013, there were 140 million cases of chickenpox and shingles worldwide.[14] Before routine immunization the number of cases occurring each year was similar to the number of people born.[9] Since immunization the number of infections in the United States has decreased nearly 90%.[9] In 2015 chickenpox resulted in 6,400 deaths globally – down from 8,900 in 1990.[6][15] Death occurs in about 1 per 60,000 cases.[9] Chickenpox was not separated from smallpox until the late 19th century.[9] In 1888 its connection to shingles was determined.[9] The first documented use of the term chicken pox was in 1658.[16] Various explanations have been suggested for the use of "chicken" in the name, one being the relative mildness of the disease.[16]

Signs and symptoms

[edit]

The early (prodromal) symptoms in adolescents and adults are nausea, loss of appetite, aching muscles, and headache.[17] This is followed by the characteristic rash or oral sores, malaise, and a low-grade fever that signals 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.[18][19]

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, 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.[18]

Because watery nasal discharge containing live virus usually precedes both exanthem (external rash) and enanthem (oral ulcers) by one to two days, the infected person 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.[20] The condition usually resolves by itself within a week or two.[21] The rash may, however, last for up to one month.[medical citation needed][22]

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.[23] 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.[22]

  • The back of a 30-year-old male after five days of the rash
    The back of a 30-year-old male after five days of the rash
  • A 3-year-old girl with a chickenpox rash on her torso
    A 3-year-old girl with a chickenpox rash on her torso
  • Lower leg of a child with chickenpox
    Lower leg of a child with chickenpox
  • A child with chickenpox
    A child with chickenpox
  • A child with chickenpox on her face.
    A child with chickenpox on her face.
  • A child with chickenpox
    A child with chickenpox
  • Chickenpox blister closeup, day 7 after start of fever
    Chickenpox blister closeup, day 7 after start of fever

Pregnancy and neonates

[edit]
Main article: Congenital varicella syndrome

During pregnancy the dangers to the fetus associated with a primary VZV infection are greater in the first six months. In the third trimester, the mother is more likely to have severe symptoms.[24] For pregnant women, antibodies produced as a result of immunization or previous infection are transferred via the placenta to the fetus.[25] Varicella infection in pregnant women could lead to spread via the placenta and infection of the fetus. If infection occurs during the first 28 weeks of gestation, this can lead to fetal varicella syndrome (also known as congenital varicella syndrome).[26] Effects on the fetus can range in severity from underdeveloped toes and fingers to severe anal and bladder malformation.[22] Possible problems include:

Infection late in gestation or immediately following birth is referred to as "neonatal varicella".[29] Maternal infection is associated with premature delivery. The risk of the baby developing the disease is greatest following exposure to infection in the period 7 days before delivery and up to 8 days following the birth. The baby may also be exposed to the virus via infectious siblings or other contacts, but this is of less concern if the mother is immune. Newborns who develop symptoms are at a high risk of pneumonia and other serious complications of the disease.[30]

Pathophysiology

[edit]
Main article: Varicella zoster virus

Exposure to VZV in a healthy child initiates the production of host immunoglobulin G (IgG), immunoglobulin M (IgM), and immunoglobulin A (IgA) antibodies; IgG antibodies persist for life and confer immunity. Cell-mediated immune responses are also important in limiting the scope and the duration of primary varicella infection. After primary infection, VZV is hypothesized to spread from mucosal and epidermal lesions to local sensory nerves. VZV then remains latent in the dorsal ganglion cells of the sensory nerves. Reactivation of VZV results in the clinically distinct syndrome of herpes zoster (i.e., shingles), postherpetic neuralgia,[31] and sometimes Ramsay Hunt syndrome type II.[32] Varicella zoster can affect the arteries in the neck and head, producing stroke, either during childhood, or after a latency period of many years.[33]

Shingles

[edit]
Main article: Herpes zoster

After a chickenpox infection, the virus remains dormant in the body's nerve tissues for about 50 years. However, this does not mean that VZV cannot be contracted later in life. The immune system usually keeps the virus at bay, but it can still manifest itself at any given age causing a different form of the viral infection called shingles (also known as herpes zoster).[34] Since the efficacy of the human immune system decreases with age, the United States Advisory Committee on Immunization Practices (ACIP) suggests that every adult over the age of 50 years get the herpes zoster vaccine.[35]

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.[36] Adults over the age of 60 who had chickenpox but not shingles are the most prone age demographic.[37]


Diagnosis

[edit]
Chickenpox

The diagnosis of chickenpox is primarily based on the signs and symptoms, with typical early symptoms followed by a characteristic rash. Confirmation of the diagnosis is by examination of the fluid within the vesicles of the rash, or by testing blood for evidence of an acute immunologic response.[38]

Vesicular fluid can be examined with a Tzanck smear, or by testing for direct fluorescent antibody. The fluid can also be "cultured", whereby attempts are made to grow the virus from a fluid sample. Blood tests can be used to identify a response to acute infection (IgM) or previous infection and subsequent immunity (IgG).[39]

Prenatal diagnosis of fetal varicella infection can be performed using ultrasound, though a delay of 5 weeks following primary maternal infection is advised. A PCR (DNA) test of the mother's amniotic fluid can also be performed, though the risk of spontaneous abortion due to the amniocentesis procedure is higher than the risk of the baby's developing fetal varicella syndrome.[30]

Prevention

[edit]

Hygiene measures

[edit]

The spread of chickenpox can be prevented by isolating affected individuals. Contagion is by exposure to respiratory droplets, or direct contact with lesions, within a period lasting from three days before the onset of the rash, to four days after the onset of the rash.[40] The chickenpox virus is susceptible to disinfectants, notably chlorine bleach (i.e., sodium hypochlorite). Like all enveloped viruses, it is sensitive to drying, heat and detergents.[22]

Vaccine

[edit]
Main article: Varicella vaccine

Chickenpox can be prevented by vaccination.[2] The side effects are usually mild, such as some pain or swelling at the injection site.[2]

A live attenuated varicella vaccine, the Oka strain, was developed by Michiaki Takahashi and his colleagues in Japan in the early 1970s.[41] In 1995, Merck & Co. licensed the "Oka" strain of the varicella virus in the United States, and Maurice Hilleman's team at Merck invented a varicella vaccine in the same year.[42][43][44]

The varicella vaccine is recommended in many countries.[12] Some countries require the varicella vaccination or an exemption before entering elementary school. A second dose is recommended five years after the initial immunization.[45] A vaccinated person is likely to have a milder case of chickenpox if they become infected.[46] Immunization within three days following household contact reduces infection rates and severity in children.[13] Being exposed to chickenpox as an adult (for example, through contact with infected children) may boost immunity to shingles. Therefore, it was thought that when the majority of children were vaccinated against chickenpox, adults might lose this natural boost, so immunity would drop and more shingles cases would occur.[47] On the other hand, current observations suggest that exposure to children with varicella is not a critical factor in the maintenance of immunity. Multiple subclinical reactivations of varicella-zoster virus may occur spontaneously and, despite not causing clinical disease, may still provide an endogenous boost to immunity against zoster.[48]

The vaccine is part of the routine immunization schedule in the US.[49] Some European countries include it as part of universal vaccinations in children,[50] but not all countries provide the vaccine.[12] In the UK as of 2014, the vaccine is only recommended in people who are particularly vulnerable to chickenpox. This is to keep the virus in circulation, thereby exposing the population to the virus at an early age when it is less harmful, and to reduce the occurrence of shingles through repeated exposure to the virus later in life.[51] In November 2023, the UK Joint Committee on Vaccination and Immunisation recommended all children be given the vaccine at ages 12 months and 18 months; however, this has not yet been implemented. In populations that have not been immunized or if immunity is questionable, a clinician may order an enzyme immunoassay. An immunoassay measures the levels of antibodies against the virus that give immunity to a person. If the levels of antibodies are low (low titer) or questionable, reimmunization may be done.[52]

Treatment

[edit]

Treatment mainly consists of easing the symptoms. As a protective measure, people are usually required to stay at home while they are infectious to avoid spreading the disease to others. Cutting the fingernails short or wearing gloves may prevent scratching and minimize the risk of secondary infections.[53]

Although there have been no formal clinical studies evaluating the effectiveness of topical application of calamine lotion (a topical barrier preparation containing zinc oxide, and one of the most commonly used interventions), it has an excellent safety profile.[54] Maintaining good hygiene and daily cleaning of skin with warm water can help to avoid secondary bacterial infection;[55] scratching may increase the risk of secondary infection.[56]

Paracetamol (acetaminophen) but not aspirin may be used to reduce fever. Aspirin use by someone with chickenpox may cause serious, sometimes fatal disease of the liver and brain, Reye syndrome. People at risk of developing severe complications who have had significant exposure to the virus may be given intra-muscular varicella zoster immune globulin (VZIG), a preparation containing high titres of antibodies to varicella zoster virus, to ward off the disease.[57][58]

Antivirals are sometimes used.[59][60]

Children

[edit]

If aciclovir by mouth is started within 24 hours of rash onset, it decreases symptoms by one day but does not affect complication rates.[61][62] Use of aciclovir, therefore, is not currently recommended for individuals with normal immune function. Children younger than 12 years old and older than one month are not meant to receive antiviral drugs unless they have another medical condition that puts them at risk of developing complications.[63]

