Research Papers And Articles About Chicken Pox And Shingles Pdf
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- Chickenpox (Varicella) Vaccines
- The burden of chickenpox disease in Sweden
- Varicella zoster virus-associated morbidity and mortality in Africa – a systematic review
Varicella-zoster virus VZV causes chickenpox and may subsequently reactivate to cause herpes zoster later in life. The exogenous boosting hypothesis states that re-exposure to circulating VZV can inhibit VZV reactivation and consequently also herpes zoster in VZV-immune individuals. Using this hypothesis, mathematical models predicted widespread chickenpox vaccination to increase herpes zoster incidence over more than 30 years.
Chickenpox (Varicella) Vaccines
Primary infection is followed by latency in ganglionic neurons. During this period, no virus particles are produced and no obvious neuronal damage occurs. Reactivation of the virus leads to virus replication, which causes zoster shingles in tissues innervated by the involved neurons, inflammation and cell death — a process that can lead to persistent radicular pain postherpetic neuralgia.
The pathogenesis of postherpetic neuralgia is unknown and it is difficult to treat. Furthermore, other zoster complications can develop, including myelitis, cranial nerve palsies, meningitis, stroke vasculopathy , retinitis, and gastroenterological infections such as ulcers, pancreatitis and hepatitis.
VZV is the only human herpesvirus for which highly effective vaccines are available. After varicella or vaccination, both wild-type and vaccine-type VZV establish latency, and long-term immunity to varicella develops. However, immunity does not protect against reactivation. Thus, two vaccines are used: one to prevent varicella and one to prevent zoster. In this Primer we discuss the pathogenesis, diagnosis, treatment, and prevention of VZV infections, with an emphasis on the molecular events that regulate these diseases.
Varicella zoster virus VZV, also known as human herpesvirus 3 is a ubiquitous alphaherpesvirus with a double-stranded DNA genome. VZV only naturally infects humans, with no animal reservoir; its main targets are T lymphocytes, epithelial cells and ganglia.
Primary infection causes varicella chickenpox , during which VZV becomes latent in ganglionic neurons. As cellular immunity to VZV wanes with advancing age or in immunocompromised individuals, VZV reactivates to cause zoster shingles. Zoster can be complicated by chronic pain postherpetic neuralgia PHN and other serious neurological and ocular disorders for example, meningoencephalitis, myelitis, cranial nerve palsies, vasculopathy, keratitis and retinopathy , as well as multiple visceral and gastrointestinal disorders, including ulcers, hepatitis and pancreatitis 1 , 2 Fig.
Antiviral drugs and vaccines against both varicella and zoster are available and are effective in treating and preventing VZV-induced disease 2. Primary infection with varicella zoster virus VZV in susceptible individuals causes varicella, which usually is harmless in healthy children whose immune system controls the infection.
VZV establishes latency in ganglionic neurons, and reactivation of viral replication and spread of the virus to the skin innervated by these neurons causes zoster. Increasing age and compromised immune function are risk factors for complications of VZV infections. However, some of these complications, such as postherpetic neuralgia, can also occur without these predisposing factors.
PowerPoint slide. VZV is highly communicable and spreads by the airborne route, with an extraordinarily high transmission rate 3 in temperate countries. Traditionally, the virus was thought to spread to others from the respiratory tract, but such evidence is scant. Instead, most virus comes from skin where it is highly concentrated in vesicles; skin cells and cell-free VZV are frequently shed and are probably the major source of infectious cell-free airborne virus 4 , 5.
Infected children without skin lesions are not contagious to others 4. The highly efficient transmission of VZV assured that, before the introduction of the varicella vaccine, most children would contract varicella before 10 years of age. Varicella in children is usually self-limiting, although complications can be unpredictable, and long-lasting immunity follows once the patient recovers.
Epidemics are also self-limiting because the high rate of transmission and disease-induced immunity deplete the pool of susceptible individuals 6. Sporadic reactivation of VZV causes zoster and provides an evolutionary advantage for the pathogen by providing a source of infection in new, susceptible birth cohorts.
