{
  "id": "chickenpox",
  "title": "Chickenpox",
  "lang": "en",
  "source_lang": "en",
  "summary": "Chickenpox is a highly contagious viral infection characterized by an itchy rash and preventable through vaccination.",
  "category": "health",
  "subcategory": "diseases",
  "type": "concept",
  "aliases": [
    "Varicella"
  ],
  "generated_at": "2026-10-13",
  "model": "pro/gpt-6.1-sol",
  "url": "https://aiwiki.page/en/chickenpox/",
  "translations": {
    "zh-Hans": {
      "url": "https://aiwiki.page/zh/chickenpox/",
      "json": "https://aiwiki.page/zh/chickenpox.json"
    }
  },
  "sections": [
    {
      "heading": "",
      "text": "Chickenpox, also called varicella, is a highly contagious infectious disease caused by primary infection with the varicella-zoster virus (VZV). Its characteristic itchy rash develops in successive crops, so spots, fluid-filled blisters, and crusts may appear together. Infection spreads principally through airborne exposure and contact with infectious lesions, and transmission can begin before the rash appears. (cdc.gov)\n\nAlthough usually self-limiting in otherwise healthy children, chickenpox can cause serious complications, including bacterial skin infections, pneumonia, and neurological disease. Adults, pregnant women, newborns, and people with impaired immune defenses are at greater risk of severe illness. After the initial infection, VZV remains latent in sensory nerve ganglia and can later reactivate as shingles, a distinct clinical manifestation of the same virus. (cdc.gov)\n\nThe development of a chickenpox vaccine transformed prevention, substantially reducing illness, hospitalization, and deaths where vaccination programs achieved high coverage. Understanding the disease encompasses its viral biology, transmission and population distribution, clinical course, diagnosis and treatment, and the vaccination and public health measures used to control it. (cdc.gov)"
    },
    {
      "heading": "Varicella-Zoster Virus and the Infection Cycle",
      "text": "Varicella-zoster virus (VZV) is a human alphaherpesvirus whose primary infection produces chickenpox, or varicella. Its genome consists of linear, double-stranded DNA, approximately 125,000 base pairs long. In 1986, A. J. Davison and J. E. Scott published a complete VZV genome sequence comprising 124,884 base pairs and identified 70 genes through sequence analysis. After primary infection, VZV can remain in the body for life; reactivation of this persistent infection causes shingles, or herpes zoster, rather than a new primary episode of chickenpox. These are therefore different phases of infection with the same virus, not diseases caused by separate pathogens. (pubmed.ncbi.nlm.nih.gov)\n\nVZV enters through the respiratory tract or conjunctiva, the membrane covering the inner eyelids and anterior surface of the eye. Initial replication occurs in the nasopharynx and regional lymph nodes. The conventional description of its subsequent spread distinguishes a primary viremia—virus entering the bloodstream—approximately four to six days after infection, which carries VZV to tissues such as the liver and spleen, from a secondary viremia following further replication that delivers virus to the skin. Supporting the involvement of circulating infected cells, infectious VZV has been recovered from blood mononuclear cells from about five days before until one to two days after the rash appears. (cdc.gov)\n\nExperimental studies identify T cells as important vehicles for this bloodstream dissemination. In 2004, Chia-Chi Ku and colleagues demonstrated that VZV-infected human T cells could transfer infectious virus to human skin grafts in mice with severe combined immunodeficiency. In that model, infected T cells reached epithelial sites of replication within 24 hours of entering the circulation. The experiments support a cell-associated route to skin infection, rather than dissemination exclusively through freely circulating virus particles. They also showed that interferon-α responses in neighboring epidermal cells restricted viral expansion: blocking the human interferon receptor accelerated lesion formation and increased recovery of infectious virus. These findings distinguish delivery of VZV to the skin from its subsequent expansion into visible lesions. (pmc.ncbi.nlm.nih.gov)\n\nDuring primary infection, VZV also reaches sensory nerve ganglia, including dorsal-root ganglia beside the spinal cord and cranial sensory ganglia such as the trigeminal ganglia. These structures contain the cell bodies of sensory neurons and become sites of viral latency. Latency differs from productive infection: the viral genome persists, but the broad program of viral gene expression and production of infectious progeny is suppressed. When reactivation occurs, productive replication resumes, and virus can travel along sensory nerves to the skin. The relationship between immune control and reactivation is distinct from the bloodstream dissemination responsible for primary chickenpox. (cdc.gov)\n\nLatency does not mean that every viral gene is completely silent. In 2018, Daniel P. Depledge, Werner J. D. Ouwendijk, and colleagues used virus-enriched RNA sequencing to identify a VZV latency-associated transcript, termed VLT, in human trigeminal ganglia. VLT was detected in all seven ganglia examined in the discovery analysis, whereas transcripts from most viral genes were absent. Its restricted expression illustrates how persistent viral DNA can remain biologically active without undergoing the coordinated replication cycle that generates infectious virus. Detection of viral DNA or a latency-associated transcript is therefore not equivalent to evidence of productive infection. (nature.com)"
    },
    {
      "heading": "Transmission and Infectious Period",
      "text": "Varicella-zoster virus (VZV) spreads through direct contact with fluid from infectious skin blisters and through airborne transmission of aerosols originating from their vesicular fluid. Both chickenpox lesions and active shingles lesions can supply infectious material. Infected respiratory secretions from people with chickenpox may also become aerosolized and contribute to transmission, although this route is described less definitively than transmission from lesions. Skin lesions are considered the major source of transmissible VZV; infection therefore does not require a susceptible person to touch a blister directly. (cdc.gov)\n\nExposure to either chickenpox or shingles (herpes zoster) can cause chickenpox in a person without immunity to VZV. The recipient develops primary infection, not shingles: shingles results from reactivation of virus already present in the body. Localized shingles is infectious from rash onset until its lesions crust, and covering the lesions reduces the likelihood of transmission. It is generally less contagious than chickenpox. CDC cites a household study in which transmission risk from shingles was approximately one-fifth of that from chickenpox; this estimate concerns transmission to susceptible contacts, not the probability that an exposed person will develop shingles. (cdc.gov)\n\nThe incubation period—the interval between exposure and development of disease—is usually 14–16 days, with a range of 10–21 days. The same interval applies