Treatment of chickenpox in children is aimed at symptoms while the immune system deals with the virus. With children younger than 12 years, cutting fingernails and keeping them clean is an important part of treatment as they are more likely to scratch their blisters more deeply than adults.[64]

Aspirin is highly contraindicated in children younger than 16 years, as it has been related to Reye syndrome.[65]

Adults

[edit]

Infection in otherwise healthy adults tends to be more severe.[66] Treatment with antiviral drugs (e.g. aciclovir or valaciclovir) is generally advised, as long as it is started within 24–48 hours from rash onset.[63] Remedies to ease the symptoms of chickenpox in adults are generally the same as those used for children. Adults are more often prescribed antiviral medication, as it is effective in reducing the severity of the condition and the likelihood of developing complications. Adults are advised to increase water intake to reduce dehydration and relieve headaches. Painkillers such as paracetamol (acetaminophen) are recommended, as they are effective in relieving itching and other symptoms such as fever or pain. Antihistamines relieve itching and may be used in cases where the itching prevents sleep because they also act as a sedative. As with children, antiviral medication is considered more useful for those adults who are more prone to develop complications. These include pregnant women or people who have a weakened immune system.[67]

Prognosis

[edit]

The duration of the visible blistering caused by varicella zoster virus varies in children usually from four to seven 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.

In adults, the disease is more severe,[68] 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),[69] bronchitis (either viral bronchitis or secondary bacterial bronchitis),[69] hepatitis,[70] and encephalitis.[71] 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.[30] Inflammation of the brain, encephalitis, can occur in immunocompromised individuals, although the risk is higher with herpes zoster.[72] Necrotizing fasciitis is also a rare complication.[73]

Varicella can be lethal to individuals 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.[74] Varicella is a particular problem in hospitals when there are patients with immune systems weakened by drugs (e.g., high-dose steroids) or HIV.[75]

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.[76]

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.[76]

Epidemiology

[edit]

Primary varicella occurs in all countries worldwide. In 2015 chickenpox resulted in 6,400 deaths globally – down from 8,900 in 1990.[6] There were 7,000 deaths in 2013.[15] Varicella is highly transmissible, with an infection rate of 90% in close contacts.[77]

In temperate countries, chickenpox is primarily a disease of children, with most cases occurring during the winter and spring, most likely due to school contact. In such countries it is one of the classic diseases of childhood, with most cases occurring in children up to age 15;[78] most people become infected before adulthood, and 10% of young adults remain susceptible.

In the United States, a temperate country, the Centers for Disease Control and Prevention (CDC) do not require state health departments to report infections of chickenpox, and only 31 states volunteered this information as of 2013.[79] A 2013 study conducted by the social media disease surveillance tool called Sickweather used anecdotal reports of chickenpox infections on social media systems Facebook and Twitter to measure and rank states with the most infections per capita, with Maryland, Tennessee and Illinois in the top three.[80]

In the tropics, chickenpox often occurs in older people and may cause more serious disease.[81] In adults, the pockmarks are darker and the scars more prominent than in children.[82]

Society and culture

[edit]

Etymology

[edit]

How the term chickenpox originated is not clear but it may be due to it being a relatively mild disease.[16] It has been said to be derived from chickpeas, based on resemblance of the vesicles to chickpeas,[16][83][84] or to come from the rash resembling chicken pecks.[84] Other suggestions include the designation chicken for a child (i.e., literally 'child pox'), a corruption of itching-pox,[83][85] or the idea that the disease may have originated in chickens.[86] Samuel Johnson explained the designation as "from its being of no very great danger".[87]

Intentional exposure

[edit]

Because chickenpox is usually more severe in adults than it is in children, some parents deliberately expose their children to the virus, for example by taking them to "chickenpox parties".[88] Doctors say that children are safer getting the vaccine, which is a weakened form of the virus, than getting the disease, which can be fatal or lead to shingles later in life.[88][89][90] Repeated exposure to chickenpox may protect against zoster.[91]

Other animals

[edit]

Humans are the only known species that the disease affects naturally.[9] However, chickenpox has been caused in animals, including chimpanzees[92] and gorillas.[93]

Research

[edit]

Sorivudine, a nucleoside analog, has been reported to be effective in the treatment of primary varicella in healthy adults (case reports only), but large-scale clinical trials are still needed to demonstrate its efficacy.[94] There was speculation in 2005 that continuous dosing of aciclovir by mouth for a period of time could eradicate VZV from the host, although further trials were required to discern whether eradication was actually viable.[95]

See also

[edit]

References

[edit]
[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Chickenpox

View on Grokipedia
from Grokipedia
Chickenpox, also known as varicella, is a highly contagious caused by the varicella-zoster virus (VZV), a member of the herpesvirus family. It typically presents as a generalized, pruritic that evolves from macules to papules, vesicles, and scabs, often accompanied by fever, , and . The disease is most common in children under 10 years old, with an of 10 to 21 days, and the illness usually lasts 4 to 7 days. Transmission occurs primarily through airborne respiratory droplets from coughing or sneezing, direct contact with the fluid from skin lesions, or contact with contaminated objects. Individuals are contagious from 1 to 2 days before the rash appears until all lesions have crusted over, with secondary attack rates ranging from 61% to 100% among susceptible close contacts. Before widespread vaccination, chickenpox affected nearly all children worldwide, peaking in winter and spring in temperate climates, and it remains endemic in many regions with low vaccine coverage. The hallmark symptom is an itchy, blister-like that begins on the , face, or trunk and spreads to the rest of the body, potentially forming up to 500 lesions. In healthy children, the disease is generally mild, with symptoms including low-grade fever and lasting 2 to 3 days before the rash. Adults, pregnant women, infants, and immunocompromised individuals often experience more severe illness. Complications can include bacterial skin infections, pneumonia, encephalitis, and rarely death, occurring in about 1% to 2% of cases, with higher risks in at-risk groups. Prior to vaccination programs, the United States saw approximately 4 million cases annually, leading to 10,500 to 13,500 hospitalizations and 100 to 150 deaths. Globally, most fatalities occur in otherwise healthy children due to the high incidence, though severe outcomes are more common in adults and vulnerable populations. Prevention is highly effective through , with two doses of the recommended for children, adolescents, and adults without prior immunity, reducing severe cases by nearly 97% in vaccinated populations. Treatment focuses on symptom relief, such as antihistamines or calamine lotion for itching and acetaminophen for fever, while antiviral medications like acyclovir may be used for high-risk patients to reduce severity. Since the introduction of routine vaccination in 1995, chickenpox incidence, hospitalizations, and deaths have declined dramatically in countries with high coverage.

Causation and Transmission

Causative Agent

Chickenpox, also known as varicella, is caused exclusively by the varicella-zoster virus (VZV), a highly contagious pathogen that infects humans worldwide. VZV belongs to the Herpesviridae family, specifically the alphaherpesvirus subfamily, and features a linear double-stranded DNA genome of approximately 125,000 base pairs. The virus encodes around 70 genes, which support its replication cycle and host interaction. Structurally, VZV consists of an enveloped icosahedral virion measuring 150-200 nm in diameter, with the envelope containing key glycoproteins such as gE and gI that form a heterodimer essential for viral entry into host cells and cell-to-cell spread. The virus was first successfully isolated and cultured in embryonic lung cells in 1953 by Thomas Weller and colleagues, marking a pivotal advancement in understanding its and enabling further research into its . VZV exhibits between wild-type strains, which cause natural , and attenuated vaccine strains like the Oka strain, developed in in the 1970s through in and cells to reduce while maintaining . Uniquely among herpesviruses, VZV is strictly human-specific with no known natural animal reservoir, and it is the only member of the family that causes a primary manifesting as a widespread vesicular (chickenpox) followed by lifelong latency in sensory dorsal root ganglia, from which it can reactivate as (shingles).

Modes of Transmission

Chickenpox, caused by the varicella-zoster virus (VZV), primarily spreads through via respiratory droplets generated by coughing or sneezing from an infected individual, as well as through direct contact with vesicular fluid from skin lesions. The virus is highly contagious, with transmission occurring person-to-person in close proximity, and it does not reliably spread through indirect contact with contaminated environmental surfaces, as VZV is labile and survives only briefly outside the host. Crowded settings, such as households, schools, or daycares, facilitate higher transmission risk due to increased opportunities for close contact. The for chickenpox is typically 10 to 21 days, with an average of 14 to 16 days following exposure to the . begins 1 to 2 days before the onset of the characteristic and continues until all lesions have crusted over, which usually occurs within 5 to 7 days after rash appearance. Among susceptible household contacts, the secondary can reach up to 90%, reflecting the 's high transmissibility in unvaccinated populations, where the (R0) is estimated at 8 to 12. Maternal VZV infection during the first 20 weeks of pregnancy carries a risk of congenital varicella syndrome in the fetus of approximately 0.4% to 2.0%. There is no evidence that fomite transmission—via contaminated objects—serves as a dominant route for VZV spread.