VZV occurs worldwide, but in some developed countries there is less concern for VZV than for other infectious agents, such as influenza virus, Ebola virus and multidrug-resistant staphylococci.
However, even in countries where varicella vaccination is routine there has not been an eradication of VZV disease. Import of varicella from countries that do not vaccinate and zoster caused by reactivation of latent wild-type VZV or vOka can occur.
Given the increasing number of immunocompromised individuals worldwide, it is important to maintain substantial levels of herd immunity against varicella in developed countries and to extend vaccination to developing countries. In addition, because of the current anti-vaccine movement in some countries, it is also wise to maintain interest in VZV research and to improve current methods to prevent and treat varicella and zoster. In this Primer article, we summarize the diseases and complications of VZV infection, how latency develops, how and when to vaccinate and treat patients, and we highlight open research questions Box 1.
Varicella occurs worldwide and is endemic in populations of sufficient size to sustain year-round transmission, with epidemics occurring every 2—3 years 3. Viral genomic studies have identified five viral clades and their geographical distribution: clades 1, 3 and 5 are of European origin; clade 2 includes Asian strains such as the parental Oka strain, from which varicella and zoster vaccines were derived; and clade 4 contains African strains 8.
Varicella epidemiology and disease burden have been studied primarily in developed countries. Although VZV seroprevalance data are becoming more widely available, additional data are needed on severe disease outcomes and deaths to better characterize the global health burden due to varicella, particularly in regions with high HIV prevalence, such as Africa and India 7. Varicella incidence ranges from 13 to 16 cases per 1, persons per year, with substantial yearly variation 3. In tropical climates, acquisition of varicella occurs at a higher overall mean age for example, at Varicella shows a strong seasonal pattern, with peak incidence during winter and spring or during the cool, dry season 3 , Outbreaks occur commonly in settings where children congregate, such as childcare centres and schools, but can also occur in other age groups and settings, including hospitals, facilities for institutionalized people, refugee camps and military and correctional facilities 12 — Although varicella is usually a self-limiting disease, it can result in serious complications and death.
Serious varicella complications include bacterial sepsis, pneumonia, encephalitis and haemorrhage 3. Adults, infants and individuals who are severely immunocompromised are at higher risk of severe complications and death. In countries where varicella vaccination is routinely recommended in childhood, varicella epidemiology has changed dramatically Fig. Furthermore, significantly less morbidity and mortality in vaccinated and in unvaccinated age groups indicate indirect vaccination effects such as herd immunity and interruption of annual epidemics 18 , The introduction of the varicella vaccine in reduced the number of varicella cases substantially data shown for Illinois, Michigan, Texas and West Virginia, USA.
Reprinted with permission from Ref. Zoster epidemiology has been described almost exclusively from developed countries with long life expectancies. The incidence and severity of zoster increase with age due to declining cell-mediated immunity to VZV 3 , Age is the most important risk factor for PHN, with the risk increasing rapidly after 50 years of age 3 , There are limited data on the age-specific incidence in low and middle income countries.
Recently, however, a higher proportion of the population has exhibited impaired immunity to VZV and develops zoster, for example, due to the growing number of elderly people, immunosuppressed organ transplant recipients, patients receiving chemotherapy for cancer or autoimmune disease, HIV-infected individuals, and patients with chronic illnesses Although mathematical modelling has predicted an increase in zoster where circulating VZV is reduced by childhood vaccination programmes 28 , the concept of exogenous VZV exposure as the only means for immune boosting remains an area of controversy see below.
Post-licensure surveillance data provide direct evidence of the impact of the varicella vaccine on zoster epidemiology 29 , Healthy varicella vaccine recipients have a lower risk of zoster than unvaccinated individuals, and this finding is consistent with pre-licensure studies demonstrating a similar effect in children with acute leukaemia The effect of varicella vaccination on overall zoster epidemiology continues to be evaluated.
