Szczepionka przeciw ospie wietrznej
Patofizjologia i mechanizm

Szczepionka przeciw ospie wietrznej (Varivax) zawiera żywy atenuowany wirus VZV szczepu Oka, który po podaniu indukuje zarówno humoralną odpowiedź immunologiczną (produkcja przeciwciał IgG specyficznych dla VZV), jak i komórkową (aktywacja limfocytów T CD4+ i CD8+). Po jednej dawce szczepionki 70-90% dzieci uzyskuje pełną ochronę przed wszystkimi postaciami ospy, a ponad 95% przed umiarkowaną i ciężką formą choroby; po dwóch dawkach skuteczność wzrasta do 97-99% i 100% odpowiednio. Ochrona utrzymuje się do 10 lat, a ekspozycja na dziki typ wirusa zwiększa poziom przeciwciał, co wspiera długotrwałą odporność. Szczepionka jest bezpieczna, a ryzyko reaktywacji wirusa szczepionkowego i rozwoju półpaśca jest znacznie niższe niż po naturalnym zakażeniu. Poekspozycyjne podanie szczepionki w ciągu 3-5 dni od kontaktu może zapobiec zakażeniu lub złagodzić przebieg choroby.

Mechanizm działania szczepionki przeciw ospie wietrznej

Szczepionka przeciw ospie wietrznej zawiera żywy atenuowany (osłabiony) wirus ospy wietrznej (VZV, Varicella-Zoster Virus) szczepu Oka. Wirus ten został pierwotnie pozyskany od dziecka z naturalną infekcją ospy wietrznej, a następnie wprowadzony do hodowli ludzkich komórek płuc zarodkowych, zaadaptowany i namnożony w hodowlach komórek zarodkowych świnki morskiej, a ostatecznie namnożony w ludzkiej linii komórek diploidalnych pochodzących z tkanek płodowych (WI-38).12

Indukcja odpowiedzi immunologicznej

Szczepionka przeciw ospie wietrznej, znana również jako Varivax, wywołuje zarówno humoralną, jak i komórkową odpowiedź immunologiczną przeciwko wirusowi ospy wietrznej.34 Po podaniu szczepionki osłabiony wirus dostaje się do organizmu, gdzie:

Szczepionka wprowadza osłabioną formę wirusa do organizmu, co prowokuje układ odpornościowy do rozpoznania wirusa jako obcego i uruchomienia mechanizmów obronnych. Odpowiedź immunologiczna obejmuje produkcję przeciwciał, które są białkami ukierunkowanymi na neutralizację wirusa.9 Dodatkowo generowane są komórki pamięci immunologicznej, zapewniające długotrwałą odporność.10

Skuteczność i czas trwania ochrony

Po podaniu pojedynczej dawki szczepionki przeciw ospie wietrznej, 70-90% dzieci uzyskuje pełną ochronę przed wszystkimi postaciami ospy wietrznej, a ponad 95% ochronę przed umiarkowaną i ciężką postacią choroby.11 Po dwóch dawkach szczepionki, 97-99% dzieci jest chronionych przed wszystkimi postaciami ospy wietrznej, a 100% przed umiarkowaną i ciężką postacią choroby.12

Dokładny czas trwania ochrony po szczepieniu nadal pozostaje nieznany, jednak badania skuteczności wykazały, że szczepionka może zapewniać ciągłą ochronę przez okres do 10 lat po szczepieniu.1314 Zaobserwowano również wzrost poziomu przeciwciał u osób zaszczepionych po ekspozycji na dziki typ wirusa ospy wietrznej, co może tłumaczyć widoczną długoterminową ochronę po szczepieniu w tych badaniach.15

Patogeneza infekcji wirusem ospy wietrznej

Aby zrozumieć mechanizm działania szczepionki, warto poznać patogenezę naturalnej infekcji wirusem ospy wietrznej. VZV jest wysoce zakaźnym wirusem, który dostaje się do organizmu gospodarza przez drogi oddechowe i spojówki.1617

Cykl replikacji naturalnego wirusa VZV

Przebieg naturalnej infekcji VZV przebiega etapami:18

  • Wirus namnaża się w miejscu wniknięcia w nosogardzieli i regionalnych węzłach chłonnych19
  • Pierwotna wiremia występuje 4-6 dni po zakażeniu i powoduje rozprzestrzenienie się wirusa do innych narządów, takich jak wątroba, śledziona i zwoje czuciowe20
  • Dalsza replikacja zachodzi w narządach wewnętrznych, po czym następuje wtórna wiremia z zakażeniem wirusowym skóry21
  • Zakażone komórki dendrytyczne błony śluzowej prawdopodobnie jako pierwsze napotykają infekcję, po czym następuje zakażenie ludzkich limfocytów T CD4+ z węzłów chłonnych, które transportują VZV bezpośrednio do skóry22

Po pierwotnej infekcji VZV rozprzestrzenia się z wykwitów śluzówkowych i skórnych do lokalnych nerwów czuciowych, pozostając w stanie latencji w komórkach zwojów grzbietowych nerwów czuciowych.2324 Reaktywacja VZV prowadzi do klinicznie odrębnego zespołu półpaśca (herpes zoster).25

Molekularne mechanizmy patogenezy VZV

Genom VZV zawiera co najmniej 71 znanych lub przewidywanych otwartych ramek odczytu (ORF). Podobnie jak wszystkie herpeswirusy, VZV ma osłonkę bogatą w lipidy, która jest pozyskiwana z błon komórkowych i do której wstawiane są glikoproteiny wirusowe.26

Cykl życiowy wirusa rozpoczyna się od wniknięcia VZV, co jest słabo poznanym procesem, który prawdopodobnie obejmuje bezpośrednią fuzję cząstek wirusowych z błoną komórkową lub endocytozę.27 VZV hamuje odpowiedzi wrodzone, aby wytworzyć wypełnioną wirusem zmianę na powierzchni skóry, gdzie zakażone keratynocyty uwalniają nowo złożone wiriony.28

Kilka białek wirusowych zakłóca odpowiedzi pośredniczone przez interferon w zakażonych komórkach:29

  • IE62 hamuje fosforylację czynnika regulacyjnego interferonu 3 (IRF3) przez kinazę TBK-1, blokując w ten sposób produkcję interferonu
  • Kinaza ORF47 zmniejsza fosforylację IRF3
  • IE63 hamuje fosforylację eukariotycznego czynnika inicjacji 2 i jego późniejsze efekty interferonowe

Fuzja komórka-komórka nie jest ściśle wymagana do rozprzestrzeniania się VZV, ponieważ wiriony uwalniane z zakażonych komórek mogą wnikać do sąsiednich komórek. Jednak tworzenie polikariotów jest klasyczną zmianą patologiczną wywoływaną przez VZV w skórze.30

Różnice między szczepem szczepionkowym a dzikim wirusem

Szczep szczepionkowy Oka został opracowany przez Michiaki Takahashi i jego współpracowników w Japonii na początku lat 70. XX wieku.3132 Szczepionka powstała poprzez seryjne pasażowanie wirusa izolowanego od chłopca z ospą wietrzną, najpierw w ludzkich fibroblastach zarodkowych, a następnie w fibroblastach zarodkowych świnki morskiej.33

Atenuacja szczepu szczepionkowego

Szczep szczepionkowy Oka wykazuje zmniejszoną replikację w ksenoprzeszczepach skóry, co jest zgodne z sytuacją u ludzi, którzy rzadko rozwijają zmiany po podskórnym podaniu szczepionki.34 Mutacje, które nagromadziły się w tym atenuowanym szczepie (poprzez pasażowanie w fibroblastach), zmniejszyły jego zdolność do pokonywania wewnętrznych barier skórnych, mimo że mutacje te nie mają wpływu na tropizm limfocytów T ani neurotropizm.35

Szczepionka jest bezpieczna i skuteczna w zapobieganiu ospie wietrznej lub zmniejszaniu jej nasilenia, a także w budowaniu długotrwałej odporności przeciwko wirusowi.36 Wirus szczepionkowy reaktywuje się również rzadziej niż typ dziki.37

Neurotropizm i latencja szczepu szczepionkowego

Szczep szczepionkowy zachowuje neurotropizm swojego dzikiego odpowiednika.38 Po podaniu szczepionki wirus namnaża się lokalnie w skórze, a niektóre cząstki wirusowe wnikają do wolnych zakończeń włókien nocyceptorowych A i C, po czym cząstki wirusowe są transportowane do ciała komórek zwojów korzeni grzbietowych (DRG), gdzie wirus wchodzi w stan latencji.39

Po kilku latach wirus szczepionkowy może reaktywować się z DRG, po czym jest przenoszony w tych samych włóknach pseudounipolarnych w kierunku antero-gradowym do uda, prezentując się jako półpasiec w dermatomie lędźwiowym na nodze.40 Reaktywacja i związane z nią powikłania występują jednak znacznie rzadziej w przypadku szczepu szczepionkowego niż dzikiego.41