Pathophysiology

Primary Infection Process

The primary infection with varicella-zoster virus (VZV) typically begins with viral entry through the respiratory mucosa, such as the conjunctiva or upper respiratory tract epithelium, following inhalation of infectious aerosols or direct contact with vesicular fluid from an infected individual. Initial replication occurs locally in epithelial cells and then in regional lymph nodes within 2 to 4 days post-exposure, producing a primary viremia that disseminates the virus to reticuloendothelial organs like the spleen and liver. This is followed by a secondary round of replication in these organs, culminating in secondary viremia around 10 to 14 days after initial exposure, during which infected T lymphocytes facilitate systemic spread, including to the skin. VZV is highly infectious in susceptible hosts. Upon reaching the skin via secondary , VZV primarily infects epidermal and dermal endothelial cells, leading to intracellular replication and cell-to-cell spread. This process induces , or separation of epidermal cells due to and cytopathic effects, resulting in the formation of intraepidermal vesicles filled with clear fluid containing high concentrations of infectious virions. The characteristic emerges approximately 14 to 16 days after exposure, beginning as erythematous macules that rapidly progress over 12 to 24 hours to papules, clear vesicles, turbid pustules, and finally crusts, with individual lesions evolving over 3 to 7 days while new crops appear in successive waves for up to 5 to 7 days. The displays a centripetal distribution, with the highest concentration of lesions on the trunk and proximal extremities, sparing the distal limbs and featuring fewer on the face relative to the central body. The acute phase elicits a robust that is essential for viral clearance. Innate immunity activates first, with type I interferons (such as IFN-α) produced by plasmacytoid dendritic cells and infected limiting early replication, alongside contributions from natural killer cells, monocytes, and neutrophils that infiltrate lesions and secrete proinflammatory cytokines like IL-6 and TNF-α. Adaptive immunity follows, with VZV-specific IgM detectable within 7 to 10 days of onset, peaking around 1 month, while IgG appears shortly thereafter and persists lifelong to confer immunity; cell-mediated responses, particularly + and + T lymphocytes, peak around 3 days post- and are critical for resolving by targeting infected cells and facilitating production. These T-cell responses, expressing skin-homing markers like cutaneous lymphocyte antigen, correlate with resolution within 1 to 2 weeks. Viral load dynamics during primary infection show peak coinciding with the onset of fever and , with detectable VZV DNA in blood ranging from 1 to 5,000 copies per 10^5 peripheral blood mononuclear cells in children, often higher and more prolonged in adults. This dissemination results in 250 to 500 total lesions in healthy children across 2 to 4 crops, while adults typically experience more severe disease with over 500 lesions, reflecting greater and immune activation.

Latency and Reactivation

Following primary varicella-zoster virus (VZV) , the virus establishes a lifelong latent in sensory neurons of the peripheral . The primary sites of latency include dorsal root ganglia, cranial ganglia, and trigeminal ganglia, where viral DNA persists as a circular without undergoing lytic replication. During this dormant phase, limited viral occurs, with open reading frames (ORF) 63 and 66 producing proteins that contribute to maintaining latency by modulating host cell processes and suppressing full viral reactivation. These proteins help the virus evade immune detection while residing episomally in the neuronal nucleus. Reactivation of latent VZV, leading to herpes zoster (), is typically spontaneous and occurs when wanes. Common triggers include age-related immune decline, physical or emotional stress, and immunosuppression from conditions such as infection or treatments like . The annual incidence of shingles is approximately 3 to 5 cases per 1,000 adults, increasing sharply with age to over 10 per 1,000 person-years in individuals older than 80. Upon reactivation, the immediate-early 62 (IE62) protein, encoded by ORF62, plays a key role by transactivating other viral genes, initiating lytic replication and spread along the affected . The pathophysiology of shingles involves viral replication in the sensory , leading to neuronal damage, , and centrifugal spread to the skin, resulting in a unilateral dermatomal accompanied by severe due to and . A significant complication is (PHN), defined as persisting beyond 90 days after onset, which affects 10 to 18% of cases and is more common in older adults. The lifetime risk of developing in unvaccinated individuals is approximately 30%, highlighting the long-term implications of primary VZV infection. Rarely, reactivation manifests as zoster sine herpete, characterized by dermatomal without a visible , though VZV DNA can be detected in or ganglia.

Clinical Features

Signs and Symptoms

Chickenpox typically begins with a prodromal phase in some cases, characterized by a mild fever of 38–39°C, , anorexia, and occurring 1–2 days before the appears; this phase is uncommon in children, affecting approximately 20% or fewer, and is more prominent in adults. The hallmark symptom is a pruritic that evolves rapidly from erythematous macules to papules and then to clear, fluid-filled vesicles, often described as "dew drops on a rose petal," before crusting and scabbing over; new crops of lesions emerge over 3–5 days, with the entire rash lasting 5–10 days. Accompanying systemic symptoms include fever that peaks at the onset of the and persists for 2–4 days, along with and ; gastrointestinal upset, such as , occurs rarely. The exhibits a centripetal distribution, concentrating centrally on the trunk, face, and scalp while sparing the palms and soles; the average number of lesions in healthy children ranges from 200 to 500. The intense pruritus associated with the rash typically peaks on days 2–4 of its appearance, and scratching can lead to secondary bacterial , such as staphylococcal or streptococcal , in 5–10% of cases.

Effects in Special Populations

Chickenpox, caused by the varicella-zoster virus (VZV), presents with increased severity and distinct risks in certain populations, including neonates, pregnant individuals, immunocompromised patients, and adults compared to children. In neonates, primary can lead to two main forms: congenital varicella and neonatal varicella. Congenital varicella occurs when maternal happens between weeks 7 and 28 of , with the highest risk (up to 2%) during weeks 13 to 20; it manifests as limb , cutaneous scars in a dermatomal distribution, ocular defects such as or cataracts, and neurological abnormalities like or cortical atrophy. Neonatal varicella, arising from maternal 5 to 10 days before or up to 2 days after delivery, carries a of 20% to 30% without antiviral treatment, often due to disseminated involving the liver, lungs, and (CNS). In pregnant individuals, VZV infection elevates maternal risks, particularly , which complicates 10% to 20% of cases, with incidence rising after 20 weeks of and mortality up to 40% if untreated; this is attributed to physiological changes like increased oxygen demand and diaphragmatic elevation. Infection during also heightens the risk of preterm labor and , though no teratogenic effects are observed after week 28, as fetal is complete. Immunocompromised patients, such as those with organ transplants or malignancies, experience disseminated VZV disease far more frequently, characterized by visceral involvement of the liver (), lungs (), and CNS ( or ), along with prolonged and higher . In solid organ transplant recipients, mortality from primary varicella can reach 10% to 20%, even with treatment, due to rapid progression and multi-organ failure. Compared to healthy children, in whom chickenpox is typically mild with low fever and recovery within 1–2 weeks, adults generally experience more severe disease with higher fever, greater systemic symptoms, increased risk of complications like bacterial skin infections, pneumonia, and encephalitis, higher hospitalization rates, and approximately 25 times higher mortality risk per case. Encephalitis occurs in approximately 1–2 per 10,000 cases overall, with increased risk in adults, while cerebellar ataxia affects about 1 in 4,000 overall but is more common in adults. Additionally, aspirin use in children with chickenpox is contraindicated due to its association with Reye's syndrome, a rare but potentially fatal encephalopathy and hepatic failure linked to salicylate exposure during viral illness. In the UK, routine childhood vaccination was recommended in 2023 and is scheduled to begin in 2026, potentially reducing adult cases in the future.

Diagnosis

Clinical Assessment

Clinical assessment of chickenpox, or varicella, primarily relies on a detailed history and , particularly in uncomplicated cases among children, where testing is often unnecessary. During history taking, clinicians inquire about recent exposure to a confirmed case of varicella or herpes zoster, which typically occurs 10 to 21 days prior to symptom onset, with an average incubation period of 14 to 16 days. Vaccination status is evaluated, as two doses of the varicella vaccine provide high protection, though breakthrough infections can occur in up to 30% of vaccinated individuals after household exposure. Immune history, including prior infection or immunocompromising conditions, is also assessed, alongside details of the prodrome—such as mild fever, malaise, and anorexia 1 to 2 days before rash appearance, which is more prominent in adolescents and adults—and the progression of the rash from macules to vesicles over hours to days. On , the hallmark is a pruritic, polymorphic characterized by lesions in various stages: erythematous macules evolving to papules, clear vesicles on an erythematous base (often described as "dew drops on a rose petal"), and eventually pustules and crusts, typically numbering 250 to 500 in unvaccinated individuals. The usually begins on the , face, trunk, and upper arms before spreading centripetally, sparing the lower extremities and palms/soles in most cases, though mucosal involvement like oral ulcers may precede it by 1 to 3 days. Fever, often low-grade (38–39°C), is checked alongside general signs of ; complications such as from poor intake or secondary bacterial skin infections are evaluated by inspecting for , warmth, or purulence around lesions, while respiratory symptoms may suggest in adults. Differential diagnosis involves distinguishing varicella from other vesicular or maculopapular rashes, such as (which features an initial and exposure history), hand-foot-and-mouth disease or enteroviral exanthems (localized to extremities and mouth with fewer systemic symptoms), ( spots and cough preceding a morbilliform rash), and disseminated (clustered lesions without the polymorphic distribution). In vaccinated individuals, breakthrough varicella presents atypically with milder symptoms, fewer than 50 lesions, and accelerated progression, often lacking a dense vesicular phase, necessitating careful comparison to these mimics. According to CDC case definitions, a probable case of primary varicella is an acute illness with a generalized vesicular rash (maculopapulovesicular) or a non-vesicular rash with epidemiologic linkage to a confirmed case; confirmed cases require laboratory evidence like PCR detection of varicella-zoster virus (VZV) DNA. For epidemiologic purposes, exposure-confirmed cases without rash may also be classified based on history alone. In outbreaks, especially among children, clinical diagnosis achieves over 85% accuracy for uncomplicated varicella, allowing rapid public health response without routine testing; however, adults frequently require laboratory confirmation due to higher risks of severe complications like pneumonia.