whether the source has chickenpox or shingles. Incubation and infectiousness are distinct: the incubation interval describes the delay before illness becomes apparent, whereas the infectious period identifies when the infected person can transmit VZV. A person with chickenpox can therefore transmit infection before the characteristic rash provides a visible indication of disease. (cdc.gov)\n\nChickenpox is considered infectious from 1–2 days before rash onset until all lesions have crusted. The endpoint depends on the condition of the lesions rather than a fixed number of days after the rash begins. Vaccinated people with breakthrough infection may develop predominantly flat or raised lesions that never form vesicles or crusts. For these non-crusting cases, the alternative endpoint is no new lesions appearing for 24 hours. Vaccination history alone does not establish that a person with an active chickenpox eruption is noninfectious. (cdc.gov)\n\nHousehold transmission illustrates the high contagiousness of chickenpox: reported secondary attack rates among susceptible household contacts range from 61% to 100%. These rates describe infection among susceptible contacts, not among every household member regardless of immunity. Breakthrough cases can also transmit VZV. In a household study of recipients of one vaccine dose, cases with fewer than 50 lesions were approximately one-third as contagious as unvaccinated cases; breakthrough cases with 50 or more lesions were as contagious as unvaccinated cases. Thus, reduced lesion numbers can accompany reduced infectiousness, but a vaccinated source remains capable of spreading infection. (cdc.gov)"
    },
    {
      "heading": "Epidemiology and Population Burden",
      "text": "Before widespread vaccination, chickenpox was predominantly a childhood infection in temperate countries, where most children acquired it by age 10. In some tropical populations, infection occurred later, leaving a larger proportion of adolescents and young adults susceptible and consequently a greater proportion of cases among adults. The reasons for this geographical difference in age distribution are not established with certainty. The distinction matters for population burden because adults have a higher risk of severe disease than otherwise healthy children. These patterns describe populations with substantial natural transmission, rather than an age distribution that necessarily persists after high vaccination coverage. (cdc.gov)\n\nSeasonality was also conspicuous before vaccination. In temperate settings, incidence generally peaked in winter and early spring, whereas tropical settings showed less pronounced seasonal variation. The CDC’s Pink Book reports that high vaccination coverage in the United States eliminated discernible seasonality. Seasonal patterns therefore need to be interpreted alongside immunization coverage: the historical winter–spring peak is not an invariant feature of chickenpox in every climate or vaccination era. (cdc.gov)\n\nThe early-1990s United States baseline was a historical national estimate of approximately 4 million cases annually, not a count of individually reported cases. Before vaccination, almost everyone eventually acquired chickenpox, so the annual number of infections approximately matched the size of the birth cohort. The CDC estimates that this burden produced 10,500–13,500 hospitalizations and 100–150 deaths each year. Approximately 90% of cases occurred before age 15, with the highest reported incidence among children aged 1–4 years. Routine vaccination began in 1995, followed by the addition of a second childhood dose in 2007; these dates distinguish the subsequent one-dose and two-dose observation periods. (cdc.gov)\n\nThe strongest long-term case comparison comes from Illinois, Michigan, Texas, and West Virginia, which continuously reported cases to the National Notifiable Diseases Surveillance System before and after vaccine introduction. Comparing 1990–1994 with 2018–2019, reported incidence declined by an average of 98.6% across these four states, with state-specific reductions of 96.5%–99.0%. A broader analysis of reporting jurisdictions found an 88.6% decline, from 28.7 cases per 100,000 population in 2005–2006 to 3.3 in 2018–2019. Coverage expanded from 25 states and the District of Columbia in 2005 to 39 states and the District in 2019. These surveillance results document large reductions, but their geographical coverage and changing reporting completeness distinguish them from a complete national enumeration of infections. (academic.oup.com)\n\nSevere outcomes were measured using separate national data sources. A 2022 study by Mona Marin and colleagues analyzed hospitalizations in the nationally representative National Inpatient Sample for 1993–2019 and death-certificate data from the National Center for Health Statistics for 1990–2019. Across all ages, the age-adjusted hospitalization rate fell approximately 90%, from 4.4 per 100,000 population in 1993–1995 to 0.4 in 2018–2019. The age-adjusted mortality rate with varicella recorded as the underlying cause declined 89%, from 0.41 per million in 1990–1994 to 0.05 in 2017–2019. Among people younger than 20, the corresponding reductions were 97% for hospitalization and more than 99% for underlying-cause mortality, using the same respective baseline and endpoint periods. (stacks.cdc.gov)"
    },
    {
      "heading": "Clinical Presentation and Disease Course",
      "text": "A brief prodrome may precede the rash, particularly in adults: fever, malaise, headache, and reduced appetite can begin 1–2 days before the skin eruption. In children, however, the rash is often the first recognized sign, without an obvious preceding illness. The early clinical pattern therefore differs by age: an adult may initially experience nonspecific constitutional symptoms, whereas a child may first present with itchy spots. Neither fever nor a recognizable prodrome is required for chickenpox to occur, especially in vaccinated patients. (cdc.gov)\n\nIn unvaccinated patients, individual lesions progress rapidly from macules—flat areas of altered skin color—to papules, which are raised solid lesions, and then to vesicles containing fluid. This progression can occur within approximately 24 hours; the vesicles subsequently dry and form crusts. Typical lesions measure about 1–4 mm across. The vesicles are superficial and fragile, with clear fluid over an erythematous, or reddened, base; some rupture or become purulent before crusting. The eruption usually begins on the scalp, face, or trunk and spreads to the limbs, with the greatest concentration on the trunk. Lesions may also affect mucosal surfaces, including the oropharynx, conjunctiva, and vagina, rather than being confined to external skin. (cdc.gov)\n\nNew lesions appear in successive crops over several days rather than developing simultaneously. Healthy, unvaccinated children commonly have approximately 250–500 lesions in two to four crops. Consequently, a single area of skin can contain fresh macules, raised papules, fluid-filled vesicles, and older crusts at the same time. This coexistence of developmental stages is a characteristic clinical feature. The eruption generally evolves into crusts over 4–7 days, although the appearance of new crops means that