Ryzyko rozwoju półpaśca jest zmniejszone u dzieci, które otrzymały szczepionkę przeciw ospie wietrznej, ale nie wyeliminowane. Według CDC z 2014 roku: „Szczepionki przeciw ospie wietrznej zawierają osłabiony żywy VZV, który może powodować utajone (uśpione) zakażenie. Szczep szczepionkowy VZV może reaktywować się później w życiu i powodować półpasiec. Jednak ryzyko zachorowania na półpasiec wywołany przez szczep szczepionkowy VZV po szczepieniu przeciwko ospie wietrznej jest znacznie niższe niż zachorowanie na półpasiec po naturalnym zakażeniu dzikim typem VZV.”42

Rola w profilaktyce poekspozycyjnej

Szczepionka przeciw ospie wietrznej jest obecnie zatwierdzona do stosowania po ekspozycji i kontroli ognisk choroby.43 Patogeneza ospy wietrznej podąża za ogólnym schematem wirusowych wysypek zaproponowanym przez Fennera.44

Mechanizm działania w profilaktyce poekspozycyjnej

Inokulacja dróg oddechowych pozwala na początkową replikację wirusa w regionalnych węzłach chłonnych. Pierwotna wiremia prowadzi do replikacji w wątrobie i śledzionie, a wtórna wiremia rozprzestrzenia wirusa (w zakażonych komórkach jednojądrzastych) do różnych narządów, w tym skóry, prowadząc do charakterystycznej wysypki.45

Odpowiedź immunologiczna uruchomiona przed wtórną wiremią może przerwać lub złagodzić kliniczną chorobę.46 Jeśli podanie szczepionki następuje w ciągu 3-5 dni po ekspozycji na wirusa ospy wietrznej, może pomóc zapobiec zakażeniu lub sprawić, że będzie ono mniej poważne.4748

Teoretyczne rozważania i dowody eksperymentalne wydają się wspierać poekspozycyjne stosowanie u dzieci szczepionek pochodzących od szczepu Oka w ciągu 3 dni od pojawienia się wysypki u przypadku wskaźnikowego.49 Pomimo szczepienia, niewielka część osób może rozwinąć łagodną, ale zakaźną ospę wietrzną, zwłaszcza jeśli były narażone na kontakt w gospodarstwie domowym.50

Nowe kierunki badań nad szczepionkami przeciw VZV

Trwają badania nad nowymi formułami szczepionek przeciwko wirusowi VZV, które mogłyby zapewnić skuteczniejszą i długotrwałą ochronę.

Szczepionki mRNA przeciwko VZV

Opracowywane są szczepionki mRNA-LNP skierowane przeciwko glikoproteinie E (gE) powierzchniowej VZV.51 Badania wykazały, że kandydaci na szczepionki mRNA-LNP wywołują silne i trwałe odpowiedzi humoralne specyficzne dla antygenu gE.52

Szczególnie godne uwagi jest to, że myszy zaszczepione szczepionkami mRNA-LNP wykazały znacznie wyższą produkcję cytokin specyficznych dla antygenu przez komórki T w porównaniu z grupą otrzymującą Shingrix, obecną standardową szczepionkę.53 Dodatkowo szczepionki mRNA-LNP indukowały długotrwałą odpowiedź pamięci immunologicznej, na co wskazuje wykrycie utrzymujących się komórek plazmatycznych długo żyjących (LLPC) specyficznych dla gE i komórek T pamięci cztery miesiące po ostatnim szczepieniu.54

Opracowano trzy wersje glikoproteiny E (gE) VZV kodowanej przez mRNA:55

  • Pełnej długości gE (gE-full length), obecna na powierzchni wirionu i naturalnie zakażonych komórek
  • Skrócona gE (gE-truncated), wytworzona przez usunięcie części domeny C-końcowej i pojedynczą substytucję aminokwasu zmieniającą jeden z motywów lokalizacji sieci trans-Golgiego (TGN)
  • Rozpuszczalna gE (gE-soluble), która jest wyrażana jako zewnątrzkomórkowa domena białka i podobna do sekwencji antygenu w Shingrix

Dane z wstępnych badań pokazują, że formulacja GLB mRNA-LNP (NOF) skutecznie dostarcza glikoproteinę gE i wywołuje silną odpowiedź immunogenną, porównywalną z Shingrix, u myszy.56 Co ważne, wykazano również, że LNP NOF, dostarczające mRNA gE pełnej długości, są mniej zapalne niż Shingrix i dlatego mogą wykazywać lepszy profil bezpieczeństwa w badaniach klinicznych u ludzi.57

Potencjalne dodatkowe korzyści ze szczepień przeciwko VZV

Badania wskazują na potencjalne dodatkowe korzyści szczepionek przeciwko VZV, wykraczające poza zapobieganie ospie wietrznej i półpaścowi. Szczepionka przeciwko półpaścowi może bezpośrednio chronić przed demencją, chociaż dokładny mechanizm tej ochrony pozostaje niejasny.58

Jedna z teorii sugeruje, że reaktywacja wirusa varicella-zoster może wywołać uszkodzenie mózgu poprzez szereg mechanizmów, w tym nagromadzenie nieprawidłowych białek i przewlekły stan zapalny. Zapobiegając reaktywacji, szczepionka przeciwko półpaścowi może teoretycznie zapobiec temu uszkodzeniu mózgu.59

Inna hipoteza zakłada, że szczepionka zapewnia ochronę nie poprzez bezpośrednie ukierunkowanie na wirusy, ale poprzez dostrojenie układu odpornościowego w sposób, który spowalnia lub zmienia przebieg demencji.60

Rozwój genetycznie zdefiniowanej żywej atenuowanej szczepionki VZV, która zapobiega zakażeniu neuronalnemu i utajonemu, oprócz pierwotnej ospy wietrznej, jest niezbędny do ostatecznego wyeliminowania VZV i, jeśli zostanie w pełni zrozumiany, ma ogromne implikacje dla wielu powiązanych herpeswirusów i innych wirusów o podobnych mechanizmach patogennych.61

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  1. 09.04.2026
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Materiały źródłowe