Laboratory Confirmation

Laboratory confirmation of varicella-zoster virus (VZV) infection is indicated when clinical diagnosis is uncertain, such as in presentations, immunocompromised patients, or scenarios requiring differentiation from other exanthems. These tests verify VZV involvement by detecting viral components or immune responses, guiding targeted interventions like antiviral therapy or isolation protocols. (PCR) serves as the gold standard for confirming VZV infection due to its rapid detection of viral DNA and superior performance metrics. Real-time PCR assays, applied to specimens like vesicle fluid, unroofed lesion scrapings, throat swabs, or (), exhibit sensitivity exceeding 95% and near-100% specificity in vesicular samples, enabling same-day results in equipped laboratories. Beyond diagnosis, PCR facilitates to distinguish wild-type VZV from vaccine-derived Oka strains, aiding epidemiological tracking in outbreaks or efficacy assessments. Serological assays detect VZV-specific antibodies to support or immunity status. IgM antibodies, signaling acute , emerge 3 to 7 days post-rash onset and peak around 2 weeks, but their interpretation is limited by frequent false positives from with other herpesviruses or prolonged detection after . In contrast, IgG antibodies indicate prior exposure or immunity; a fourfold or greater rise in IgG titers between acute- and convalescent-phase sera (collected 2-4 weeks apart) confirms recent primary with high specificity, though this method delays definitive results. Direct fluorescent (DFA) testing provides a quick alternative by scrapings for VZV antigens, yielding results in 15 to 30 minutes with specificity over 95%, making it valuable for point-of-care decisions. However, its sensitivity, approximately 88%, lags behind PCR, particularly in early or healed s, limiting its use as a standalone confirmatory tool. Viral remains a historical option but is rarely employed in modern practice due to technical demands and delays. Specimens are inoculated into human diploid cells (e.g., ), where VZV exhibits slow cytopathic effects detectable in 1 to 2 weeks, resulting in sensitivity below 50% compared to molecular methods and rendering it impractical for acute . The Tzanck smear offers a simple, bedside cytodiagnostic approach by examining scrapings for multinucleated giant cells characteristic of herpesvirus infections, with results in minutes. Despite its historical role, it has low specificity around 50%, as these cells also appear in cases, and variable sensitivity (50-75%); it retains niche utility in outbreaks, immunocompromised settings, or resource-poor environments for preliminary screening.

Prevention Strategies

Vaccination

The is a live designed to prevent chickenpox caused by the varicella-zoster virus (VZV). It utilizes the Oka strain of VZV, which was originally isolated from a child with chickenpox in in the 1970s and attenuated through in embryonic lung cell cultures, guinea pig embryo cells, and diploid cell cultures more than 30 times to reduce its virulence while maintaining immunogenicity. Two primary formulations are available: single-antigen vaccines like Varivax, which contains only the attenuated VZV, and combination vaccines like ProQuad, which incorporates , , , and varicella (MMRV) components for simultaneous protection against multiple diseases. The demonstrates high efficacy in preventing varicella and its complications. A single dose is approximately 82% effective against any form of chickenpox and 95-100% effective against severe disease, while two doses increase protection to 90-98% against any disease and nearly 100% against severe outcomes, including hospitalization and death. Two doses also reduce outbreak incidence by over 90% in vaccinated populations, with immunity persisting for more than 20 years based on long-term follow-up studies showing sustained levels and low breakthrough rates. Vaccination schedules vary by age and region but emphasize early administration to maximize herd immunity. In the United States, the Advisory Committee on Immunization Practices (ACIP) recommends two doses for children: the first at 12-15 months of age and the second at 4-6 years, with a minimum interval of 3 months between doses for those under 13 years and 4 weeks for adolescents and adults. In September 2025, ACIP updated recommendations to prefer administration of separate MMR and varicella vaccines over MMRV for children aged 12 through 47 months to reduce the risk of febrile seizures associated with the combination vaccine. Catch-up vaccination is advised for unvaccinated individuals, including adolescents and adults, using the same two-dose regimen to address gaps in immunity. Internationally, the United Kingdom announced a universal childhood varicella vaccination program in 2025, with rollout beginning in January 2026 offering two doses of the MMRV vaccine at 12 months and 18 months, alongside catch-up vaccination for older children. Safety profiles are favorable, with most adverse events being mild and self-limiting. Common side effects include injection-site reactions such as , redness, or swelling in up to 20% of recipients, along with low-grade fever in about 10-15% and a mild varicella-like in approximately 5% of cases, typically appearing 1-3 weeks post-vaccination. The vaccine is contraindicated in pregnant individuals due to theoretical risks to the , those with severe immunosuppression (e.g., from or ), and anyone with a history of to vaccine components like or neomycin. Breakthrough infections in vaccinated individuals are generally milder, with fewer lesions (often <50) and shorter duration compared to unvaccinated cases, and they pose lower transmission risk. Recent advancements include the 2024 phase IIa trial of the , an investigational live engineered with ORF7 deletion for dual and neural , which demonstrated humoral comparable to the Oka-based in children aged 3-12 years across three dose levels, with a favorable safety profile and no serious adverse events. While adoption of MMRV formulations like ProQuad continues in some regions for convenience in reducing injection numbers and improving compliance, particularly in international routine immunization programs expanding combination use, the 2025 ACIP update highlights preferences for separate vaccines in young children.

Non-Vaccine Measures

Non-vaccine measures play a crucial role in limiting the spread of chickenpox (varicella), particularly in settings with low coverage or during outbreaks, by emphasizing isolation, , and targeted prophylaxis. These strategies focus on interrupting transmission through direct contact with respiratory droplets or vesicular fluid from infected individuals, who remain contagious from 1-2 days before onset until all lesions crust over. The (WHO) endorses these approaches as essential tools, especially in resource-limited environments where uptake is incomplete, to reduce secondary attack rates that can reach 61-100% among susceptible household contacts. Isolation protocols are a cornerstone of prevention, requiring infected individuals to avoid contact with others until lesions have fully crusted, typically 5-7 days after rash appearance, to minimize airborne and contact transmission. In community settings such as schools and workplaces, exclusion is recommended during this period, with return permitted once no new lesions develop and crusting is complete; this measure helps contain outbreaks by preventing exposure in high-density environments. Healthcare facilities implement stricter contact and airborne precautions, including placement in negative-pressure rooms if available or closed isolation rooms otherwise, with care provided only by immune personnel wearing like N95 respirators and gloves to avert nosocomial spread. These protocols have demonstrated effectiveness in reducing transmission, with studies indicating that timely isolation can lower secondary attack rates by up to 50% when combined with other measures. Hygiene practices further support containment by targeting the virus's primary modes of spread. Frequent handwashing with and water, avoidance of touching or scratching lesions to prevent autoinoculation or fomite transfer (though play a limited role), and covering all lesions with non-permeable dressings are advised for infected persons. Infected individuals should dispose of tissues or materials contaminated with respiratory secretions properly and avoid sharing personal items like towels or utensils; surfaces potentially exposed to vesicular fluid should be disinfected with standard hospital-grade agents. The WHO highlights these practices as simple yet vital for reducing contagion in households and communities, particularly where increases risk. Post-exposure prophylaxis with varicella-zoster immune globulin (VZIG), such as VariZIG, is recommended for high-risk susceptible individuals exposed to chickenpox to attenuate or prevent . Administration should occur as soon as possible, ideally within 96 hours of exposure but up to 10 days, targeting groups like neonates born to mothers with varicella around delivery, immunocompromised persons, and pregnant women without immunity. VZIG provides by supplying antibodies, significantly reducing the severity of infection in these populations, with clinical data showing it prevents moderate-to-severe varicella in approximately 70-90% of cases when given promptly. Community-level measures enhance individual efforts during outbreaks through coordinated responses. identifies exposed susceptibles for monitoring or prophylaxis, while education campaigns inform the public about the contagious period (10-21 days post-exposure for potential onset) and recognition of early symptoms to prompt voluntary isolation. In settings like schools or childcare facilities, exclusion of cases until crusting and, if needed, temporary closure may be enacted when attack rates exceed 5% or multiple linked cases occur, preventing wider dissemination; for example, guidelines suggest cohorting immune and non-immune groups or excluding unvaccinated susceptibles for after the last case. The WHO advocates these interventions in low-vaccine contexts to curb epidemics, with overall non-vaccine strategies estimated to reduce household transmission by 30-50% through integrated application.