individual lesions are at different points in that process. (cdc.gov)\n\nUncomplicated chickenpox in otherwise healthy children is usually mild and self-limiting. Fever may reach approximately 102°F (38.9°C), and fever and other systemic symptoms generally subside within 2–4 days after rash onset; the overall symptomatic illness typically lasts 4–7 days. Thus, constitutional symptoms may improve while the skin eruption is still evolving. Adolescents and adults are more likely than healthy young children to develop severe illness and complications, so the usual mild childhood course does not describe all age groups. (cdc.gov)\n\nBreakthrough chickenpox is infection with wild-type varicella-zoster virus occurring more than 42 days after vaccination, not simply any rash following a vaccine dose. It usually causes fewer than 50 lesions, little or no fever, and a shorter illness than chickenpox in unvaccinated patients. The eruption is often predominantly maculopapular, with few or no vesicles, making its appearance less distinctive and its clinical recognition more difficult. These are typical patterns rather than guarantees: approximately 25%–30% of breakthrough cases among children who received one vaccine dose have clinical features resembling unvaccinated disease, and rare severe cases with dissemination to internal organs have been reported. (cdc.gov)"
    },
    {
      "heading": "Complications and Severe Disease",
      "text": "Secondary bacterial infections of skin lesions and underlying soft tissues are the most common complications in children. Important pathogens include Staphylococcus aureus and group A Streptococcus. These infections can produce cellulitis or progress to necrotizing fasciitis, in which deeper soft tissues are destroyed, and invasive streptococcal disease with bloodstream infection or toxic shock syndrome. Sepsis represents a systemic complication rather than merely an infected skin lesion. Bacterial infection is a major reason for chickenpox-related hospitalization and can be fatal; its cause is distinct from the varicella-zoster virus responsible for the original eruption. (cdc.gov)\n\nPneumonia following chickenpox may be primary viral pneumonia, caused by varicella-zoster virus involvement of the lungs, or secondary bacterial pneumonia. This distinction separates a direct complication of the viral infection from an additional infection by another pathogen. Primary viral pneumonia is uncommon in immunocompetent children but is the most common complication in adults. Secondary bacterial pneumonia is more frequent in children younger than one year. Consequently, pulmonary complications do not have the same distribution or underlying cause across age groups. (cdc.gov)\n\nComplications affecting the central nervous system include cerebellar ataxia, characterized by impaired balance and coordination, and encephalitis, involving inflammation of the brain. Cerebellar involvement is the most common neurological manifestation and generally has a favorable outcome. The CDC’s Pink Book gives approximate frequencies of one cerebellar ataxia episode per 4,000 chickenpox cases and one encephalitis episode per 50,000 cases in unvaccinated children; these estimates should not be applied indiscriminately to vaccinated populations or adults. Encephalitis can cause seizures and coma, and diffuse cerebral involvement is more common in adults than in children. Other uncommon neurological complications include aseptic meningitis, transverse myelitis, and Guillain–Barré syndrome. (cdc.gov)\n\nRare bleeding complications include thrombocytopenia, a reduction in circulating platelets, hemorrhagic varicella, and purpura fulminans. These are distinct from the ordinary vesicular rash and can accompany severe disease. Fatal outcomes can result from bacterial, pulmonary, neurological, or hemorrhagic complications. Severe illness is more frequent in infants, adults, pregnant patients, and people with impaired immunity, although serious complications and deaths also occur in previously healthy children and adults. Vaccinated people can develop severe breakthrough disease, despite its usually milder course. (cdc.gov)\n\nReye syndrome is a separate, rare complication associated with aspirin or other salicylate exposure during childhood chickenpox. It affects the liver and brain and may present during recovery with vomiting and lethargy, progressing to delirium or coma. Case-control investigations documented the association between salicylate use during antecedent viral illness and subsequent Reye syndrome. These findings prompted a United States Surgeon General advisory in June 1982. Later surveillance documented a marked decline in Reye syndrome alongside declining aspirin use in children; Reye syndrome following chickenpox has consequently become very rare. (portugues.cdc.gov)"
    },
    {
      "heading": "Pregnancy, Newborns, and Immunocompromised Patients",
      "text": "Chickenpox during pregnancy carries an increased risk of severe maternal illness, particularly viral pneumonia, which can be fatal. Maternal complications and fetal effects are distinct: serious illness in the pregnant patient does not necessarily imply congenital abnormalities, and fetal risk depends strongly on gestational timing. Some studies have reported more frequent or more severe varicella pneumonia during the third trimester, but this association has not been consistently demonstrated. (cdc.gov)\n\nMaternal infection during early pregnancy can cause congenital varicella syndrome, a pattern of fetal injury rather than simply an acute rash in the newborn. Characteristic findings include skin scars following a dermatomal distribution, underdevelopment of an extremity, microcephaly, ocular and neurological abnormalities, and low birth weight. The estimated risk following maternal chickenpox in the first or early second trimester is approximately 0.4–2.0%; most exposed pregnancies therefore do not result in this syndrome. The cutaneous, limb, and neurological abnormalities distinguish congenital varicella syndrome from infection acquired around delivery. (cdc.gov)\n\nGestational timing was quantified in a prospective study by G. Enders and colleagues, published in 1994, which followed pregnancies in Germany and the United Kingdom between 1980 and 1993. Among 1,373 women with maternal varicella, nine cases of congenital varicella syndrome were identified, all following infection during the first 20 weeks. Two affected infants occurred among 472 pregnancies with infection before 13 weeks, an observed risk of 0.4%; seven occurred among 351 pregnancies with infection at 13–20 weeks, an observed risk of 2.0%. These are estimates from defined gestational subgroups, not a uniform risk applying throughout pregnancy. The same study followed 366 women with maternal shingles and found no infants with clinical evidence of intrauterine infection in that group. (pubmed.ncbi.nlm.nih.gov)\n\nSevere neonatal varicella is particularly associated with maternal rash beginning five days before through two days after delivery. In this interval, the infant may be exposed to varicella-zoster virus before sufficient protective maternal antibody has been transferred across the placenta. When maternal rash begins more than five days before birth, neonatal