Most studies examining the overall population rates of zoster in developed countries the United States, the United Kingdom, Canada, Spain, Japan and Australia show increasing incidence trends in these countries, regardless of whether they have varicella vaccination programmes 3 , 7. In the United States, where the varicella vaccine has been used for 20 years in children, increases in zoster incidence started years before the use of the varicella vaccine and the rate of increase is similar before and after implementation of the vaccination programme 3 , 29 , Primary infection.
Following transmission to susceptible hosts, VZV proliferates in the oral pharynx tonsils , infects T cells that enter the circulation and disseminate virus to the skin and possibly other organs; infection is at first controlled by innate immunity 32 , VZV can remodel diverse T cell populations to facilitate skin trafficking VZV DNA can be detected in T cells viraemia as early as 10 days prior to the occurrence of a rash and can persist for a week afterwards Initially, innate immunity delays viral multiplication in the skin, which provides time for adaptive immunity to develop Eventually, cutaneous innate immune responses are overcome by the virus, and there is substantial viral replication in the skin and sometimes the viscera , resulting in the characteristic rash of varicella 33 Fig.
Important and unpredictable complications of varicella in previously healthy children include encephalitis, haemorrhagic manifestations, and bacterial superinfections involving skin, blood, bones and lungs.
Severe varicella in an month-old infant who, during the incubation period, had received dexamethasone as part of therapy for pneumococcal meningitis. Pictured on day 5 of the rash, when he was still systemically unwell and acquiring new lesions. The infant made a full recovery with intravenous acyclovir therapy. In this process of lytic infection Fig. As described for other herpesviruses, gene expression is thought to proceed in an orderly cascade, beginning with immediate early genes, then early genes, followed by late genes.
In latency, however, gene expression is restricted and possibly blocked Fig. In reactivation, all VZV genes are expressed, again resulting in lytic infection 2. The virus capsid is then transported to the cell nucleus, where the viral DNA becomes circular. The full set of viral proteins, including immediate early IE , early E and late L proteins, are expressed and enter the nucleus.
New virions then bud in a two-step process. This full cycle of viral replication leads to substantial cell damage and eventually lysis; the acidic environmental in the endosome damages the virus particles and reduces their infectiousness. The micrograph shows VZV infection of guinea pig enteric neurons showing lytic infection Isolated neurons were cultured in vitro and infected with cell-free VZV to induce infection.
The neurons were analysed 48 h after infection with cell-associated virus; after lytic infection, neurons die with 48—72 h. The neuron is filled with cytoplasmic glycoprotein E immunoreactivity and the immunoreactivity of ORF29p has almost entirely translocated to the nucleus arrow. Furthermore, no viral proteins are found in the nucleus. Latent infection causes no easily observable changes of cell morphology see micrograph. The micrograph shows VZV infection of guinea pig enteric neurons showing latent infection The neurons were analysed 2 weeks after infection with cell-free VZV; after latent infection, neurons survive in vitro for as long as cultures can be maintained.
Note that ORF29p immunoreactivity is confined to the cytoplasm; there is no nuclear immunoreactivity arrow. TGN, trans-Golgi network. Adapted from Ref. VZV is latent in neurons of cranial nerve ganglia, dorsal root ganglia, and enteric and autonomic ganglia 2 , Because sites of zoster often correspond to those most involved in varicella face and trunk , VZV has long been thought to enter epidermal nerve endings during varicella and undergo retrograde axonal transport to reach neuronal cell bodies in the ganglia.