Management and Treatment

Supportive Therapy

Supportive therapy for chickenpox focuses on alleviating discomfort, preventing secondary bacterial infections, and promoting recovery through non-specific measures. In healthy children, the majority of cases—95% to 100%—resolve completely with supportive care alone, without the need for antiviral intervention. Guidelines from the Centers for Disease Control and Prevention (CDC) and the (AAP) emphasize maintaining comfort, hydration, and to minimize complications. To relieve itching, a common and distressing symptom, patients can apply calamine lotion to affected areas or take cool baths infused with baking soda, uncooked , or colloidal oatmeal. Oral antihistamines such as diphenhydramine may be used for severe pruritus, particularly in children, while cool compresses provide additional soothing. Caregivers should trim fingernails short and encourage avoiding scratching to prevent skin excoriation and bacterial ; mittens can be worn during for young children. Fever and pain are managed primarily with acetaminophen, which is preferred for its safety profile in children. Aspirin should be strictly avoided due to its association with Reye's syndrome, a rare but serious condition with an incidence of fewer than 2 cases per year in the United States since 1994, often linked to viral illnesses like chickenpox when salicylates are used. Ibuprofen is also generally discouraged in children with chickenpox owing to potential increased risk of skin infections. Skin care involves keeping lesions clean and dry to reduce risk; if signs of bacterial appear, such as increased redness or , warm soaks may be applied under medical guidance. Regular handwashing with and for at least 20 seconds is recommended if blisters are accidentally scratched. Adequate hydration is essential, with encouragement of oral fluid intake to counter fever-related , alongside sufficient rest in a comfortable environment. Isolation measures, such as staying home from school or work until lesions crust over (typically 5-7 days after onset), are critical to prevent transmission, as chickenpox is highly contagious.

Pharmacological Interventions

Pharmacological interventions for chickenpox primarily involve antiviral agents to mitigate in severe or high-risk cases, such as immunocompromised individuals, neonates, or adults with complicated . Acyclovir remains the cornerstone antiviral, administered orally at a dose of 20 mg/kg four times daily for 5 to 7 days in children older than 2 years who are at increased risk for moderate to severe varicella. For immunocompromised patients or neonates with severe manifestations, intravenous acyclovir is recommended at 10 mg/kg every 8 hours, typically for 7 to 10 days or until clinical improvement, followed by oral therapy if necessary. These regimens reduce the duration of fever by approximately 1 day, the total number of skin lesions by 2 to 3 days, and overall severity in otherwise healthy children when initiated early. In high-risk populations such as immunocompromised children, acyclovir significantly reduces complications; for example, one study showed it decreased the incidence of cutaneous dissemination from 43% to 8% compared to . Alternative antivirals with improved oral , such as valacyclovir or , are preferred for adults due to simpler dosing schedules and equivalent against varicella-zoster virus (VZV). Valacyclovir is typically dosed at 1 gram orally three times daily for 7 days in adults with uncomplicated chickenpox, while may be used at 500 mg three times daily for 7 days. These prodrugs of acyclovir and , respectively, achieve higher plasma concentrations, potentially improving compliance, though they are not routinely recommended for healthy children owing to limited additional benefit over acyclovir and higher costs. For optimal antiviral effect across all agents, treatment should commence within 24 to 72 hours of rash onset, as delayed initiation diminishes benefits on lesion formation and symptom resolution. In patients with , acyclovir or valacyclovir substantially reduces VZV dissemination and associated morbidity when used therapeutically. Adjunct pharmacological measures address secondary complications rather than the primary viral infection. Antibiotics are indicated solely for bacterial superinfections, such as or arising from scratching, with cephalexin (25-50 mg/kg/day divided every 6-8 hours in children or 500 mg four times daily in adults) as a first-line option for methicillin-sensitive or coverage. Varicella-zoster immune globulin (VZIG), administered intramuscularly at 125 units/10 kg (maximum 625 units) within 10 days of exposure, serves as in susceptible high-risk individuals to attenuate or prevent severe disease, though it does not supplant .

Outcomes and Prognosis

Short-Term Recovery

Chickenpox typically resolves within 2 to 3 weeks in uncomplicated cases among healthy individuals. The progresses from macules to vesicles and pustules, with crusting occurring by days 7 to 10 after onset, after which the scabs gradually fall off over the ensuing 1 to 2 weeks. Fever and usually subside within 3 to 5 days of symptom appearance. Contagiousness ceases once all lesions have crusted over, typically around day 7, allowing individuals to return to normal activities provided no open sores remain. Natural infection with varicella-zoster virus confers lifelong immunity in most cases through both humoral (IgG antibody-mediated) and cellular responses. This provides over 90% protection against reinfection, although rare mild breakthrough cases can occur, often with fewer lesions than the primary episode. Common short-term sequelae include scarring from scratching or secondary bacterial infections, affecting 10% to 20% of cases, particularly on the face. Fatigue and general malaise may persist for 1 to 2 weeks post-rash resolution. Rare acute complications, such as (occurring in approximately 1 per 50,000 cases in unvaccinated children), may lead to seizures and coma but generally resolve with supportive care and antivirals. Recovery is influenced by factors such as age, with younger children experiencing faster and milder symptoms compared to adolescents or adults. Adequate hydration and supportive measures, including rest and antipruritics to prevent , can shorten the overall duration by about 1 day. In healthy children, over 95% of cases are self-limiting without intervention beyond symptom relief.

Long-Term Complications

The primary long-term complication of chickenpox arises from the latency of the varicella-zoster virus (VZV), which can reactivate later in life as , or . Approximately one in three people who contract chickenpox will experience over their lifetime, with incidence increasing with age and . A significant consequence of shingles is postherpetic neuralgia (PHN), characterized by persistent nerve pain in the affected dermatome that can last months to years. PHN develops in 10–20% of cases among older adults, with rates rising to 50% or higher in those over 80 years. Management typically involves first-line therapies such as , an anticonvulsant that stabilizes nerve activity, and tricyclic antidepressants (TCAs) like amitriptyline, which modulate pain signaling pathways. Rare chronic sequelae of chickenpox or its reactivation include ocular complications, such as and , which are uncommon and may lead to corneal inflammation or vision impairment if untreated. Neurological effects are also uncommon but notable, with associated with an elevated risk; studies report an of approximately 1.9 for ischemic stroke within 30 days post-infection, particularly when involving the ophthalmic branch of the . Natural chickenpox infection establishes long-lasting T-cell memory that initially provides stronger protection against reactivation compared to , though this immunity wanes over decades without exogenous boosting from community VZV exposure. In contrast, the chickenpox reduces shingles risk by about 80% in healthy vaccinated children relative to those with natural infection, but reduced circulation of wild-type virus may diminish natural immune boosting in adults. Historically, chickenpox contributed to 100–150 deaths annually in the United States before vaccine introduction in 1995, often from secondary bacterial infections or in otherwise healthy individuals. Post-, mortality has plummeted by over 97%, with fewer than 10 deaths reported yearly, predominantly among immunocompromised adults. zoster rates among adults in the United States gradually increased from 1998 to 2019, potentially attributable to aging populations and diminished natural immune reinforcement following widespread childhood , though recent data indicate rates have plateaued or declined.