disease is usually milder because passive antibody transfer has had time to occur. The interval between maternal rash onset and neonatal rash onset is usually 9–15 days, although it can be as short as two days. Historical reports placed neonatal case fatality as high as 30% without antiviral treatment; this figure describes severe perinatal disease, not the risk among all newborns exposed to chickenpox. (cdc.gov)\n\nPremature infants constitute an additional vulnerable group. CDC guidance identifies exposed hospitalized infants born at 28 weeks’ gestation or later as being at risk when their mothers lack evidence of immunity. Hospitalized infants born before 28 weeks, or weighing 1,000 grams or less at birth, are considered at risk regardless of maternal immunity. Very premature infants may not have acquired sufficient maternal antibody before birth, so maternal protection cannot be assumed to provide equivalent neonatal protection. (cdc.gov)\n\nPatients with immunodeficiency, leukemia or lymphoma, or immune suppression caused by chemotherapy or high-dose systemic corticosteroids can develop progressive, disseminated chickenpox. Their illness may involve unusually numerous lesions, continued formation of new lesions beyond seven days, lesions on the palms and soles, or hemorrhagic lesions. Dissemination to internal organs can produce pneumonia, hepatitis, encephalitis, and disseminated intravascular coagulation; fulminant disease may involve several organ systems. In children with HIV infection, particularly those with low CD4 counts, new crops of lesions can persist for weeks or months and evolve into non-healing, necrotic ulcers. These prolonged or atypical manifestations differ from the usual self-limited eruption in immunocompetent children. (cdc.gov)"
    },
    {
      "heading": "Diagnosis and Laboratory Investigation",
      "text": "Clinical diagnosis rests on recognition of a generalized, itchy rash in which macules, papules, fluid-filled vesicles, and crusts coexist because lesions appear in successive crops. This pattern is less dependable in vaccinated patients: breakthrough disease may produce fewer than 50 lesions, predominantly maculopapular rather than vesicular, with little or no fever. Mild, atypical eruptions can resemble other skin disorders, so vaccination history and contact with a confirmed case help interpret the presentation but do not replace laboratory confirmation. Laboratory testing has become increasingly important as vaccination reduces both the frequency of characteristic disease and clinicians’ familiarity with it. (cdc.gov)\n\nLesion-based polymerase chain reaction (PCR) is the preferred confirmatory test. It detects varicella-zoster virus (VZV) DNA directly rather than measuring the patient’s immune response, and real-time methods can produce results within several hours. The principal specimens are vesicular fluid, epithelial cells from the lesion base, and scabs. In clinical collection, a vesicle is opened and its base swabbed to obtain infected cells; collecting fluid alone may miss this important material. Scabs are excellent PCR specimens even after vesicles have crusted. When vaccinated patients have only maculopapular lesions, abrasion and swabbing can provide suitable cellular material, although adequate collection is more difficult. (cdc.gov)\n\nA negative result does not necessarily exclude chickenpox, particularly when the specimen contains insufficient lesion material. For confirmation of a cutaneous eruption, saliva, nasopharyngeal secretions, urine, and other non-lesion samples are less reliable than skin specimens and can yield false-negative results. Conversely, detecting VZV establishes the presence of the virus but does not by itself distinguish primary chickenpox from reactivated shingles; the clinical distribution and history remain relevant. The same PCR technology is used to investigate both forms of VZV disease. (cdc.gov)\n\nSerum IgM testing has substantially lower sensitivity than lesion PCR and is prone to poor specificity. A positive result may accompany recent VZV activity, but IgM can be produced during primary infection, reinfection, or reactivation, so it cannot reliably distinguish these events. IgG testing serves a different purpose: a single positive result documents antibodies arising from previous infection or vaccination, not the cause of a current rash. Paired acute and convalescent samples showing at least a fourfold rise in IgG can support acute infection, but this approach is less sensitive than lesion PCR, delays confirmation, and may fail in previously infected or vaccinated people with high baseline antibody levels. (cdc.gov)\n\nCommercial IgG assays generally detect immunity following natural infection more readily than vaccine-induced antibodies, which often occur at lower concentrations. Consequently, a negative commercial IgG result after vaccination does not necessarily indicate absence of immunity. Routine postvaccination antibody testing is therefore not recommended in CDC guidance. More sensitive purified-glycoprotein enzyme-linked immunosorbent assays have been used in research to measure vaccine responses, but are not commercially available for routine testing. (cdc.gov)\n\nSpecialized strain-discriminating PCR and genotyping distinguish wild-type VZV from the Oka-derived vaccine strain. These investigations are used, for example, for suspected vaccine-associated rash occurring 7–42 days after vaccination, shingles in a vaccine recipient, or suspected transmission of vaccine-strain virus. CDC and designated public-health reference laboratories provide such differentiation. Viral culture and direct fluorescent antibody testing are alternative detection methods, but both are less sensitive than PCR; culture also takes longer. Direct fluorescent antibody testing requires particularly careful specimen collection and handling, while a Tzanck smear lacks specificity for VZV and is not recommended for confirmation. (cdc.gov)"
    },
    {
      "heading": "Treatment and Clinical Management",
      "text": "Supportive care addresses itching, fever, discomfort, and maintenance of hydration. Calamine lotion and cool baths are used for symptomatic relief, while measures that limit scratching reduce damage to the skin and the risk of secondary infection. Acetaminophen, also called paracetamol, is used for fever and pain. Pediatric care excludes aspirin because its use during chickenpox is associated with Reye syndrome; CDC guidance dated April 24, 2024, also reports the American Academy of Pediatrics’ recommendation to avoid ibuprofen where possible because of its association with serious bacterial skin infections. Fluid intake and assessment for dehydration are additional components of care, particularly when a child is drinking poorly. These measures relieve symptoms but do not directly inhibit viral replication. (cdc.gov)\n\nAcyclovir acts against varicella-zoster virus (VZV) through a different mechanism. Viral thymidine kinase initiates its conversion to a phosphorylated compound, and cellular enzymes produce the active triphosphate. This metabolite inhibits viral DNA polymerase and terminates the growing viral DNA chain. Evidence for oral treatment of uncomplicated disease primarily concerns early administration. A