Varicella-associated viraemia, however, is an even more likely means by which neurons may be latently infected, particularly enteric or other neurons that lack cutaneous projections. For example, latent VZV has been found in the dorsal root ganglia of children with no history of varicella and no epidermal involvement
The burden of chickenpox disease in Sweden
Varicella-zoster virus VZV causes clinically significant illness during acute and recurrent infection accompanied by robust innate and acquired immune responses. Varicella-zoster virus subverts pattern recognition receptor sensing to modulate antigen presentation and IFN-I production. During primary infection, VZV hijacks T cells to disseminate to the skin and establishes latency in ganglia. Durable T- and B-cell memory formed within a few weeks of infection is boosted by reactivation or re-exposure. Antigen-specific T cells are recruited and potentially retained in VZV-infected skin to counteract reactivation. In latently VZV-infected ganglia, however, virus-specific T cells have not been recovered, suggesting that local innate immune responses control VZV latency. Antibodies prevent primary VZV infection, whereas T cells are fundamental to resolving disease, limiting severity, and preventing reactivation.
Varicella-zoster virus VZV causes clinically significant illness during acute and recurrent infection accompanied by robust innate and acquired immune responses. Varicella-zoster virus subverts pattern recognition receptor sensing to modulate antigen presentation and IFN-I production. During primary infection, VZV hijacks T cells to disseminate to the skin and establishes latency in ganglia. Durable T- and B-cell memory formed within a few weeks of infection is boosted by reactivation or re-exposure. Antigen-specific T cells are recruited and potentially retained in VZV-infected skin to counteract reactivation. In latently VZV-infected ganglia, however, virus-specific T cells have not been recovered, suggesting that local innate immune responses control VZV latency.
Healthy varicella vaccine recipients have a lower risk of zoster than unvaccinated individuals, and this finding is consistent with pre-licensure studies.
Varicella zoster virus-associated morbidity and mortality in Africa – a systematic review
Coronavirus Guidelines. Visit free Relief Central. Prime PubMed is provided free to individuals by: Unbound Medicine. Children hospitalised with four common viral diseases showed epidemiological differences but few socioeconomic variations.
The following information was supplied regarding data availability:. McDonald, W. Chickenpox and shingles ABM.
Metrics details. Chickenpox vaccine is not included in the routine childhood vaccination programme in Sweden. The aim of this study was to estimate the baseline of national chickenpox disease burden, as comprehensive studies, required for an assessment regarding vaccine introduction, are lacking.
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Chickenpox , also known as varicella , is a highly contagious disease caused by the initial infection with varicella zoster virus VZV. Chickenpox is an airborne disease which spreads easily from one person to the next through the coughs and sneezes of an infected person. Since its introduction in , the varicella vaccine has resulted in a decrease in the number of cases and complications from the disease. Chickenpox occurs in all parts of the world. The early prodromal symptoms in adolescents and adults are nausea, loss of appetite, aching muscles, and headache.
Universal childhood vaccination against varicella began in the United States as a 1-dose schedule in , changing to a 2-dose schedule in The exogenous boosting hypothesis, which postulates that reexposure to circulating wild-type varicella delays the onset of herpes zoster, predicts a transient increase in the incidence of herpes zoster, peaking in adults 15—35 years after the start of varicella vaccination. This was a retrospective study of administrative claims data from the MarketScan Commercial and Medicare databases between — Outcome measures were the incidences of herpes zoster per person-years, by calendar year and age category, and the annual rates of change in herpes zoster by age category, in an interrupted time series regression analysis, for the periods of — prevaccine , — 1-dose vaccination period , and — 2-dose vaccination period. Although the annual incidence of herpes zoster in adults has continued to increase, the rates of change decreased during both the 1- and 2-dose vaccination periods. The hypothesized increase in herpes zoster predicted from modelling of the exogenous boosting hypothesis was not observed.
Metrics details. Varicella zoster virus VZV causes varicella and herpes zoster. These vaccine preventable diseases are common globally. Most available data on VZV epidemiology are from industrialised temperate countries and cannot be used to guide decisions on the immunization policy against VZV in Africa. This systematic review aims to review the published data on VZV morbidity and mortality in Africa. All published studies conducted in Africa from to were eligible. Eligible studies must have reported any VZV epidemiological measure incidence, prevalence, hospitalization rate and mortality rate.
Chickenpox is an infection caused by the varicella-zoster virus. Most cases are in children under age 15, but older children and adults can get it.
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