Epidemiological Profile

Global Incidence and Distribution

Chickenpox, caused by the varicella-zoster virus, affects an estimated 84-87 million people annually worldwide based on systematic analyses, with cases predominantly in low- and middle-income countries in and where access to healthcare is limited. According to the 2019, there were about 84 million incident cases and 14,553 deaths globally; by 2021, incident cases had increased slightly to approximately 87 million (including herpes zoster), while deaths and disability-adjusted life years (DALYs) continued to decline, with age-standardized DALY rates down about 36% since 1990. Pre-vaccination era incidence rates hovered around 1-2% of the per year in many regions, underscoring the disease's ubiquity before widespread efforts. In the United States, prior to the introduction of the in 1995, approximately 4 million cases occurred annually, a figure that has since declined to fewer than 150,000 cases per year due to vaccination coverage. The disease exhibits distinct age and seasonal patterns globally. Incidence peaks among children under 10 years old, particularly those aged 1-4 years, who account for the majority of cases in both vaccinated and unvaccinated populations. In regions like China, a 2021 meta-analysis of VZV IgG seroprevalence in the healthy population (n=46,828) reported age-specific positivity rates of 17% (95% CI: 8%–28%) in the 0~ age group, 95% (95% CI: 94%–97%) in the 30~ age group, and 95% (95% CI: 90%–98%) in the ≥40 age group, illustrating cumulative immunity from primary infections. In temperate climates, outbreaks are more common during winter and spring months, with cycles occurring every 2-5 years, whereas in tropical regions, transmission persists year-round with less pronounced seasonality. These patterns are influenced by environmental factors such as and , which affect viral stability and human behavior. The COVID-19 pandemic temporarily reduced transmission due to measures (2020-2022), but cases rebounded post-restrictions. High-burden areas are concentrated in low-income countries, where systems are often inadequate, leading to underreporting of cases. In tropical settings, particularly rural areas, a higher proportion of infections occur in adults due to delayed primary exposure from lower childhood transmission rates, resulting in more severe outcomes. Socioeconomic factors, including household overcrowding and poor ventilation, significantly elevate transmission risk by facilitating close contact among susceptible individuals. More recent analyses indicate a decline in global DALYs to around 0.9 million by 2019 amid partial adoption, with further reductions by 2021. The introduction of the varicella vaccination program in the United States in 1995 has dramatically reduced chickenpox incidence, with cases declining by more than 97% from over 4 million annually in the early to fewer than 150,000 by recent years. Hospitalizations fell by 97%, from 10,500–13,500 to under 1,400 per year, while deaths decreased by 97%, from 100–150 to fewer than 30 annually. Over the program's first 25 years, it prevented an estimated 91 million cases and generated $23.4 billion in healthcare cost savings. National Health and Nutrition Examination Survey (NHANES) data from 1999–2004 indicate high post-vaccination immunity levels, with varicella-zoster virus (VZV) seroprevalence of 93.6% among ages 6–19 years and 98.0% among ages 20–49 years. Globally, more than 45 countries have implemented routine universal varicella programs as of 2024, with the prequalifying several vaccines, including BARYCELA by GC Biopharma in 2023 and VarV by Sinovac in 2022, to facilitate broader access in low- and middle-income settings. In the , a routine MMRV program is scheduled to begin rollout in January 2026, targeting children from one year of age, with a goal of achieving at least 95% coverage to establish . Vaccination has led to unintended epidemiological shifts, including a rise in adult incidence, attributed to reduced natural boosting from childhood varicella exposure; in the , rates among those aged 30 years and older increased during the vaccination era, with some studies noting annual rises of 3–5% in certain cohorts post-program implementation. Breakthrough varicella in vaccinated individuals is typically milder than natural infection, featuring fewer than 50 lesions and reduced fever in most cases, though severe outcomes can occur in 25–30% of breakthroughs. Achieving against varicella requires 80–90% population coverage, as the virus's (R0) ranges from 8–12; outbreaks persist in communities with coverage below 85%, such as school settings with rates under 54%, underscoring the need for sustained high uptake. In 2025, the WHO Strategic Advisory Group of Experts (SAGE) recommended a life-course approach, including two-dose childhood schedules and targeted for at-risk groups like immunocompromised individuals and healthcare workers, to address ongoing varicella and zoster burdens. Recent 2024 data indicate the varicella-zoster treatment market grew to USD 1.75 billion, with a projected 4.5% through 2034, driven by shifting demographics including an aging population increasing zoster cases among those over 60.

Historical and Cultural Context

Etymology and Naming

The term "chickenpox" emerged in English during the , with the first documented use appearing in 1658, likely reflecting the disease's relatively mild nature compared to the more severe . English physician Richard Morton (1637–1698) further popularized the name by describing it as a gentler form of pox, emphasizing its lesser danger and distinguishing it from the deadly variola major. Several etymological theories explain the inclusion of "chicken," including a possible derivation from the or French word for chickpea ("chiche" or "pois"), due to the resemblance of the rash's vesicles to the legume's size and shape; alternatively, "chicken" may evoke the perceived triviality of the illness, akin to a minor ailment in . Italian physician Giovanni Filippo Ingrassia (1510–1580) first differentiated varicella from in 1553 based on clinical observations during outbreaks in , marking one of the earliest formal medical distinctions. The term "varicella," derived from the Latin "variola" (meaning "spotted" or "shabby," a term originally for ) with the diminutive suffix "-ella" to signify a milder variant, first appeared in in the 18th century. The term gained traction in by the , with English physician William Heberden providing a detailed description in 1767 that clearly separated it from , solidifying "varicella" as the preferred clinical name. Earlier accounts trace the disease's recognition to the 9th-century Persian physician Rhazes (Al-Razi, 865–925), who offered the first clear description of its vesicular rash as distinct from and in his treatise on infectious diseases. In French-speaking regions, the name reflected similar etymological roots, with "varicelle" (a direct adaptation of the Latin term) commonly used, though folk references sometimes likened it to "chiche-pois" for the appearance. Today, while "chickenpox" endures in everyday language, international standards like the World Health Organization's (ICD-10 code B01) employ "varicella" for precision in medical and epidemiological contexts.

Traditional and Social Practices

In historical contexts, particularly in and the from the 18th to the , parents often intentionally exposed their children to chickenpox to induce a mild case and confer lifelong immunity, a practice known as "chickenpox parties." These gatherings involved inviting susceptible children to play with an infected child, reflecting the view of the disease as an inevitable childhood milestone rather than a severe threat. This approach declined sharply after the introduction of the in 1995, as provided a safer alternative for immunity. Prior to widespread , deliberate exposure was a common strategy in the U.S., with some parents organizing "chickenpox parties" to avoid more severe adult cases. Folk remedies for chickenpox emphasized symptom relief through natural applications, such as herbal poultices made from clays similar to modern calamine lotion to soothe itching and prevent scarring, or baths to reduce inflammation. Isolation rituals were also prevalent, with affected individuals confined to specific rooms or homes to limit spread, often accompanied by herbal teas like for restlessness. In some cultures, chickenpox was perceived as a marking childhood resilience; for instance, in South Indian traditions, pox illnesses were attributed to the Mariyamman "arriving" in the body, prompting devotional rituals rather than medical intervention alone. Non-Western practices, such as Ayurvedic treatments, historically addressed chickenpox (termed masurika) using antiviral herbs like neem leaves for cooling poultices and for anti-inflammatory effects, alongside blood purification therapies to support recovery. Social stigma surrounding chickenpox led to formalized measures starting in the 1800s, when European and American health authorities enacted laws isolating infected households to curb outbreaks of contagious diseases, including varicella. By the early , school exclusion policies became standardized, requiring children with active rashes to stay home until lesions crusted over, a practice enforced in U.S. public schools to protect vulnerable students. These regulations underscored the disease's perceived threat despite its generally mild course in children. Culturally, chickenpox appeared in 19th-century as a routine childhood affliction, symbolizing and recovery, as seen in depictions of life amid minor epidemics. In modern media, awareness campaigns have shifted focus to prevention, with initiatives like the U.S. CDC's promotion highlighting the disease's risks and the vaccine's benefits, reducing cases by over 97% since 1995.

Zoonotic and Comparative Aspects

Infection in Other Animals

Varicella-zoster virus (VZV) exhibits strict host specificity and naturally infects only s, with no documented animal reservoirs, distinguishing it from other alphaherpesviruses such as the (Cercopithecine herpesvirus 1) that naturally circulates in rhesus macaques and poses zoonotic risks to s. This human exclusivity arises from VZV's reliance on specific human cellular receptors and immune interactions, preventing efficient replication in non-human species under natural conditions. To study VZV pathogenesis, latency, and reactivation, researchers have developed experimental animal models despite the virus's host restrictions. Guinea pigs, when inoculated with adapted VZV strains, support limited viral replication in ganglia and skin, enabling investigations into latency establishment and immune responses; for instance, intravenous injection of VZV-infected T cells into guinea pigs results in viral DNA detection in multiple neural tissues. Simian models using Old World nonhuman primates, such as rhesus macaques, provide closer analogs through infection with simian varicella virus (SVV), a closely related alphaherpesvirus that mimics VZV's lifecycle. Additionally, mice engineered with humanized immune systems, including human hematopoietic stem cells and dorsal root ganglia xenografts, allow for VZV dissemination and latency studies, facilitating vaccine efficacy testing. These models, while imperfect, have advanced understanding of VZV neurotropism without relying on natural infections. Related viruses in animals offer comparative insights into VZV . SVV, endemic in African green monkeys and other nonhuman primates, causes acute varicella-like illness followed by latency and zoster reactivation, sharing 70-75% genomic homology and collinear arrangement with VZV. virus (PRV), also known as suid herpesvirus 1, infects pigs and other mammals as an alphaherpesvirus analog to VZV, inducing similar neuropathic symptoms and neuronal latency, though it lacks the dermatotropic rash of varicella. In veterinary contexts, SVV outbreaks in primate colonies are monitored, with differentials including canine herpesvirus, which causes distinct respiratory and reproductive diseases in dogs but can present overlapping vesicular lesions. VZV demonstrates no zoonotic potential, with no natural spillover events from humans to animals or vice versa reported, and laboratory accidents involving cross-species transmission remaining exceedingly rare due to the virus's human tropism. Recent studies, such as those in 2023 examining SVV infection in rhesus macaques, have utilized this model to elucidate zoster pathogenesis, revealing robust central nervous system inflammatory responses during reactivation without fulminant encephalitis.