multicenter, placebo-controlled trial published in 1991 enrolled 815 otherwise healthy children aged 2–12 years, with treatment beginning within 24 hours of rash onset. Mean lesion counts were 294 in the acyclovir group and 347 in the placebo group; 21% and 38%, respectively, developed more than 500 lesions. Healing and symptom resolution were faster with acyclovir, but the trial found no significant difference in complications and did not establish prevention of rare, serious outcomes. (dailymed.nlm.nih.gov)\n\nClinical selection therefore distinguishes modest reductions in uncomplicated illness from treatment of patients at greater risk. CDC’s April 2024 clinical guidance, citing the American Academy of Pediatrics, identifies oral acyclovir or valacyclovir as options for selected groups, including otherwise healthy people older than 12 years, people with chronic skin or lung disorders, and those receiving long-term salicylates or certain corticosteroid regimens. Routine oral antiviral treatment is not recommended for otherwise healthy children with typical, uncomplicated chickenpox. Maximum benefit is associated with initiation within the first 24 hours after the rash appears. (cdc.gov)\n\nSevere or disseminated disease changes the treatment approach: intravenous acyclovir is used for complications such as viral pneumonia, encephalitis, severe hepatitis, or thrombocytopenia, and for varicella in immunocompromised patients. Pregnancy complicated by varicella pneumonia is another indication for intravenous treatment. Thus, immune status and organ involvement, rather than rash extent alone, influence route selection. Acyclovir-resistant VZV, encountered especially in immunocompromised patients, may require foscarnet under specialist management. (cdc.gov) Acyclovir is cleared through the kidneys; clinical management includes attention to renal function, hydration, and dose adjustment when clearance is reduced. Hospital pediatric guidance also emphasizes fluid-balance recording because dehydration can increase the risk of acyclovir-associated renal impairment. (dailymed.nlm.nih.gov)\n\nSecondary bacterial infection requires assessment and treatment distinct from antiviral therapy. Increasing redness, warmth, tenderness, or purulent discharge around lesions can indicate bacterial involvement. Antibiotics may be used for infected skin lesions, whereas serious bacterial complications can require intravenous antibiotics and additional hospital care. Antibiotics act against bacteria, not VZV; conversely, suppression of VZV replication with acyclovir does not replace antibacterial treatment when bacterial infection is present. (cdc.gov)"
    },
    {
      "heading": "Immunity and the Relationship to Shingles",
      "text": "Primary varicella infection induces both antibody responses and T-cell–mediated immunity. VZV-specific antibodies, including persistent immunoglobulin G (IgG), contribute to protection against subsequent exposure, while cellular responses are particularly important in controlling infected cells and limiting disease. These defenses have distinct functions: circulating antibodies do not by themselves prevent reactivation of virus already present in sensory ganglia. In a 2009 study led by Adriana Weinberg, involving 981 older adults who developed herpes zoster during a vaccine trial and 1,362 who did not, stronger VZV-specific cellular responses at zoster onset correlated with less severe disease; antibody concentrations did not show the same protective association. (ncbi.nlm.nih.gov)\n\nRecovery from chickenpox usually provides long-lasting, often lifelong protection against another clinical episode. A second episode is uncommon in otherwise healthy people, although it occurs more frequently in people with impaired immunity. Protection against illness is not equivalent to preventing every subsequent infection: re-exposure to wild-type VZV can boost antibody concentrations without producing recognizable chickenpox or detectable virus in the bloodstream. Nor does recovery eliminate the original virus. Persistent infection therefore explains how a person can remain protected against a second generalized episode of chickenpox yet develop shingles, or herpes zoster, decades later. (cdc.gov)\n\nThe association between aging and shingles principally concerns declining VZV-specific cellular immunity rather than a simple disappearance of antibodies. A 2010 study by Weinberg and colleagues analyzed VZV-responsive immune-cell measurements from 752 healthy and 200 HIV-infected participants; among healthy participants with previous chickenpox, the modeled response peaked at approximately 34 years of age. This population-level finding does not establish an individual threshold for reactivation. Aging and immunosuppression are established risk factors for shingles, but neither makes reactivation inevitable, and shingles can also occur in younger people without recognized immune impairment. (pubmed.ncbi.nlm.nih.gov)\n\nDuring reactivation, VZV resumes productive replication in sensory neurons, and newly formed virus travels along nerves to the skin. Unlike chickenpox’s generalized, predominantly trunk-centered eruption, shingles usually produces clustered vesicles within a dermatome—the skin territory supplied by a particular sensory nerve. The eruption is generally unilateral and does not cross the body’s midline; pain or abnormal sensation may precede it by two to four days. Disseminated shingles is an important exception, particularly in immunocompromised patients. Shingles represents renewed activity of the persistent infection, not an acute complication of the original chickenpox episode or a newly acquired infection that directly produces zoster. (cdc.gov)\n\nThe molecular mechanisms maintaining viral latency and initiating reactivation remain incompletely defined. Latency involves suppressed productive replication, not continuous production of infectious virus. In 2018, Daniel P. Depledge, Werner J. D. Ouwendijk, and colleagues identified a VZV latency-associated transcript, termed VLT, in human trigeminal-ganglion neurons. In laboratory co-transfection experiments, the latency-associated form of VLT selectively suppressed expression of ORF61, a viral gene involved in regulating productive infection. This provides evidence for a viral mechanism that may help restrain replication, but it does not establish the complete sequence of events triggering shingles in humans. How neuronal regulation and host immune defenses interact to maintain latency—and why that balance fails at a particular time—remains unresolved. (nature.com)"
    },
    {
      "heading": "Vaccines and Immunization Programs",