  • #1 Varicella vaccine – Wikipedia
    https://en.wikipedia.org/wiki/Varicella_vaccine
    The varicella-zoster vaccine is made from the Oka/Merck strain of live attenuated varicella virus. The Oka virus was initially obtained from a child with natural varicella, introduced into human embryonic lung cell cultures, adapted to and propagated in embryonic guinea pig cell cultures, and finally propagated in a human diploid cell line originally derived from fetal tissues (WI-38).
  • #2 Varicella Vaccine
    https://www.pediatriconcall.com/drugs/varicella-vaccine/1036
    Varicella Virus Vaccine is a live, attenuated varicella virus vaccine. The virus was initially obtained from a child with natural varicella, then introduced into human embryonic lung cell cultures, adapted to and propagated in embryonic guinea pig cell cultures and finally propagated in human diploid cell cultures. […] A mild chicken-pox with vesiculopapular rash and a low fever commonly occur after the first injection.
  • #3 Varicella (Chickenpox) Vaccine – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK441946/
    Varicella-zoster virus (chickenpox) is an acute febrile rash illness that was very common in children in the United States before the universal vaccination program existed. […] The FDA approves using the live varicella virus vaccine to provide immunity for preventing varicella in individuals 12 months older. […] This activity reviews the mechanism of action, indications, contraindications, adverse effects of this vaccine, and the front-line personnel involved in preventing the disease. […] Evaluate the mechanism of action of the varicella vaccine. […] The varicella-zoster vaccine contains live attenuated varicella-zoster vaccine (Oka strain). This vaccine induces both humoral and cell-mediated immune responses. It produces an IgG humoral immune response in individuals, and the cell-mediated immune response is caused by varicella-zoster-specific activation of both CD4+ T-helper and CD8+ T-lymphocyte cells. The protection duration is still unknown; however, some efficacy trials have shown that the vaccine can offer continued protection for up to 10 years after vaccination.
  • #4 Everything You Need To Know About The Chickenpox Vaccine
    https://justtheinserts.com/chickenpox/
    VARIVAX induces both cell-mediated and humoral immune responses to varicella-zoster virus. […] The relative contributions of humoral immunity and cell-mediated immunity to protection from varicella are unknown. […] The duration of protection of VARIVAX is unknown; however, long-term efficacy studies have demonstrated continued protection up to 10 years after vaccination. […] A boost in antibody levels has been observed in vaccinees following exposure to wild-type varicella which could account for the apparent long-term protection after vaccination in these studies.
  • #5 Varicella (Chickenpox) Vaccine – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK441946/
    Varicella-zoster virus (chickenpox) is an acute febrile rash illness that was very common in children in the United States before the universal vaccination program existed. […] The FDA approves using the live varicella virus vaccine to provide immunity for preventing varicella in individuals 12 months older. […] This activity reviews the mechanism of action, indications, contraindications, adverse effects of this vaccine, and the front-line personnel involved in preventing the disease. […] Evaluate the mechanism of action of the varicella vaccine. […] The varicella-zoster vaccine contains live attenuated varicella-zoster vaccine (Oka strain). This vaccine induces both humoral and cell-mediated immune responses. It produces an IgG humoral immune response in individuals, and the cell-mediated immune response is caused by varicella-zoster-specific activation of both CD4+ T-helper and CD8+ T-lymphocyte cells. The protection duration is still unknown; however, some efficacy trials have shown that the vaccine can offer continued protection for up to 10 years after vaccination.
  • #6 Varicella vaccine : Indications, Uses, Dosage, Drugs Interactions, Side effects
    https://medicaldialogues.in/generics/varicella-vaccine-2726218
    The varicella vaccine has a potential physiological mechanism that plays a role in its pharmacodynamics, involving its interaction with the immune system. […] When administered, the live, attenuated virus in the vaccine stimulates the immune system. Mainly, immunoglobulin G (IgG), produced as a result, helps identify and neutralize the virus. When the immune system develops a rapid and effective defence against the varicella-zoster virus in the future, it is due to this memory activation that long-term immunity is established. Due to this strong immune response, which offers some protection against varicella, the vaccination is beneficial in avoiding chickenpox and its associated complications. […] The varicella vaccine is injected, and the vaccine’s active ingredients enter the bloodstream.
  • #7 Varicella (Chickenpox) Vaccine – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK441946/
    Varicella-zoster virus (chickenpox) is an acute febrile rash illness that was very common in children in the United States before the universal vaccination program existed. […] The FDA approves using the live varicella virus vaccine to provide immunity for preventing varicella in individuals 12 months older. […] This activity reviews the mechanism of action, indications, contraindications, adverse effects of this vaccine, and the front-line personnel involved in preventing the disease. […] Evaluate the mechanism of action of the varicella vaccine. […] The varicella-zoster vaccine contains live attenuated varicella-zoster vaccine (Oka strain). This vaccine induces both humoral and cell-mediated immune responses. It produces an IgG humoral immune response in individuals, and the cell-mediated immune response is caused by varicella-zoster-specific activation of both CD4+ T-helper and CD8+ T-lymphocyte cells. The protection duration is still unknown; however, some efficacy trials have shown that the vaccine can offer continued protection for up to 10 years after vaccination.
  • #8 Varicella (Chickenpox) Vaccine | Treatment & Management | Point of Care
    https://www.statpearls.com/point-of-care/30981
    The varicella-zoster vaccine contains live attenuated varicella-zoster vaccine (Oka strain). This vaccine induces both humoral and cell-mediated immune responses. It produces an IgG humoral immune response in individuals, and the cell-mediated immune response is caused by varicella-zoster-specific activation of both CD4+ T-helper and CD8+ T-lymphocyte cells. The protection duration is still unknown; however, some efficacy trials have shown that the vaccine can offer continued protection for up to 10 years after vaccination. […] The varicella vaccine is now FDA-approved to give for post-exposure use and outbreak control. The vaccine should be given as soon as possible after exposure, but it has shown effectiveness in preventing or modifying disease within 3 to 5 days post-exposure.
  • #9 Varicella Vaccine And Covid Vaccine | Travelvax
    https://www.travelvax.com.au/latest-news/varicella-vaccine-and-covid-vaccine
    The varicella vaccine, commonly known as the chickenpox vaccine, plays a crucial role in preventing varicella-zoster virus (VZV) (herpes zoster) infection. This vaccine is a live attenuated vaccine, meaning it contains a weakened form of the virus that causes chickenpox. Live attenuated vaccines use viruses or bacteria that have been weakened so that they cannot cause the disease in a healthy person but can still stimulate an immune response. […] The varicella vaccine works by introducing the weakened virus into the body. This prompts the immune system to recognise the virus as foreign and mount a defence. The immune response involves the production of antibodies, which are proteins that target and neutralise the virus. […] Additionally, memory cells are generated, providing long-term immunity. If the vaccinated person is later exposed to the actual virus, their immune system can quickly recognise and respond, preventing or significantly reducing the severity of the infection.
  • #10 Varicella vaccine : Indications, Uses, Dosage, Drugs Interactions, Side effects
    https://medicaldialogues.in/generics/varicella-vaccine-2726218
    The varicella vaccine is approved for active immunization against the varicella-zoster virus, prevents varicella (chickenpox), and reduces the severity of chickenpox infection in individuals, particularly children and adults. […] The varicella vaccine involves the absorption of the vaccine subcutaneously, distribution throughout the body, minimal metabolism, and primarily strengthening immunity by producing antibodies with insignificant excretion, enabling protection against the varicella-zoster virus. […] The varicella vaccination works by embedding a live but weakened strain of the varicella-zoster virus (VZV) inside the body. This vaccine activates by exposing you to a small amount of the virus or a viral protein, which prompts the body to produce immunity against the disease. The virus is weakened before being administered, activating the immune system without causing sickness. The immune system responds to the presence of the weakened virus by creating antibodies that are specifically directed against the varicella-zoster virus. Long-lasting defence is provided by these antibodies that remain in the body. These antibodies offer enduring protection because they stay in the body. The immune system can quickly identify and neutralize the virus if the wild-type VZV is exposed in the future, preventing or significantly reducing the risk of varicella (chickenpox).
  • #11 Chickenpox (Varicella) – Factsheets – Immunisation Advisory Centre
    https://www.immune.org.nz/factsheets/chickenpox-varicella
    The chickenpox vaccine contains weakened live chickenpox (varicella zoster) viruses. […] Immunisation against chickenpox may not protect every person completely. […] After a single chickenpox vaccine dose, 70-90% of children are expected to be fully protected against all chickenpox and more than 95% protected from moderate to severe chickenpox. […] After two chickenpox vaccine doses, 97-99% of children are protected against all chickenpox and 100% protected from moderate to severe chickenpox. […] Protection after one dose of vaccine before 13 years of age can provide many years but probably not lifelong protection. […] Protection after two doses of vaccine appears to be very long term for most people immunised, however, it is not known if it is lifelong at this stage. […] Available information suggests that chickenpox immunisation may reduce the risk of developing shingles later in life in comparison with those who had wild-type disease.