Current Research Directions

Vaccine Developments

Recombinant subunit vaccines represent a significant advancement in herpes zoster (HZ) prevention, with GlaxoSmithKline's Shingrix, approved by the FDA in 2017, demonstrating over 90% efficacy against HZ in adults aged 50 and older. This non-live vaccine uses a recombinant glycoprotein E antigen combined with an AS01B adjuvant, providing robust humoral and cell-mediated immunity without the risks associated with live-attenuated strains. In 2025, a clinical study reported favorable immunogenicity of Shingrix in varicella-zoster virus (VZV)-naïve, immunocompromised pediatric patients, eliciting humoral responses in nearly all cases while maintaining an acceptable safety profile. Live-attenuated vaccine developments continue to refine the original Oka , with the VZV-7D —an ORF7-deficient variant designed for enhanced skin and neuro-attenuation—advancing through Phase II trials in 2024. This showed seroconversion rates and geometric mean titers comparable to the standard Oka in children aged 3-12 years, with a potentially reduced risk of vaccine-associated complications. Additionally, trials exploring higher-potency formulations, such as a Phase III study in healthy adults aged 13-55 years, have demonstrated improved and safety over existing controls, supporting potential adaptations for adult populations. Combination vaccines like MMRV (measles, , , and varicella) have seen increased adoption, accounting for approximately 15% of first-dose administrations in U.S. programs by early 2025, amid updated ACIP guidance favoring separate doses for younger children but retaining MMRV for boosters. The World Health Organization's Strategic Advisory Group of Experts (SAGE) in 2025 endorsed a life-course approach integrating varicella and HZ vaccination into national programs to address VZV transmission across age groups, emphasizing universal strategies to break disease cycles. Challenges persist in deploying live-attenuated varicella vaccines, particularly in tropical regions where cold chain maintenance is disrupted by high temperatures and logistical constraints, leading to potential potency loss during storage and transport. Efficacy against breakthrough HZ remains a concern, as childhood varicella vaccination reduces but does not eliminate reactivation risk, with long-term studies indicating 70-90% protection against severe outcomes yet variable durability in preventing mild HZ episodes. Shingrix has achieved strong market performance, with Q3 2025 sales of approximately £0.8 billion (up 13% year-over-year). A 2025 study linked Shingrix vaccination to a 32% lower risk for dementia onset (hazard ratio approximately 0.68).

Therapeutic and Epidemiological Studies

Recent therapeutic trials have explored novel antivirals for varicella-zoster virus (VZV) infections, particularly in cases of resistance or severe manifestations like herpes zoster (HZ). , a conjugate of , has shown potential efficacy as prophylaxis against VZV reactivation in hematopoietic cell transplant patients, reducing incidence in small cohorts despite limited data on direct treatment for primary chickenpox. In 2025, ongoing studies are examining HZ outcomes in vaccinated cohorts, revealing that while varicella vaccination reduces primary infections, it may contribute to a delayed rise in HZ due to diminished natural boosting of immunity. Epidemiological modeling has increasingly focused on the post-vaccination dynamics of HZ, attributing observed increases to the exogenous boosting hypothesis, where reduced exposure to wild-type VZV in vaccinated populations leads to waning over time. A 2024 CDC report documented an approximately 30% rise in HZ hospitalizations among adults from 2011 to 2022 following widespread varicella , highlighting the need for targeted HZ strategies. In tropical regions, assessments indicate a higher burden of chickenpox in adults due to lower childhood transmission rates influenced by , with significant underreporting—estimated at up to 50% in parts of —exacerbating gaps in global surveillance. Surveillance efforts have advanced through genomic sequencing of VZV strains during outbreaks, enabling precise tracking of transmission chains and identification, as demonstrated in recent nosocomial and community investigations. Emerging AI-driven applications for are being piloted to improve early detection in resource-limited settings, though validation studies remain preliminary. The VZV treatment market is projected to grow at a (CAGR) of 4.5% from 2024 to 2034, driven by demand for antivirals and supportive therapies amid rising HZ incidence. Future directions emphasize universal screening for VZV immunity to guide prophylaxis in at-risk groups, alongside investigations into climate's role in altering chickenpox —such as reduced winter peaks in tropical areas potentially prolonging susceptibility windows. These efforts aim to address gaps in low-resource regions and refine models for long-term control.