      "text": "Varicella vaccines contain live attenuated varicella-zoster virus rather than inactivated virus or isolated viral proteins. The United States products use virus derived from the Oka strain, weakened through serial passage in cell cultures. Single-antigen preparations, such as Varivax, protect against varicella alone; measles–mumps–rubella–varicella (MMRV) vaccines, such as ProQuad, combine four vaccine components in one injection. In the United States, single-antigen vaccine is licensed from 12 months of age, whereas MMRV is licensed for children aged 12 months through 12 years. Product licensing and age limits are distinct from the schedules adopted by immunization programs. (cdc.gov)\n\nOne-dose and two-dose strategies differ principally in their prevention of infection and breakthrough disease, rather than solely in protection against severe illness. CDC summarizes post-licensure evidence as approximately 82% effectiveness against varicella of any severity after one dose and approximately 92% after two doses; one-dose protection against severe disease is already very high. A second dose boosts immunity and reduces breakthrough infections, but does not guarantee that infection cannot occur. A clinical trial with ten-year follow-up found fewer breakthrough cases among two-dose recipients than among one-dose recipients. These effectiveness estimates concern clinical disease and should not be interpreted as identical to the proportion developing detectable antibodies. (cdc.gov)\n\nEvidence-of-immunity criteria determine eligibility for routine and catch-up vaccination. CDC guidance dated July 15, 2024, accepts documented age-appropriate vaccination, laboratory evidence of immunity or laboratory-confirmed disease, and healthcare-provider diagnosis or verification of previous varicella or shingles. Birth in the United States before 1980 is also accepted in some settings, but not for healthcare personnel, pregnant women, or immunocompromised people. Commercial antibody assays can detect immunity following natural infection but may miss lower antibody concentrations after vaccination, producing false-negative results. Consequently, a negative commercial test does not necessarily invalidate documented vaccination. (cdc.gov)\n\nCommon adverse reactions include injection-site discomfort, fever, and a mild varicella-like rash; serious vaccine-associated illness is rare. Formulation matters: post-licensure studies in children aged 12–23 months found approximately one additional febrile seizure per 2,300–2,600 first-dose MMRV recipients during days 5–12, compared with separate MMR and varicella injections at the same visit. The increased risk was not observed with the second MMRV dose at ages 4–6 years. Established contraindications include a severe allergic reaction to a previous dose or component, pregnancy, and substantial immunosuppression. Restrictions are not uniform across all immune disorders: selected people with HIV infection and adequate immune function may receive single-antigen vaccine under defined protocols, whereas MMRV has stricter exclusions. (cdc.gov)\n\nNational programs differ in timing and vaccine selection. CDC’s July 2024 guidance specifies a routine United States two-dose schedule at 12–15 months and 4–6 years, with catch-up vaccination for susceptible older children, adolescents, and adults. England introduced routine MMRV vaccination on January 1, 2026, offering doses at 12 and 18 months. Its implementation also includes birth-cohort-specific transitional arrangements, rather than applying the new infant schedule retrospectively to every child. These are population-program schedules, not individualized prescribing instructions. (cdc.gov)\n\nThe World Health Organization position paper published on November 21, 2025, superseded its June 2014 varicella guidance. It recommends childhood vaccination where varicella constitutes an important public-health problem and favors two doses for effective prevention, while recognizing that a one-dose program can reduce mortality and severe morbidity but controls circulation and outbreaks less effectively. Either single-antigen or MMRV vaccines may be used. Instead of imposing a universal minimum coverage percentage, the paper calls for high national and subnational coverage, with countries setting targets according to disease burden, affordability, cost-effectiveness, seroprevalence, and age at infection. This framework permits different national implementation choices while distinguishing program objectives from individual clinical eligibility. (who.int)"
    },
    {
      "heading": "Surveillance, Exposure Management, and Outbreak Control",
      "text": "In the United States, standardized case definitions distinguish surveillance classifications from individual clinical diagnosis. The 2024 definition, approved by the Council of State and Territorial Epidemiologists in June 2023, accepts an acute generalized rash with or without vesicles when no alternative diagnosis is more likely. A case is confirmed when compatible clinical illness accompanies confirmatory laboratory evidence, or when a vesicular generalized rash accompanies a qualifying epidemiological link, including contact with a laboratory-confirmed case or a person with shingles. A vesicular rash without such confirmation can constitute a probable case; non-vesicular illness requires additional epidemiological or laboratory support. PCR testing of scabs, vesicular fluid, or scrapings from non-vesicular lesions is the preferred laboratory confirmation method. Positive IgM is supportive rather than confirmatory evidence. (ndc.services.cdc.gov)\n\nCase-based public-health surveillance connects reports from clinicians, laboratories, schools, and institutions with health departments. Reporting obligations vary by jurisdiction; states transmit notifications through the National Notifiable Diseases Surveillance System. In 2002, CSTE recommended establishing case-based surveillance by 2005, while varicella-related deaths became nationally notifiable on January 1, 1999. Investigation records include age, illness and rash onset dates, lesion characteristics, laboratory results, exposure setting, and epidemiological links. Vaccination records specify dose numbers and administration dates; severity records include lesion counts, complications, hospitalization, and death. Recording pregnancy and immunocompromising conditions helps identify exposures involving people at elevated risk of severe disease. (cdc.gov)\n\nCDC defines an outbreak as at least three cases related by place and epidemiological linkage, although a single suspected case can trigger control measures. In schools, childcare facilities, residential institutions, and healthcare settings, investigations combine active case finding, laboratory sampling, an outbreak line list, and reconstruction of exposure during each case’s infectious period. For larger outbreaks, CDC recommends laboratory confirmation of three to five cases, particularly early in the investigation. Classroom exposure usually makes the entire class a contact group. Investigators assess documented vaccination, laboratory evidence of immunity, and verified previous varicella or shingles to identify susceptible contacts. Active surveillance continues for 42 days—two full incubation periods—after rash onset in the last identified case. (cdc.gov)\n\nCases are excluded from communal settings until all lesions have crusted; cases with only non-vesicular lesions remain excluded until no new lesions appear for 24 hours. Healthcare infection control combines standard, airborne, and contact precautions, with a negative-pressure isolation room where available. Residential institutions use immediate closed-room isolation and separation from susceptible residents. (cdc.gov) CDC’s healthcare-personnel guidance dated March 23, 2026, distinguishes immune exposed staff, who generally remain at work