  • #12 Chickenpox (Varicella) – Factsheets – Immunisation Advisory Centre
    https://www.immune.org.nz/factsheets/chickenpox-varicella
    The chickenpox vaccine contains weakened live chickenpox (varicella zoster) viruses. […] Immunisation against chickenpox may not protect every person completely. […] After a single chickenpox vaccine dose, 70-90% of children are expected to be fully protected against all chickenpox and more than 95% protected from moderate to severe chickenpox. […] After two chickenpox vaccine doses, 97-99% of children are protected against all chickenpox and 100% protected from moderate to severe chickenpox. […] Protection after one dose of vaccine before 13 years of age can provide many years but probably not lifelong protection. […] Protection after two doses of vaccine appears to be very long term for most people immunised, however, it is not known if it is lifelong at this stage. […] Available information suggests that chickenpox immunisation may reduce the risk of developing shingles later in life in comparison with those who had wild-type disease.
  • #13 Varicella (Chickenpox) Vaccine – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK441946/
    Varicella-zoster virus (chickenpox) is an acute febrile rash illness that was very common in children in the United States before the universal vaccination program existed. […] The FDA approves using the live varicella virus vaccine to provide immunity for preventing varicella in individuals 12 months older. […] This activity reviews the mechanism of action, indications, contraindications, adverse effects of this vaccine, and the front-line personnel involved in preventing the disease. […] Evaluate the mechanism of action of the varicella vaccine. […] The varicella-zoster vaccine contains live attenuated varicella-zoster vaccine (Oka strain). This vaccine induces both humoral and cell-mediated immune responses. It produces an IgG humoral immune response in individuals, and the cell-mediated immune response is caused by varicella-zoster-specific activation of both CD4+ T-helper and CD8+ T-lymphocyte cells. The protection duration is still unknown; however, some efficacy trials have shown that the vaccine can offer continued protection for up to 10 years after vaccination.
  • #14 Everything You Need To Know About The Chickenpox Vaccine
    https://justtheinserts.com/chickenpox/
    VARIVAX induces both cell-mediated and humoral immune responses to varicella-zoster virus. […] The relative contributions of humoral immunity and cell-mediated immunity to protection from varicella are unknown. […] The duration of protection of VARIVAX is unknown; however, long-term efficacy studies have demonstrated continued protection up to 10 years after vaccination. […] A boost in antibody levels has been observed in vaccinees following exposure to wild-type varicella which could account for the apparent long-term protection after vaccination in these studies.
  • #15 Everything You Need To Know About The Chickenpox Vaccine
    https://justtheinserts.com/chickenpox/
    VARIVAX induces both cell-mediated and humoral immune responses to varicella-zoster virus. […] The relative contributions of humoral immunity and cell-mediated immunity to protection from varicella are unknown. […] The duration of protection of VARIVAX is unknown; however, long-term efficacy studies have demonstrated continued protection up to 10 years after vaccination. […] A boost in antibody levels has been observed in vaccinees following exposure to wild-type varicella which could account for the apparent long-term protection after vaccination in these studies.
  • #16 Chapter 22: Varicella | Pink Book | CDC
    https://www.cdc.gov/pinkbook/hcp/table-of-contents/chapter-22-varicella.html?utm_medium=email&utm_source=transaction
    VZV enters the host through the respiratory tract and conjunctiva. […] It replicates at the site of entry in the nasopharynx and in regional lymph nodes. […] A primary viremia occurs 4 to 6 days after infection and disseminates the virus to other organs, such as the liver, spleen, and sensory ganglia. […] Further replication occurs in the viscera, followed by a secondary viremia, with viral infection of the skin.
  • #17 Varicella (chickenpox) | The Australian Immunisation Handbook
    https://immunisationhandbook.health.gov.au/contents/vaccine-preventable-diseases/varicella-chickenpox
    Varicella is a highly contagious viral infection. Primary infection with VZV causes varicella (chickenpox). After primary infection, VZV establishes latency in the dorsal root ganglia. Reactivation of the latent virus manifests as herpes zoster (shingles). […] The average incubation period is 14–16 days (range 10–21 days). This may be longer in people who are immunocompromised, especially after receiving zoster immunoglobulin. The period of infectivity is from 48 hours before the onset of the rash until all lesions have crusted over. […] Varicella spreads: by respiratory secretions, including aerosol transmission; from the vesicle fluid of the skin lesions of varicella or herpes zoster infection.
  • #18 Chickenpox: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/1131785-overview
    Varicella-zoster virus is transmitted person to person primarily through the respiratory route by inhalation of aerosols from vesicular fluid of skin lesions of varicella or herpes zoster. It can also spread by direct contact with the vesicular fluid of skin lesions and possibly infected respiratory tract secretions. Varicella-zoster virus enters the host through the upper respiratory tract or the conjunctiva. After initial inhalation of contaminated respiratory droplets, the virus infects the conjunctivae or the mucosae of the upper respiratory tract, with viral proliferation occurring in regional lymph nodes 2-4 days after infection. This is followed by primary viremia on days 4-6 post-infection, and a secondary round of viral replication in internal organs, notably the liver and spleen, leading to a secondary viremia 14-16 days post-infection, characterized by diffuse viral invasion of capillary endothelial cells and the epidermis.
  • #19 Chapter 22: Varicella | Pink Book | CDC
    https://www.cdc.gov/pinkbook/hcp/table-of-contents/chapter-22-varicella.html?utm_medium=email&utm_source=transaction
    VZV enters the host through the respiratory tract and conjunctiva. […] It replicates at the site of entry in the nasopharynx and in regional lymph nodes. […] A primary viremia occurs 4 to 6 days after infection and disseminates the virus to other organs, such as the liver, spleen, and sensory ganglia. […] Further replication occurs in the viscera, followed by a secondary viremia, with viral infection of the skin.
  • #20 Chapter 22: Varicella | Pink Book | CDC
    https://www.cdc.gov/pinkbook/hcp/table-of-contents/chapter-22-varicella.html?utm_medium=email&utm_source=transaction
    VZV enters the host through the respiratory tract and conjunctiva. […] It replicates at the site of entry in the nasopharynx and in regional lymph nodes. […] A primary viremia occurs 4 to 6 days after infection and disseminates the virus to other organs, such as the liver, spleen, and sensory ganglia. […] Further replication occurs in the viscera, followed by a secondary viremia, with viral infection of the skin.
  • #21 Chapter 22: Varicella | Pink Book | CDC
    https://www.cdc.gov/pinkbook/hcp/table-of-contents/chapter-22-varicella.html?utm_medium=email&utm_source=transaction
    VZV enters the host through the respiratory tract and conjunctiva. […] It replicates at the site of entry in the nasopharynx and in regional lymph nodes. […] A primary viremia occurs 4 to 6 days after infection and disseminates the virus to other organs, such as the liver, spleen, and sensory ganglia. […] Further replication occurs in the viscera, followed by a secondary viremia, with viral infection of the skin.
  • #22 Evaluation the aggressive reaction of varicella in young adult immune system compared to children immune response – MedCrave online
    https://medcraveonline.com/MOJPB/evaluation-the-aggressive-reaction-of-varicella-in-young-adult-immune-system-compared-to-children-immune-response.html
    The immune system is a defense system, both children, and adult have the same reaction toward pathogen, uses multiple defense mechanisms evolved to recognize and neutralize pathogens also have the ability to distinguish self from non-self cells, but in case of Varicella-zoster virus (VZV) that cause chicken pox, the immune system reacts differently in young healthy adult usually have an aggressive reaction serious complications can lead to death, compare with children infection is usually mild. […] The response of the immune system in case of primary infection with VZV in children and adult (healthy young adult), raising the questions, why varicella is more aggressive in adult in most cases? And why is mild in most children infection? […] VZV enters through the respiratory tract and conjunctiva, Chickenpox infection is started in mucosal sites, most of varicella zoster virus inoculated in the upper respiratory tract. The first defense cells have been proposed to encounter the infection is the dendritic cells (DC) of the mucosa following infection of human tonsillar CD4+ T cells that express skin homing markers that allow them to transport VZV directly from the lymph node to the skin.
  • #23 Chickenpox: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/1131785-overview
    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 crucial in limiting the scope and duration of primary varicella infection. After primary infection, VZV is hypothesized to spread from mucosal and epidermal lesions to local sensory nerves, remaining latent in the dorsal ganglion cells of the sensory nerves. Reactivation of VZV results in the clinically distinct syndrome of herpes zoster (shingles).
  • #24
    https://link.springer.com/article/10.1007/s12250-014-3516-9
    Varicella zoster virus (VZV) is the causative agent of varicella (chicken pox) and herpes zoster (shingles). After primary infection, the virus remains latent in sensory ganglia, and reactivates upon weakening of the cellular immune system due to various conditions, erupting from sensory neurons and infecting the corresponding skin tissue. The current varicella vaccine (v-Oka) is highly attenuated in the skin, yet retains its neurovirulence and may reactivate and damage sensory neurons. […] The development of a genetically-defined live-attenuated VZV vaccine that prevents neuronal and latent infection, in addition to primary varicella, is imperative for eventual eradication of VZV, and, if fully understood, has vast implications for many related herpesviruses and other viruses with similar pathogenic mechanisms.