References

  1. https://www.cdc.gov/chickenpox/about/index.html
  2. https://www.who.int/news-room/questions-and-answers/item/chickenpox
  3. https://www.cdc.gov/chickenpox/hcp/clinical-overview/index.html
  4. https://www.cdc.gov/pinkbook/hcp/table-of-contents/chapter-22-varicella.html
  5. https://www.canada.ca/en/public-health/services/laboratory-biosafety-biosecurity/pathogen-safety-data-sheets-risk-assessment/varicella-zoster-virus.html
  6. https://pmc.ncbi.nlm.nih.gov/articles/PMC3413377/
  7. https://pmc.ncbi.nlm.nih.gov/articles/PMC5373811/
  8. https://www.nobelprize.org/prizes/medicine/1954/weller/biographical/
  9. https://www.ncbi.nlm.nih.gov/books/NBK47446/
  10. https://journals.asm.org/doi/10.1128/cmr.00052-13
  11. https://pmc.ncbi.nlm.nih.gov/articles/PMC8151998/
  12. https://www.cdc.gov/chickenpox/hcp/clinical-guidance/index.html
  13. https://publications.aap.org/redbook/book/755/chapter/14083489/Varicella-Zoster-Virus-Infections
  14. https://www.ncbi.nlm.nih.gov/books/NBK448191/
  15. https://emedicine.medscape.com/article/1131785-overview
  16. https://pmc.ncbi.nlm.nih.gov/articles/PMC4066823/
  17. https://journals.asm.org/doi/10.1128/jvi.01227-21
  18. https://pmc.ncbi.nlm.nih.gov/articles/PMC6151075/
  19. https://academic.oup.com/jid/article/197/Supplement_2/S58/848608
  20. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0003789
  21. https://pmc.ncbi.nlm.nih.gov/articles/PMC6070824/
  22. https://pmc.ncbi.nlm.nih.gov/articles/PMC523280/
  23. https://pmc.ncbi.nlm.nih.gov/articles/PMC6667558/
  24. https://pmc.ncbi.nlm.nih.gov/articles/PMC3176736/
  25. https://pmc.ncbi.nlm.nih.gov/articles/PMC8298014/
  26. https://pmc.ncbi.nlm.nih.gov/articles/PMC4591524/
  27. https://pmc.ncbi.nlm.nih.gov/articles/PMC4628253/
  28. https://pmc.ncbi.nlm.nih.gov/articles/PMC114479/
  29. https://www.ncbi.nlm.nih.gov/books/NBK441824/
  30. https://pmc.ncbi.nlm.nih.gov/articles/PMC8847496/
  31. https://www.cdc.gov/pinkbook/hcp/table-of-contents/chapter-23-zoster.html
  32. https://pmc.ncbi.nlm.nih.gov/articles/PMC7336347/
  33. https://www.cdc.gov/chickenpox/hcp/communication-resources/varicella-diagnosis-fact-sheet.html
  34. https://www.cdc.gov/chickenpox/hcp/clinical-signs/index.html
  35. https://www.verywellhealth.com/chicken-pox-pictures-4020407
  36. https://www.immunize.org/wp-content/uploads/catg.d/p4202.pdf
  37. https://www.sciencedirect.com/topics/immunology-and-microbiology/chickenpox
  38. https://myhealth.alberta.ca/Health/pages/conditions.aspx?hwid=zm2591
  39. https://immunisationhandbook.health.gov.au/contents/vaccine-preventable-diseases/varicella-chickenpox
  40. https://www.streetervillepediatrics.com/chicken-pox.html
  41. https://www.cdc.gov/chickenpox/signs-symptoms/index.html
  42. https://www.ncbi.nlm.nih.gov/books/NBK568794/
  43. https://pmc.ncbi.nlm.nih.gov/articles/PMC9762609/
  44. https://pmc.ncbi.nlm.nih.gov/articles/PMC3155623/
  45. https://pmc.ncbi.nlm.nih.gov/articles/PMC11857854/
  46. https://pubmed.ncbi.nlm.nih.gov/3044096/
  47. https://pmc.ncbi.nlm.nih.gov/articles/PMC3029559/
  48. https://pmc.ncbi.nlm.nih.gov/articles/PMC8567532/
  49. https://pmc.ncbi.nlm.nih.gov/articles/PMC5726865/
  50. https://www.cdc.gov/chickenpox/treatment/index.html
  51. https://www.ninds.nih.gov/health-information/disorders/reyes-syndrome
  52. https://www.gov.uk/government/publications/childhood-varicella-vaccination-programme-jcvi-advice-14-november-2023/jcvi-statement-on-a-childhood-varicella-chickenpox-vaccination-programme
  53. https://www.cdc.gov/surv-manual/php/table-of-contents/chapter-17-varicella.html
  54. https://pmc.ncbi.nlm.nih.gov/articles/PMC9231738/
  55. https://www.cdc.gov/chickenpox/php/laboratories/index.html
  56. https://pmc.ncbi.nlm.nih.gov/articles/PMC5370824/
  57. https://pubmed.ncbi.nlm.nih.gov/23035203/
  58. https://emedicine.medscape.com/article/1131785-workup
  59. https://www.cdc.gov/vaccines/vpd/varicella/hcp/about-vaccine.html
  60. https://pmc.ncbi.nlm.nih.gov/articles/PMC11959904/
  61. https://www.fda.gov/media/147563/download
  62. https://www.cdc.gov/chickenpox/hcp/vaccine-considerations/index.html
  63. https://www.merckmanuals.com/professional/infectious-diseases/immunization/varicella-vaccine
  64. https://academic.oup.com/jid/article/226/Supplement_4/S425/6764809
  65. https://www.sciencedirect.com/science/article/pii/S0264410X21004011
  66. https://www.cdc.gov/acip/downloads/slides-2025-09-18-19/policy-recs-mmrv-briefing-508.pdf
  67. https://www.cdc.gov/vaccines/hcp/imz-schedules/child-adolescent-catch-up.html
  68. https://www.gov.uk/government/news/free-chickenpox-vaccination-offered-for-first-time-to-children
  69. https://adc.bmj.com/content/110/8/586
  70. https://www.cdc.gov/vaccine-safety/vaccines/varicella.html
  71. https://www.canada.ca/en/public-health/services/publications/healthy-living/canadian-immunization-guide-part-4-active-vaccines/page-24-varicella-chickenpox-vaccine.html
  72. https://academic.oup.com/jid/article/197/Supplement_2/S165/844351
  73. https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(24)00159-2/fulltext
  74. https://www.linkedin.com/pulse/north-america-mmrv-vaccines-market-size-yxege/
  75. https://www.vaccineadvisor.com/news/acip-changes-recommendation-for-mmr-varicella-vaccination/
  76. https://www.health.state.mn.us/diseases/varicella/school/index.html
  77. https://pmc.ncbi.nlm.nih.gov/articles/PMC7339085/
  78. https://open.alberta.ca/dataset/35d7f99e-a724-44f2-bea3-46c40be11eb9/resource/a7037a5c-004d-41e5-85f4-7833a9ba8838/download/health-phdmg-varicella-chickenpox-2021-09.pdf
  79. https://www.cdc.gov/mmwr/preview/mmwrhtml/mm6228a4.htm
  80. https://www.ncbi.nlm.nih.gov/books/NBK563284/
  81. https://www.cdc.gov/chickenpox/php/outbreak-control/index.html
  82. https://www.vdh.virginia.gov/content/uploads/sites/13/2016/03/Communicable_Disease_Chart.pdf
  83. https://publications.aap.org/pediatriccare/article/doi/10.1542/aap.ppcqr.396143/1544/Chickenpox
  84. https://emedicine.medscape.com/article/969773-treatment
  85. https://www.ncbi.nlm.nih.gov/books/NBK526101/
  86. https://emedicine.medscape.com/article/1131785-treatment
  87. https://clinicalinfo.hiv.gov/en/guidelines/hiv-clinical-guidelines-adult-and-adolescent-opportunistic-infections/varicella-zoster
  88. https://pmc.ncbi.nlm.nih.gov/articles/PMC8407192/
  89. https://pubmed.ncbi.nlm.nih.gov/2826611/
  90. https://www.nejm.org/doi/full/10.1056/NEJM199111283252203
  91. https://www.ncbi.nlm.nih.gov/books/NBK47401/
  92. https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/613970
  93. https://pubmed.ncbi.nlm.nih.gov/11737678/
  94. https://www.cdc.gov/infection-control/hcp/healthcare-personnel-epidemiology-control/varicella.html
  95. https://www.cdc.gov/shingles/hcp/clinical-overview/index.html
  96. https://www.ncbi.nlm.nih.gov/books/NBK493198/
  97. https://pmc.ncbi.nlm.nih.gov/articles/PMC3956687/
  98. https://pmc.ncbi.nlm.nih.gov/articles/PMC3693437/
  99. https://academic.oup.com/cid/article/76/3/e1335/6633277
  100. https://www.cdc.gov/chickenpox/vaccination-impact/index.html
  101. https://academic.oup.com/jid/article/226/Supplement_4/S407/6764826
  102. https://www.cdc.gov/shingles/data-research/index.html
  103. https://pubmed.ncbi.nlm.nih.gov/34936114/
  104. https://www.frontiersin.org/journals/public-health/articles/10.3389/fpubh.2025.1654535/full
  105. https://doi.org/10.3760/cma.j.cn112338-20210308-00185
  106. https://pmc.ncbi.nlm.nih.gov/articles/PMC10503957/
  107. https://onlinelibrary.wiley.com/doi/10.1002/jmv.70458
  108. https://pmc.ncbi.nlm.nih.gov/articles/PMC9151238/
  109. https://pubmed.ncbi.nlm.nih.gov/37224620/
  110. https://pmc.ncbi.nlm.nih.gov/articles/PMC2966667/
  111. https://extranet.who.int/prequal/vaccines/list-prequalified-vaccines
  112. https://www.gov.uk/government/publications/introduction-of-a-routine-varicella-mmrv-vaccination-programme/introduction-of-a-routine-varicella-mmrv-vaccination-programme-for-children-at-one-year-and-at-18-months
  113. https://www.cdc.gov/acip/downloads/slides-2023-02-22-24/Varicella-01-Marin-508.pdf
  114. https://pmc.ncbi.nlm.nih.gov/articles/PMC8475589/
  115. https://www.sciencedirect.com/science/article/abs/pii/S0264410X09018362
  116. https://cdn.who.int/media/docs/default-source/immunization/sage/2025/march/sage_march_2025_highlights_final.pdf
  117. https://www.gminsights.com/industry-analysis/varicella-zoster-virus-infection-treatment-market
  118. https://pmc.ncbi.nlm.nih.gov/articles/PMC1118558/
  119. https://pmc.ncbi.nlm.nih.gov/articles/PMC9997050/
  120. https://pubmed.ncbi.nlm.nih.gov/20803570/
  121. https://www.etymonline.com/word/varicella
  122. https://pmc.ncbi.nlm.nih.gov/articles/PMC4628852/
  123. https://dermnetnz.org/topics/chickenpox
  124. https://www.icd10data.com/ICD10CM/Codes/A00-B99/B00-B09/B01-
  125. https://www.cuimc.columbia.edu/news/rising-shingles-cases-adults-put-unvaccinated-kids-risk
  126. https://www.usnews.com/news/articles/2015/04/10/parents-still-seek-natural-exposure-to-viruses
  127. https://www.healthline.com/health/home-remedies-for-chickenpox
  128. https://www.mdpi.com/2077-1444/10/3/147
  129. https://journals.lww.com/jras/fulltext/2021/05040/effect_of_add_on_ayurveda_treatment_in_the.3.aspx
  130. https://undergradjournal.history.ucsb.edu/our-journal/past-issues/fall-2021/isero/
  131. https://pmc.ncbi.nlm.nih.gov/articles/PMC3486720/
  132. https://www.nytimes.com/1895/10/02/archives/health-of-the-children-rules-made-to-prevent-the-spread-of.html
  133. https://pmc.ncbi.nlm.nih.gov/articles/PMC5381807/
  134. https://www.sciencedirect.com/science/article/pii/S2590053622000726
  135. https://pmc.ncbi.nlm.nih.gov/articles/PMC4235715/
  136. https://www.frontiersin.org/journals/microbiology/articles/10.3389/fmicb.2019.01634/full
  137. https://pmc.ncbi.nlm.nih.gov/articles/PMC6631480/
  138. https://pmc.ncbi.nlm.nih.gov/articles/PMC9577235/
  139. https://pubmed.ncbi.nlm.nih.gov/32244386/
  140. https://pmc.ncbi.nlm.nih.gov/articles/PMC7866336/
  141. https://pubmed.ncbi.nlm.nih.gov/37886544/
  142. https://www.fda.gov/media/108793/download
  143. https://www.researchgate.net/publication/394003896_Safety_Immunogenicity_and_Efficacy_of_the_Shingrix_Vaccine_in_Immunocompromised_Varicella_Zoster_Virus_Naive_Pediatric_Patients
  144. https://pubmed.ncbi.nlm.nih.gov/38614117/
  145. https://www.tandfonline.com/doi/full/10.1080/14760584.2025.2514527
  146. https://www.sciencedirect.com/science/article/pii/S1045105614000487
  147. https://www.gsk.com/en-gb/media/press-releases/gsk-delivers-strong-q3-performance-and-upgrades-2025-guidance/
  148. https://www.gsk.com/media/4apgltkt/press-release-aaic.pdf
  149. https://pmc.ncbi.nlm.nih.gov/articles/PMC6310478/
  150. https://wwwnc.cdc.gov/eid/article/30/12/24-0538_article
  151. https://pmc.ncbi.nlm.nih.gov/articles/PMC4838733/
  152. https://www.thelancet.com/journals/lanwpc/article/PIIS2666-6065%2822%2900254-1/fulltext
  153. https://pmc.ncbi.nlm.nih.gov/articles/PMC5079377/
  154. https://www.researchgate.net/publication/387937375_Intelligent_skin_disease_prediction_system_using_transfer_learning_and_explainable_artificial_intelligence
  155. https://www.researchandmarkets.com/reports/6174861/varicella-zoster-virus-infection-treatment
  156. https://terrance.who.int/mediacentre/data/sage/SAGE_Docs_Ppt_Apr2014/6_session_varicella_herpes_zoster/Apr2014_session6_Presentation2_varicella.pdf
  157. https://www.sciencedirect.com/science/article/pii/S0264410X21015371
Add your contribution
Related Hubs
User Avatar
No comments yet.