under daily symptom monitoring, from susceptible exposed staff, who are generally excluded from day 8 after first exposure through day 21 after last exposure. After immune-globulin prophylaxis, that exclusion extends through day 28. (cdc.gov)\n\nPost-exposure vaccination and varicella-zoster immune globulin serve distinct functions within public-health protocols. Vaccination stimulates active immunity in eligible susceptible contacts; administration within three to five days of exposure may prevent illness or reduce its severity. Vaccination later in an outbreak can protect against subsequent exposures rather than reliably prevent infection already acquired. (cdc.gov) Immune globulin supplies preformed antibodies for selected susceptible contacts at high risk of severe disease who cannot receive vaccine, including pregnant or immunocompromised people and specified neonatal or premature-infant groups. The United States product, VariZIG, is administered as soon as possible and within ten days of exposure. It provides passive protection rather than establishing durable vaccine-induced immunity, and its potential to prolong incubation accounts for monitoring through 28 days after exposure. (cdc.gov)"
    },
    {
      "heading": "Historical Recognition and Vaccine Development",
      "text": "Chickenpox was historically confused with smallpox, because both diseases produced generalized eruptions containing fluid-filled lesions. In 1767, the English physician William Heberden provided a detailed clinical description of chickenpox as a separate disease. He noted that its blisters could mature by the second or third day of the eruption, whereas comparable smallpox lesions developed more slowly. This distinction preceded reliable routine differentiation, which the Centers for Disease Control and Prevention places near the end of the nineteenth century. The diagnostic differences were consequential: chickenpox typically produces superficial lesions in successive crops, leaving blisters and crusts together on the same body region; ordinary smallpox produces deeper, firmer lesions that are generally at the same developmental stage within a given region. Recognizing these patterns helped distinguish two separate infections rather than treating chickenpox as a mild form of smallpox. (publications.aap.org)\n\nExperimental investigation subsequently established the infectious basis of chickenpox and made vaccine development technically possible. In 1875, Rudolf Steiner demonstrated transmission by inoculating volunteers with fluid from chickenpox vesicles. In 1954, Thomas Weller isolated varicella-zoster virus in cell culture from vesicular material obtained from patients with chickenpox or shingles. Cultivation supplied a means of propagating the agent outside patients, an essential step toward preparing and evaluating a live-virus vaccine. These laboratory milestones were distinct from the earlier clinical recognition of chickenpox as a separate disease. (cdc.gov)\n\nIn Japan during the early 1970s, Michiaki Takahashi and colleagues developed the live attenuated Oka vaccine strain from virus isolated from an otherwise healthy child with chickenpox. Attenuation involved sequential propagation in human embryonic lung cells, guinea-pig embryonic cells, and human diploid WI-38 cells. The resulting preparation contained living virus with reduced virulence rather than chemically inactivated virus. Takahashi’s team reported hospital use in The Lancet in November 1974 and described its development in the Biken Journal in March 1975. The latter study tested preparations in susceptible children aged 1–10 years, reported antibody responses, and observed no clinical reactions attributable to vaccination in the children studied. These were early experimental findings, not a substitute for the subsequent clinical evaluation required for broad licensing. (cdc.gov)\n\nThe United States licensed single-antigen varicella vaccine in 1995 for people aged 12 months or older. In 2005, it licensed the combined measles–mumps–rubella–varicella vaccine, abbreviated MMRV, for children aged 12 months through 12 years. MMRV placed protection against varicella and three other infections in one vaccine product; it did not represent the discovery of a new chickenpox pathogen or a new principle of attenuation. Licensing and immunization-policy decisions were separate milestones: the initial American routine childhood program used one dose, while continued outbreaks prompted a two-dose recommendation in 2006. These dates describe the historical development of the program rather than a complete statement of present-day vaccination policy. (cdc.gov)\n\nThe transition to vaccine-era control can be measured against the early-1990s American baseline, when an estimated four million chickenpox cases occurred annually and approximately 90% occurred before age 15. Two active-surveillance sites recorded an approximately 90% decline in incidence between 1995 and 2005. The changing age distribution also reflected reduced childhood transmission: peak incidence in active-surveillance sites shifted from ages 3–6 years to ages 9–11 years during 1995–2004. The remaining school outbreaks, including outbreaks initiated by vaccinated children with mild disease, helped explain the subsequent move beyond the original one-dose strategy. These observations document successive stages of disease control, not eradication of varicella-zoster virus. (cdc.gov)"
    }
  ],
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  ],
  "sources": [
    {
      "title": "Chapter 22: Varicella",
      "url": "https://www.cdc.gov/pinkbook/hcp/table-of-contents/chapter-22-varicella.html?CDC_AAref_Val=https%3A%2F%2Fwww.cdc.gov%2Fvaccines%2Fpubs%2Fpinkbook%2Fvaricella.html"
    },
    {
      "title": "The complete DNA sequence of varicella-zoster virus",
      "url": "https://pubmed.ncbi.nlm.nih.gov/3018124/"
    },
    {
      "title": "Varicella-Zoster Virus Transfer to Skin by T Cells and Modulation of Viral Replication by Epidermal Cell Interferon-α",
      "url": "https://pmc.ncbi.nlm.nih.gov/articles/PMC2213285/"
    },
    {
      "title": "Chapter 23: Zoster",
      "url": "https://www.cdc.gov/pinkbook/hcp/table-of-contents/chapter-23-zoster.html"
    },
    {
      "title": "A spliced latency-associated VZV transcript maps antisense to the viral transactivator gene 61",
      "url": "https://www.nature.com/articles/s41467-018-03569-2"
    },
    {
      "title": "Clinical Overview of Chickenpox (Varicella)",
      "url": "https://www.cdc.gov/chickenpox/hcp/clinical-overview/index.html"
    },
    {
      "title": "Varicella (Chickenpox)",
      "url": "https://www.cdc.gov/chickenpox/downloads/Fact-sheet-Varicella-diagnosis-508.pdf"
    },
    {
      "title": "About Chickenpox",
      "url": "https://www.cdc.gov/chickenpox/about/index.html"
    },
    {
      "title": "Chapter 17: Varicella | Manual for the Surveillance of Vaccine-Preventable Diseases | CDC",
      "url": "https://www.cdc.gov/surv-manual/php/table-of-contents/chapter-17-varicella.html"
    },
    {
      "title": "Decline in Severe Varicella Disease During the United States Varicella Vaccination Program: Hospitalizations and Deaths, 1990–2019",
      "url": "https://stacks.cdc.gov/view/cdc/131793/cdc_131793_DS1.pdf"