  • #25 Chickenpox: Background, Pathophysiology, Etiology
    https://emedicine.medscape.com/article/1131785-overview
    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 crucial in limiting the scope and duration of primary varicella infection. After primary infection, VZV is hypothesized to spread from mucosal and epidermal lesions to local sensory nerves, remaining latent in the dorsal ganglion cells of the sensory nerves. Reactivation of VZV results in the clinically distinct syndrome of herpes zoster (shingles).
  • #26 Molecular mechanisms of varicella zoster virus pathogenesis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC4066823/
    The VZV genome has at least 71 known or predicted ORFs. Similar to all herpesviruses, VZV has a lipid-rich envelope, which is acquired from cellular membranes and into which viral glycoproteins are inserted. Within the envelope, a tegument layer that is predominantly composed of viral regulatory proteins surrounds an icosahedral nucleocapsid core that contains the linear double-stranded DNA genome. The viral life cycle begins with VZV entry, which is a poorly understood process that is presumed to involve either direct fusion of viral particles with the plasma membrane or endocytosis. […] Investigating VZV pathogenesis is challenging as VZV is a highly human-specific virus that has little or no capacity to infect other species. This obstacle can be overcome by using human tissue xenografts in mice with severe combined immunodeficiency (SCID). Infecting foetal thymus-liver T cell, skin and dorsal root ganglia (DRG) xenografts enables studies of the three major tissue tropisms of VZV: T cell-, skin- and neuro-tropism. In these models, innate responses that modulate infectious processes can be assessed independently of adaptive immunity, which is absent in SCID mice.
  • #27 Molecular mechanisms of varicella zoster virus pathogenesis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC4066823/
    The VZV genome has at least 71 known or predicted ORFs. Similar to all herpesviruses, VZV has a lipid-rich envelope, which is acquired from cellular membranes and into which viral glycoproteins are inserted. Within the envelope, a tegument layer that is predominantly composed of viral regulatory proteins surrounds an icosahedral nucleocapsid core that contains the linear double-stranded DNA genome. The viral life cycle begins with VZV entry, which is a poorly understood process that is presumed to involve either direct fusion of viral particles with the plasma membrane or endocytosis. […] Investigating VZV pathogenesis is challenging as VZV is a highly human-specific virus that has little or no capacity to infect other species. This obstacle can be overcome by using human tissue xenografts in mice with severe combined immunodeficiency (SCID). Infecting foetal thymus-liver T cell, skin and dorsal root ganglia (DRG) xenografts enables studies of the three major tissue tropisms of VZV: T cell-, skin- and neuro-tropism. In these models, innate responses that modulate infectious processes can be assessed independently of adaptive immunity, which is absent in SCID mice.
  • #28 Molecular mechanisms of varicella zoster virus pathogenesis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC4066823/
    VZV suppresses innate responses to produce a virus-filled lesion at the skin surface, where infected keratinocytes release newly-assembled virions. Several viral proteins interfere with IFN-mediated responses in infected cells: IE62 inhibits the phosphorylation of IFN regulatory factor 3 (IRF3) by TANK-binding kinase 1 (TBK-1), thus blocking IFN production, ORF47 kinase reduces IRF3 phosphorylation and IE63 inhibits the phosphorylation of the eukaryotic initiation factor 2 and its downstream IFN effects. […] Cell-cell fusion is not strictly required for VZV spread, as virions that are released from infected cells can enter adjacent cells. However, polykaryocyte formation is the classic pathological change that is induced by VZV in the skin. This pattern suggests that VZV reprogrammes infected cells to overcome the normal preservation of plasma membrane boundaries between differentiated cells and to mediate fusion of human skin cells in vivo, leading to facilitated virus spread, which overcomes innate barriers. […] Glycoprotein gB and the heterodimer that is formed by gH and gL constitute the minimal VZV fusion complex and are candidates for mediating virus-induced cell fusion as well as virion entry.
  • #29 Molecular mechanisms of varicella zoster virus pathogenesis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC4066823/
    VZV suppresses innate responses to produce a virus-filled lesion at the skin surface, where infected keratinocytes release newly-assembled virions. Several viral proteins interfere with IFN-mediated responses in infected cells: IE62 inhibits the phosphorylation of IFN regulatory factor 3 (IRF3) by TANK-binding kinase 1 (TBK-1), thus blocking IFN production, ORF47 kinase reduces IRF3 phosphorylation and IE63 inhibits the phosphorylation of the eukaryotic initiation factor 2 and its downstream IFN effects. […] Cell-cell fusion is not strictly required for VZV spread, as virions that are released from infected cells can enter adjacent cells. However, polykaryocyte formation is the classic pathological change that is induced by VZV in the skin. This pattern suggests that VZV reprogrammes infected cells to overcome the normal preservation of plasma membrane boundaries between differentiated cells and to mediate fusion of human skin cells in vivo, leading to facilitated virus spread, which overcomes innate barriers. […] Glycoprotein gB and the heterodimer that is formed by gH and gL constitute the minimal VZV fusion complex and are candidates for mediating virus-induced cell fusion as well as virion entry.
  • #30 Molecular mechanisms of varicella zoster virus pathogenesis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC4066823/
    VZV suppresses innate responses to produce a virus-filled lesion at the skin surface, where infected keratinocytes release newly-assembled virions. Several viral proteins interfere with IFN-mediated responses in infected cells: IE62 inhibits the phosphorylation of IFN regulatory factor 3 (IRF3) by TANK-binding kinase 1 (TBK-1), thus blocking IFN production, ORF47 kinase reduces IRF3 phosphorylation and IE63 inhibits the phosphorylation of the eukaryotic initiation factor 2 and its downstream IFN effects. […] Cell-cell fusion is not strictly required for VZV spread, as virions that are released from infected cells can enter adjacent cells. However, polykaryocyte formation is the classic pathological change that is induced by VZV in the skin. This pattern suggests that VZV reprogrammes infected cells to overcome the normal preservation of plasma membrane boundaries between differentiated cells and to mediate fusion of human skin cells in vivo, leading to facilitated virus spread, which overcomes innate barriers. […] Glycoprotein gB and the heterodimer that is formed by gH and gL constitute the minimal VZV fusion complex and are candidates for mediating virus-induced cell fusion as well as virion entry.
  • #31 Varicella vaccine – Wikipedia
    https://en.wikipedia.org/wiki/Varicella_vaccine
    Varicella vaccine, also known as chickenpox vaccine, is a vaccine that protects against chickenpox. One dose of vaccine prevents 95% of moderate disease and 100% of severe disease. Two doses of vaccine are more effective than one. If given to those who are not immune within five days of exposure to chickenpox it prevents most cases of the disease. Vaccinating a large portion of the population also protects those who are not vaccinated. It is given by injection just under the skin. […] A live attenuated varicella vaccine, the Oka strain, was developed by Michiaki Takahashi and his colleagues in Japan in the early 1970s. American vaccinologist Maurice Hilleman’s team developed a chickenpox vaccine in the United States in 1981, based on the „Oka strain” of the varicella virus. The chickenpox vaccine first became commercially available in 1984. It was first licensed for use in the US by Merck, under the brand name Varivax, in 1995.
  • #32 The Biology of Varicella-Zoster Virus Replication in the Skin
    https://www.mdpi.com/1999-4915/14/5/982
    The glycoproteins that are essential in skin pathogenesis in vivo encompass the glycoprotein gE (encoded by ORF68), which is essential for VZV replication and cell–cell spread in skin. […] The varicella vaccine was generated by Takahashi and colleagues in 1974 by serial passaging, first in human embryonic fibroblasts and then in in guinea pig embryo fibroblasts, of VZV virus isolated from a boy with chickenpox. […] The vaccine is safe and effective in preventing chickenpox or reducing the severity of it, as well as in building a long-last immunity against the virus. […] Understanding the molecular mechanisms causing attenuation in skin of the existing VZV vaccine will shed light on pivotal events of VZV skin replication that could be targeted by new antiviral drugs, as well as pave the way for the generation of novel vaccines that could be directed to a wider number of recipients, including immunocompromised children.
  • #33 The Biology of Varicella-Zoster Virus Replication in the Skin
    https://www.mdpi.com/1999-4915/14/5/982
    The glycoproteins that are essential in skin pathogenesis in vivo encompass the glycoprotein gE (encoded by ORF68), which is essential for VZV replication and cell–cell spread in skin. […] The varicella vaccine was generated by Takahashi and colleagues in 1974 by serial passaging, first in human embryonic fibroblasts and then in in guinea pig embryo fibroblasts, of VZV virus isolated from a boy with chickenpox. […] The vaccine is safe and effective in preventing chickenpox or reducing the severity of it, as well as in building a long-last immunity against the virus. […] Understanding the molecular mechanisms causing attenuation in skin of the existing VZV vaccine will shed light on pivotal events of VZV skin replication that could be targeted by new antiviral drugs, as well as pave the way for the generation of novel vaccines that could be directed to a wider number of recipients, including immunocompromised children.
  • #34 Molecular mechanisms of varicella zoster virus pathogenesis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC4066823/
    The pathogenesis of VZV infection can be modelled by infecting xenografts of human foetal tissues in mice with severe combined immunodeficiency (SCID). The xenografts are maintained for prolonged periods, as SCID mice lack T cell responses that mediate rejection of these foreign tissues. […] The importance of the IFN and IFN response is evident from the enlarged lesions in skin xenografts that form if it is blocked with an antibody that targets the IFN and IFN receptor. During varicella in the human host, T cell-mediated immunity only occurs late in infection and is rarely detected until skin lesions have developed. […] Notably, replication of the vaccine virus Oka is reduced in skin xenografts, which is consistent with the situation in humans, who rarely develop lesions after subcutaneous inoculation of the vaccine. Thus, the mutations that have accumulated in this attenuated strain (via passage in fibroblasts) have reduced its capacity to overcome intrinsic cutaneous barriers, even though the mutations have no effect on T cell tropism or neurotropism.
  • #35 Molecular mechanisms of varicella zoster virus pathogenesis
    https://pmc.ncbi.nlm.nih.gov/articles/PMC4066823/
    The pathogenesis of VZV infection can be modelled by infecting xenografts of human foetal tissues in mice with severe combined immunodeficiency (SCID). The xenografts are maintained for prolonged periods, as SCID mice lack T cell responses that mediate rejection of these foreign tissues. […] The importance of the IFN and IFN response is evident from the enlarged lesions in skin xenografts that form if it is blocked with an antibody that targets the IFN and IFN receptor. During varicella in the human host, T cell-mediated immunity only occurs late in infection and is rarely detected until skin lesions have developed. […] Notably, replication of the vaccine virus Oka is reduced in skin xenografts, which is consistent with the situation in humans, who rarely develop lesions after subcutaneous inoculation of the vaccine. Thus, the mutations that have accumulated in this attenuated strain (via passage in fibroblasts) have reduced its capacity to overcome intrinsic cutaneous barriers, even though the mutations have no effect on T cell tropism or neurotropism.
  • #36 The Biology of Varicella-Zoster Virus Replication in the Skin
    https://www.mdpi.com/1999-4915/14/5/982
    The glycoproteins that are essential in skin pathogenesis in vivo encompass the glycoprotein gE (encoded by ORF68), which is essential for VZV replication and cell–cell spread in skin. […] The varicella vaccine was generated by Takahashi and colleagues in 1974 by serial passaging, first in human embryonic fibroblasts and then in in guinea pig embryo fibroblasts, of VZV virus isolated from a boy with chickenpox. […] The vaccine is safe and effective in preventing chickenpox or reducing the severity of it, as well as in building a long-last immunity against the virus. […] Understanding the molecular mechanisms causing attenuation in skin of the existing VZV vaccine will shed light on pivotal events of VZV skin replication that could be targeted by new antiviral drugs, as well as pave the way for the generation of novel vaccines that could be directed to a wider number of recipients, including immunocompromised children.
  • #37 Chickenpox – Drugs, Targets, Patents – Synapse
    https://synapse.patsnap.com/disease/157f7a978dfd43f3b31de0cebedb99fa
    The varicella vaccine is a live attenuated varicella zoster virus (VZV), first produced by Michiaki Takahashi (1974). […] Subsequent development of the fluorescent antibody to VZV membrane antigen test (FAMA), an immune correlate, permitted vaccine efficacy to be established, initially in immunodeficient and then in typical children and adults. […] Varicella vaccine is effective and safe; universal vaccination has almost eliminated varicella; moreover, endogenous boosting from subclinical VZV reactivation has evidently prevented an anticipated epidemic of zoster from occurring in response to the vaccine-induced loss of circulating varicella. […] The vaccine virus, moreover, reactivates less frequently than wild-type and an adjuvanted subunit vaccine against VZV gE safely prevents zoster. […] VZV establishes latency and reactivates in sympathetic and enteric neurons; therefore, in addition to the painful cutaneous rash and postherpetic neuralgia of zoster, VZV reactivation can be an occult cause of vasculopathy, stroke, intestinal dysmotility, and achalasia.
  • #38 Twelve Children with Varicella Vaccine Meningitis: Neuropathogenesis of Reactivated Live Attenuated Varicella Vaccine Virus
    https://www.mdpi.com/1999-4915/12/10/1078
    The cerebrospinal fluid indices are shown in Table 2. […] Thus, the live attenuated varicella vaccine virus has retained the neurotropism of its wild-type counterpart. […] The vaccine virus replicates in the skin after reactivation. Thereafter, progeny viruses enter sensory neurons and are transported retrograde to the DRG within 1–2 days. […] Altogether, therefore, within one episode of VZV reactivation, before a strong adaptive immune response, there are two or more round trips of the virus transported between DRG and skin or between DRG and spinal cord.
  • #39 Twelve Children with Varicella Vaccine Meningitis: Neuropathogenesis of Reactivated Live Attenuated Varicella Vaccine Virus
    https://www.mdpi.com/1999-4915/12/10/1078
    Varicella vaccine is a live attenuated varicella-zoster virus (VZV). […] The most serious complication in healthy children is probably central nervous system infection, which is caused by reactivation of the vaccine virus from the dorsal root ganglia (DRG), usually years after the first varicella vaccination. […] After review of prior models, we propose a pathogenesis model. Every child around the age of 1 year is given an initial injection of the live attenuated varicella vaccine in the thigh. Virus replicates locally in the skin; some viral particles enter the free endings of A and C nociceptor fibers, after which the viral particles are transported to the soma of lumbar DRG, where the virus enters a latent state. […] Several years later, the vaccine virus reactivates from the DRG, after which the virus is carried in the same pseudounipolar fibers anterograde to the thigh, presenting as herpes zoster in a lumbar dermatome on the leg.
  • #40 Twelve Children with Varicella Vaccine Meningitis: Neuropathogenesis of Reactivated Live Attenuated Varicella Vaccine Virus
    https://www.mdpi.com/1999-4915/12/10/1078
    Varicella vaccine is a live attenuated varicella-zoster virus (VZV). […] The most serious complication in healthy children is probably central nervous system infection, which is caused by reactivation of the vaccine virus from the dorsal root ganglia (DRG), usually years after the first varicella vaccination. […] After review of prior models, we propose a pathogenesis model. Every child around the age of 1 year is given an initial injection of the live attenuated varicella vaccine in the thigh. Virus replicates locally in the skin; some viral particles enter the free endings of A and C nociceptor fibers, after which the viral particles are transported to the soma of lumbar DRG, where the virus enters a latent state. […] Several years later, the vaccine virus reactivates from the DRG, after which the virus is carried in the same pseudounipolar fibers anterograde to the thigh, presenting as herpes zoster in a lumbar dermatome on the leg.
  • #41 Varicella vaccine – Wikipedia
    https://en.wikipedia.org/wiki/Varicella_vaccine
    Varicella vaccine is 70% to 90% effective for preventing varicella and more than 95% effective for preventing severe varicella. Follow-up evaluations have taken place in the United States of children immunized that revealed protection for at least 11 years. Studies were conducted in Japan which indicated protection for at least 20 years. […] The long-term duration of protection from varicella vaccine is unknown, but there are now persons vaccinated twenty years ago with no evidence of waning immunity, while others have become vulnerable in as few as six years. […] The risk of developing shingles is reduced for children who receive the varicella vaccine, but not eliminated. The CDC stated in 2014: „Chickenpox vaccines contain weakened live VZV, which may cause latent (dormant) infection. The vaccine-strain VZV can reactivate later in life and cause shingles. However, the risk of getting shingles from vaccine-strain VZV after chickenpox vaccination is much lower than getting shingles after natural infection with wild-type VZV.”
  • #42 Varicella vaccine – Wikipedia
    https://en.wikipedia.org/wiki/Varicella_vaccine
    Varicella vaccine is 70% to 90% effective for preventing varicella and more than 95% effective for preventing severe varicella. Follow-up evaluations have taken place in the United States of children immunized that revealed protection for at least 11 years. Studies were conducted in Japan which indicated protection for at least 20 years. […] The long-term duration of protection from varicella vaccine is unknown, but there are now persons vaccinated twenty years ago with no evidence of waning immunity, while others have become vulnerable in as few as six years. […] The risk of developing shingles is reduced for children who receive the varicella vaccine, but not eliminated. The CDC stated in 2014: „Chickenpox vaccines contain weakened live VZV, which may cause latent (dormant) infection. The vaccine-strain VZV can reactivate later in life and cause shingles. However, the risk of getting shingles from vaccine-strain VZV after chickenpox vaccination is much lower than getting shingles after natural infection with wild-type VZV.”
  • #43 Varicella (Chickenpox) Vaccine | Treatment & Management | Point of Care
    https://www.statpearls.com/point-of-care/30981
    The varicella-zoster vaccine contains live attenuated varicella-zoster vaccine (Oka strain). This vaccine induces both humoral and cell-mediated immune responses. It produces an IgG humoral immune response in individuals, and the cell-mediated immune response is caused by varicella-zoster-specific activation of both CD4+ T-helper and CD8+ T-lymphocyte cells. The protection duration is still unknown; however, some efficacy trials have shown that the vaccine can offer continued protection for up to 10 years after vaccination. […] The varicella vaccine is now FDA-approved to give for post-exposure use and outbreak control. The vaccine should be given as soon as possible after exposure, but it has shown effectiveness in preventing or modifying disease within 3 to 5 days post-exposure.