    },
    {
      "title": "Clinical Features of Chickenpox (Varicella) | CDC",
      "url": "https://www.cdc.gov/chickenpox/hcp/clinical-signs/index.html"
    },
    {
      "title": "Varicella Diagnosis Fact Sheet | CDC",
      "url": "https://www.cdc.gov/chickenpox/hcp/communication-resources/varicella-diagnosis-fact-sheet.html"
    },
    {
      "title": "Clinical Overview of Chickenpox (Varicella) | CDC",
      "url": "https://www.cdc.gov/chickenpox/hcp/clinical-overview/?CDC_AAref_Val=https%3A%2F%2Fwww.cdc.gov%2Fchickenpox%2Fhcp%2Findex.html"
    },
    {
      "title": "Chickenpox Symptoms and Complications | CDC",
      "url": "https://www.cdc.gov/chickenpox/signs-symptoms/index.html"
    },
    {
      "title": "How to Treat Chickenpox | CDC",
      "url": "https://portugues.cdc.gov/chickenpox/treatment/index.html"
    },
    {
      "title": "Surgeon General's Advisory on the Use of Salicylates and Reye Syndrome | CDC",
      "url": "https://www.cdc.gov/mmwr/preview/mmwrhtml/00001108.htm"
    },
    {
      "title": "Reye Syndrome -- Ohio, Michigan | CDC",
      "url": "https://www.cdc.gov/mmwr/preview/mmwrhtml/00049023.htm"
    },
    {
      "title": "Clinical Guidance for People at Risk for Severe Varicella",
      "url": "https://www.cdc.gov/chickenpox/hcp/clinical-guidance/index.html"
    },
    {
      "title": "Consequences of varicella and herpes zoster in pregnancy: prospective study of 1739 cases.",
      "url": "https://pubmed.ncbi.nlm.nih.gov/7802767/"
    },
    {
      "title": "Prevention of Varicella: Recommendations of the Advisory Committee on Immunization Practices (ACIP)",
      "url": "https://www.cdc.gov/MMWR/Preview/MMWRhtml/rr5604a1.htm"
    },
    {
      "title": "Laboratory Testing for Varicella-Zoster Virus (VZV)",
      "url": "https://www.cdc.gov/chickenpox/php/laboratories/index.html"
    },
    {
      "title": "Specimen Collection for Varicella-Zoster Virus (VZV) Testing",
      "url": "https://www.cdc.gov/chickenpox/php/laboratories/collecting-vzv-specimens.html"
    },
    {
      "title": "Chapter 22: Laboratory Support for Surveillance of Vaccine-Preventable Diseases",
      "url": "https://www.cdc.gov/surv-manual/php/table-of-contents/chapter-22-laboratory-support.html"
    },
    {
      "title": "How to Treat Chickenpox",
      "url": "https://www.cdc.gov/chickenpox/treatment/index.html"
    },
    {
      "title": "Chickenpox",
      "url": "https://www.nhs.uk/conditions/chickenpox/?trk=public_post_comment-text"
    },
    {
      "title": "DailyMed — ACYCLOVIR tablet",
      "url": "https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=34a38cdf-04e8-4006-a9f5-4a0831117d61"
    },
    {
      "title": "A controlled trial of acyclovir for chickenpox in normal children",
      "url": "https://pubmed.ncbi.nlm.nih.gov/1944438/"
    },
    {
      "title": "Varicella zoster infection (chickenpox): management in children (1008)",
      "url": "https://clinicalguidelines.scot.nhs.uk/ggc-paediatric-guidelines/ggc-paediatric-guidelines/infectious-disease/varicella-zoster-infection-chickenpox-management-in-children-1008/?searchTerm=lfts+in+asymptomatic"
    },
    {
      "title": "Chickenpox and Shingles",
      "url": "https://www.nth.nhs.uk/resources/chickenpox-and-shingles/"
    },
    {
      "title": "Antibiotics",
      "url": "https://www.nhs.uk/medicines/antibiotics/"
    },
    {
      "title": "Chapter 22: Varicella | Pink Book | CDC",
      "url": "https://www.cdc.gov/pinkbook/hcp/table-of-contents/chapter-22-varicella.html"
    },
    {
      "title": "VZV: immunobiology and host response",
      "url": "https://www.ncbi.nlm.nih.gov/books/NBK47434/"
    },
    {
      "title": "Varicella-Zoster Virus–Specific Immune Responses to Herpes Zoster in Elderly Participants in a Trial of a Clinically Effective Zoster Vaccine",
      "url": "https://pmc.ncbi.nlm.nih.gov/articles/PMC4014851/"
    },
    {
      "title": "Influence of age and nature of primary infection on varicella-zoster virus-specific cell-mediated immune responses",
      "url": "https://pubmed.ncbi.nlm.nih.gov/20170376/"
    },
    {
      "title": "Varicella (Chickenpox) Vaccination: Information for Health Care Providers",
      "url": "https://www.cdc.gov/vaccines/hcp/by-disease/varicella.html"
    },
    {
      "title": "Chickenpox (Varicella) Vaccine Safety",
      "url": "https://www.cdc.gov/vaccine-safety/vaccines/varicella.html"
    },
    {
      "title": "Varicella Vaccine Recommendations",
      "url": "https://www.cdc.gov/chickenpox/hcp/vaccine-considerations/index.html"
    },
    {
      "title": "MMRV vaccination: information for healthcare professionals",
      "url": "https://www.gov.uk/government/publications/mmrv-programme-information-for-healthcare-practitioners/mmrv-vaccination-information-for-healthcare-professionals?preview=8973505"
    },
    {
      "title": "WHO position paper on varicella vaccines – November 2025",
      "url": "https://www.who.int/publications/i/item/who-wer10047-567-590"
    },
    {
      "title": "WHO position paper on varicella vaccines – November 2025, full text",
      "url": "https://www.nitag-resource.org/sites/default/files/2025-12/WER10047-567-590.pdf"
    },
    {
      "title": "Varicella / Chickenpox 2024 Case Definition",
      "url": "https://ndc.services.cdc.gov/case-definitions/varicella-2024/"
    },
    {
      "title": "Chickenpox Reporting and Surveillance",
      "url": "https://www.cdc.gov/chickenpox/php/conducting-surveillance/index.html"
    },
    {
      "title": "Instructions for Completing the Varicella Surveillance Worksheet (Appendix 20-6)",
      "url": "https://www.cdc.gov/surv-manual/downloads/appendix20-varicella-instruct-508.pdf"
    },
    {
      "title": "Varicella-Zoster Virus | Infection Control",
      "url": "https://www.cdc.gov/infection-control/hcp/healthcare-personnel-epidemiology-control/varicella.html"
    },
    {
      "title": "Updated Recommendations for Use of VariZIG — United States, 2013",
      "url": "https://cdc.gov/mmwr/preview/mmwrhtml/mm6228a4.htm"
    },
    {
      "title": "Evaluating Patients For Smallpox",
      "url": "https://www.cdc.gov/smallpox/media/pdfs/2024/11/smallpox-diagnostic-algorithm-poster-2-pages.pdf"
    },
    {
      "title": "Prevention of Varicella: Recommendations of the Advisory Committee on Immunization Practices (ACIP)",
      "url": "https://www.cdc.gov/MMWR/Preview/mmwrhtml/00042990.htm"
    },
    {
      "title": "Live vaccine used to prevent the spread of varicella in children in hospital",
      "url": "https://pubmed.ncbi.nlm.nih.gov/4139526/"
    },
    {
      "title": "Development of a live attenuated varicella vaccine",
      "url": "https://pubmed.ncbi.nlm.nih.gov/167707/"
    },
    {
      "title": "Epidemiology of Varicella During the 2-Dose Varicella Vaccination Program — United States, 2005–2014",
      "url": "https://www.cdc.gov/mmwr/volumes/65/wr/mm6534a4.htm"
    },
    {
      "title": "MMWR Weekly / Vol. 61 / No. 32",
      "url": "https://www.cdc.gov/mmwr/PDF/wk/mm6132.pdf"
    },
    {
      "title": "Prevention of Varicella: Recommendations of the Advisory Committee on Immunization Practices (ACIP)",
      "url": "https://www.cdc.gov/mmwr/pdf/rr/rr5604.pdf"
    }
  ],
  "license": "https://creativecommons.org/licenses/by/4.0/"
}