  • #44 Varicella vaccine in post-exposure prophylaxis
    https://www1.health.gov.au/internet/main/publishing.nsf/Content/cda-pubs-cdi-2001-cdi2501-cdi2501e.htm
    Evidence concerning the effectiveness of Oka-based varicella vaccines when administered following exposure to varicella zoster virus in domestic and hospital settings is reviewed. The pathogenesis of chickenpox follows the general scheme for viral exanthems proposed by Fenner. Respiratory tract inoculation allows initial viral replication in regional lymph nodes. Primary viraemia leads to replication in the liver and spleen, and secondary viraemia disseminates virus (within infected mononuclear cells) to various organs including the skin leading to the characteristic rash. An immune response mounted prior to the secondary viraemia may abort or ameliorate clinical disease. […] Theoretical considerations and experimental evidence appear to support the post-exposure use in children of Oka-derived varicella vaccines within 3 days of rash onset in the index case. Despite vaccination, a small proportion will develop mild, but infectious, chickenpox, especially if they have been exposed in the household setting. Controlled studies of post-exposure prophylaxis in adults using both Varilrix and Varivax II are still needed, whilst the applicability of this approach to disease control in health care facilities and in community settings warrants wider discussion.
  • #45 Varicella vaccine in post-exposure prophylaxis
    https://www1.health.gov.au/internet/main/publishing.nsf/Content/cda-pubs-cdi-2001-cdi2501-cdi2501e.htm
    Evidence concerning the effectiveness of Oka-based varicella vaccines when administered following exposure to varicella zoster virus in domestic and hospital settings is reviewed. The pathogenesis of chickenpox follows the general scheme for viral exanthems proposed by Fenner. Respiratory tract inoculation allows initial viral replication in regional lymph nodes. Primary viraemia leads to replication in the liver and spleen, and secondary viraemia disseminates virus (within infected mononuclear cells) to various organs including the skin leading to the characteristic rash. An immune response mounted prior to the secondary viraemia may abort or ameliorate clinical disease. […] Theoretical considerations and experimental evidence appear to support the post-exposure use in children of Oka-derived varicella vaccines within 3 days of rash onset in the index case. Despite vaccination, a small proportion will develop mild, but infectious, chickenpox, especially if they have been exposed in the household setting. Controlled studies of post-exposure prophylaxis in adults using both Varilrix and Varivax II are still needed, whilst the applicability of this approach to disease control in health care facilities and in community settings warrants wider discussion.
  • #46 Varicella vaccine in post-exposure prophylaxis
    https://www1.health.gov.au/internet/main/publishing.nsf/Content/cda-pubs-cdi-2001-cdi2501-cdi2501e.htm
    Evidence concerning the effectiveness of Oka-based varicella vaccines when administered following exposure to varicella zoster virus in domestic and hospital settings is reviewed. The pathogenesis of chickenpox follows the general scheme for viral exanthems proposed by Fenner. Respiratory tract inoculation allows initial viral replication in regional lymph nodes. Primary viraemia leads to replication in the liver and spleen, and secondary viraemia disseminates virus (within infected mononuclear cells) to various organs including the skin leading to the characteristic rash. An immune response mounted prior to the secondary viraemia may abort or ameliorate clinical disease. […] Theoretical considerations and experimental evidence appear to support the post-exposure use in children of Oka-derived varicella vaccines within 3 days of rash onset in the index case. Despite vaccination, a small proportion will develop mild, but infectious, chickenpox, especially if they have been exposed in the household setting. Controlled studies of post-exposure prophylaxis in adults using both Varilrix and Varivax II are still needed, whilst the applicability of this approach to disease control in health care facilities and in community settings warrants wider discussion.
  • #47 Your Child’s Vaccines: Chickenpox Vaccine (for Parents) | Nemours KidsHealth
    https://kidshealth.org/en/parents/varicella-vaccine.html
    The varicella vaccine protects against chickenpox (varicella), a common and very contagious childhood viral illness. It also protects against shingles. It is a live attenuated vaccine, which means it contains a weakened form of the virus. […] Chickenpox used to be common in the U.S., causing many hospitalizations and even deaths. Since the vaccine was introduced in 1995, it has prevented millions of infections every year. It prevents severe illness in almost all kids who are vaccinated. It’s also very effective in preventing mild illness. Vaccinated kids who do get chickenpox generally have a mild case. […] If a person with no immunity to the virus is exposed to someone with chickenpox or shingles, they are likely to get infected because the virus is so contagious. Giving the vaccine within 3 to 5 days after exposure can help to prevent the infection or make it less serious.
  • #48 Varicella (Chickenpox) Vaccine | Treatment & Management | Point of Care
    https://www.statpearls.com/point-of-care/30981
    The varicella-zoster vaccine contains live attenuated varicella-zoster vaccine (Oka strain). This vaccine induces both humoral and cell-mediated immune responses. It produces an IgG humoral immune response in individuals, and the cell-mediated immune response is caused by varicella-zoster-specific activation of both CD4+ T-helper and CD8+ T-lymphocyte cells. The protection duration is still unknown; however, some efficacy trials have shown that the vaccine can offer continued protection for up to 10 years after vaccination. […] The varicella vaccine is now FDA-approved to give for post-exposure use and outbreak control. The vaccine should be given as soon as possible after exposure, but it has shown effectiveness in preventing or modifying disease within 3 to 5 days post-exposure.
  • #49 Varicella vaccine in post-exposure prophylaxis
    https://www1.health.gov.au/internet/main/publishing.nsf/Content/cda-pubs-cdi-2001-cdi2501-cdi2501e.htm
    Evidence concerning the effectiveness of Oka-based varicella vaccines when administered following exposure to varicella zoster virus in domestic and hospital settings is reviewed. The pathogenesis of chickenpox follows the general scheme for viral exanthems proposed by Fenner. Respiratory tract inoculation allows initial viral replication in regional lymph nodes. Primary viraemia leads to replication in the liver and spleen, and secondary viraemia disseminates virus (within infected mononuclear cells) to various organs including the skin leading to the characteristic rash. An immune response mounted prior to the secondary viraemia may abort or ameliorate clinical disease. […] Theoretical considerations and experimental evidence appear to support the post-exposure use in children of Oka-derived varicella vaccines within 3 days of rash onset in the index case. Despite vaccination, a small proportion will develop mild, but infectious, chickenpox, especially if they have been exposed in the household setting. Controlled studies of post-exposure prophylaxis in adults using both Varilrix and Varivax II are still needed, whilst the applicability of this approach to disease control in health care facilities and in community settings warrants wider discussion.
  • #50 Varicella vaccine in post-exposure prophylaxis
    https://www1.health.gov.au/internet/main/publishing.nsf/Content/cda-pubs-cdi-2001-cdi2501-cdi2501e.htm
    Evidence concerning the effectiveness of Oka-based varicella vaccines when administered following exposure to varicella zoster virus in domestic and hospital settings is reviewed. The pathogenesis of chickenpox follows the general scheme for viral exanthems proposed by Fenner. Respiratory tract inoculation allows initial viral replication in regional lymph nodes. Primary viraemia leads to replication in the liver and spleen, and secondary viraemia disseminates virus (within infected mononuclear cells) to various organs including the skin leading to the characteristic rash. An immune response mounted prior to the secondary viraemia may abort or ameliorate clinical disease. […] Theoretical considerations and experimental evidence appear to support the post-exposure use in children of Oka-derived varicella vaccines within 3 days of rash onset in the index case. Despite vaccination, a small proportion will develop mild, but infectious, chickenpox, especially if they have been exposed in the household setting. Controlled studies of post-exposure prophylaxis in adults using both Varilrix and Varivax II are still needed, whilst the applicability of this approach to disease control in health care facilities and in community settings warrants wider discussion.
  • #51 Potent and long-lasting humoral and cellular immunity against varicella zoster virus induced by mRNA-LNP vaccine | npj Vaccines
    https://www.nature.com/articles/s41541-024-00865-5
    Varicella zoster virus (VZV) is a highly contagious human herpes virus responsible for causing chickenpox (varicella) and shingles (herpes zoster). […] In this study, we aimed to evaluate immunogenicity and memory response induced by three mRNA-LNP-based vaccine candidates targeting VZVs surface glycoprotein E (gE). […] Our results demonstrate that the mRNA-LNP-based vaccine candidates elicited robust and durable humoral responses specific to the gE antigen. Notably, mice vaccinated with the mRNA-LNP vaccines exhibited significantly higher antigen-specific T-cell cytokine production compared to the group receiving Shingrix, the current standard of care vaccine. […] Additionally, mRNA-LNP vaccines induced long-lasting memory response, as evidenced by detection of persistent gE-specific Long-Lived Plasma Cells (LLPCs) and memory T cells four months after final immunization.
  • #52 Potent and long-lasting humoral and cellular immunity against varicella zoster virus induced by mRNA-LNP vaccine | npj Vaccines
    https://www.nature.com/articles/s41541-024-00865-5
    Varicella zoster virus (VZV) is a highly contagious human herpes virus responsible for causing chickenpox (varicella) and shingles (herpes zoster). […] In this study, we aimed to evaluate immunogenicity and memory response induced by three mRNA-LNP-based vaccine candidates targeting VZVs surface glycoprotein E (gE). […] Our results demonstrate that the mRNA-LNP-based vaccine candidates elicited robust and durable humoral responses specific to the gE antigen. Notably, mice vaccinated with the mRNA-LNP vaccines exhibited significantly higher antigen-specific T-cell cytokine production compared to the group receiving Shingrix, the current standard of care vaccine. […] Additionally, mRNA-LNP vaccines induced long-lasting memory response, as evidenced by detection of persistent gE-specific Long-Lived Plasma Cells (LLPCs) and memory T cells four months after final immunization.
  • #53 Potent and long-lasting humoral and cellular immunity against varicella zoster virus induced by mRNA-LNP vaccine | npj Vaccines
    https://www.nature.com/articles/s41541-024-00865-5
    Varicella zoster virus (VZV) is a highly contagious human herpes virus responsible for causing chickenpox (varicella) and shingles (herpes zoster). […] In this study, we aimed to evaluate immunogenicity and memory response induced by three mRNA-LNP-based vaccine candidates targeting VZVs surface glycoprotein E (gE). […] Our results demonstrate that the mRNA-LNP-based vaccine candidates elicited robust and durable humoral responses specific to the gE antigen. Notably, mice vaccinated with the mRNA-LNP vaccines exhibited significantly higher antigen-specific T-cell cytokine production compared to the group receiving Shingrix, the current standard of care vaccine. […] Additionally, mRNA-LNP vaccines induced long-lasting memory response, as evidenced by detection of persistent gE-specific Long-Lived Plasma Cells (LLPCs) and memory T cells four months after final immunization.
  • #54 Potent and long-lasting humoral and cellular immunity against varicella zoster virus induced by mRNA-LNP vaccine | npj Vaccines
    https://www.nature.com/articles/s41541-024-00865-5
    Varicella zoster virus (VZV) is a highly contagious human herpes virus responsible for causing chickenpox (varicella) and shingles (herpes zoster). […] In this study, we aimed to evaluate immunogenicity and memory response induced by three mRNA-LNP-based vaccine candidates targeting VZVs surface glycoprotein E (gE). […] Our results demonstrate that the mRNA-LNP-based vaccine candidates elicited robust and durable humoral responses specific to the gE antigen. Notably, mice vaccinated with the mRNA-LNP vaccines exhibited significantly higher antigen-specific T-cell cytokine production compared to the group receiving Shingrix, the current standard of care vaccine. […] Additionally, mRNA-LNP vaccines induced long-lasting memory response, as evidenced by detection of persistent gE-specific Long-Lived Plasma Cells (LLPCs) and memory T cells four months after final immunization.
  • #55 Potent and long-lasting humoral and cellular immunity against varicella zoster virus induced by mRNA-LNP vaccine | npj Vaccines
    https://www.nature.com/articles/s41541-024-00865-5
    These findings underscore the potential of our mRNA-LNP-based vaccine candidates in generating potent immune responses against VZV, offering promising prospects for their clinical development as an effective prophylactic vaccine against herpes zoster. […] We, therefore, aimed to develop a safe and effective mRNA vaccine against herpes zoster that would generate robust virus-specific cell-mediated and humoral immune responses and induce long-term immunological memory. […] Here, we designed three versions of the VZV glycoprotein E, gE, encoded by the mRNA: (i) full-length gE (gE-full length), as present on the surface of the virion and naturally infected cells, (ii) truncated gE (gE-truncated), generated by deleting a part of the C-terminal domain and a single amino acid substitution altering one of the trans-Golgi network (TGN) localization motifs, and (iii) soluble gE (gE-soluble), which is expressed as the extracellular domain of the protein and similar to the antigen sequence in Shingrix.
  • #56 Potent and long-lasting humoral and cellular immunity against varicella zoster virus induced by mRNA-LNP vaccine | npj Vaccines
    https://www.nature.com/articles/s41541-024-00865-5
    Taken together, the data from this preliminary study shows that the GLB mRNA-LNP (NOF) formulation is successful in delivering the gE glycoprotein and successful in eliciting a strong immunogenic response, comparable to Shingrix, in mice. […] Importantly, we also showed that the NOF LNPs, delivering the gE full-length mRNA, was less inflammatory than Shingrix and therefore could demonstrate better safety profile in human clinical studies. […] In summary, we designed and evaluated the immunogenicity of three different mRNA-LNP vaccine candidates that encoded for three distinct VZV gE antigen variants. All three candidates, when delivered via novel NOF LNPs, were well-tolerated in rats and highly immunogenic and induced potent humoral, cellular, and immunological memory responses in mice.
  • #57 Potent and long-lasting humoral and cellular immunity against varicella zoster virus induced by mRNA-LNP vaccine | npj Vaccines
    https://www.nature.com/articles/s41541-024-00865-5
    Taken together, the data from this preliminary study shows that the GLB mRNA-LNP (NOF) formulation is successful in delivering the gE glycoprotein and successful in eliciting a strong immunogenic response, comparable to Shingrix, in mice. […] Importantly, we also showed that the NOF LNPs, delivering the gE full-length mRNA, was less inflammatory than Shingrix and therefore could demonstrate better safety profile in human clinical studies. […] In summary, we designed and evaluated the immunogenicity of three different mRNA-LNP vaccine candidates that encoded for three distinct VZV gE antigen variants. All three candidates, when delivered via novel NOF LNPs, were well-tolerated in rats and highly immunogenic and induced potent humoral, cellular, and immunological memory responses in mice.
  • #58 Shingles vaccine may directly guard against dementia, study hints | Live Science
    https://www.livescience.com/health/alzheimers-dementia/shingles-vaccine-may-directly-guard-against-dementia-study-hints
    The shingles vaccine helps prevent reactivation of the virus that causes chickenpox. The chickenpox virus remains in the body after an initial infection and can later cause shingles. […] The shingles vaccine helps to build immunity and prevent reactivation of the virus, and it’s thus highly effective at preventing shingles and its complications, such as long-term nerve pain, vision loss and a higher risk of bacterial skin infections. […] More studies are needed to understand the mechanism behind the vaccine’s protective effect against dementia, as that’s currently unclear. One theory suggests that reactivation of the varicella-zoster virus may trigger brain damage through a range of mechanisms, including the buildup of abnormal proteins and chronic inflammation. By preventing reactivation, the shingles vaccine may theoretically prevent this brain damage. […] Another hypothesis is that the vaccine provides protection not by targeting viruses directly but by tuning the immune system in a way that slows or alters the course of dementia.
  • #59 Shingles vaccine may directly guard against dementia, study hints | Live Science
    https://www.livescience.com/health/alzheimers-dementia/shingles-vaccine-may-directly-guard-against-dementia-study-hints
    The shingles vaccine helps prevent reactivation of the virus that causes chickenpox. The chickenpox virus remains in the body after an initial infection and can later cause shingles. […] The shingles vaccine helps to build immunity and prevent reactivation of the virus, and it’s thus highly effective at preventing shingles and its complications, such as long-term nerve pain, vision loss and a higher risk of bacterial skin infections. […] More studies are needed to understand the mechanism behind the vaccine’s protective effect against dementia, as that’s currently unclear. One theory suggests that reactivation of the varicella-zoster virus may trigger brain damage through a range of mechanisms, including the buildup of abnormal proteins and chronic inflammation. By preventing reactivation, the shingles vaccine may theoretically prevent this brain damage. […] Another hypothesis is that the vaccine provides protection not by targeting viruses directly but by tuning the immune system in a way that slows or alters the course of dementia.
  • #60 Shingles vaccine may directly guard against dementia, study hints | Live Science
    https://www.livescience.com/health/alzheimers-dementia/shingles-vaccine-may-directly-guard-against-dementia-study-hints
    The shingles vaccine helps prevent reactivation of the virus that causes chickenpox. The chickenpox virus remains in the body after an initial infection and can later cause shingles. […] The shingles vaccine helps to build immunity and prevent reactivation of the virus, and it’s thus highly effective at preventing shingles and its complications, such as long-term nerve pain, vision loss and a higher risk of bacterial skin infections. […] More studies are needed to understand the mechanism behind the vaccine’s protective effect against dementia, as that’s currently unclear. One theory suggests that reactivation of the varicella-zoster virus may trigger brain damage through a range of mechanisms, including the buildup of abnormal proteins and chronic inflammation. By preventing reactivation, the shingles vaccine may theoretically prevent this brain damage. […] Another hypothesis is that the vaccine provides protection not by targeting viruses directly but by tuning the immune system in a way that slows or alters the course of dementia.
  • #61
    https://link.springer.com/article/10.1007/s12250-014-3516-9
    Varicella zoster virus (VZV) is the causative agent of varicella (chicken pox) and herpes zoster (shingles). After primary infection, the virus remains latent in sensory ganglia, and reactivates upon weakening of the cellular immune system due to various conditions, erupting from sensory neurons and infecting the corresponding skin tissue. The current varicella vaccine (v-Oka) is highly attenuated in the skin, yet retains its neurovirulence and may reactivate and damage sensory neurons. […] The development of a genetically-defined live-attenuated VZV vaccine that prevents neuronal and latent infection, in addition to primary varicella, is imperative for eventual eradication of VZV, and, if fully understood, has vast implications for many related herpesviruses and other viruses with similar pathogenic mechanisms.