Molluscum contagiosum
Patofizjologia i mechanizm

Molluscum contagiosum (MCV) to przewlekła, zlokalizowana infekcja skóry wywołana przez dwuniciowy wirus DNA z rodziny Poxviridae, który zakaża keratynocyty naskórka, powodując charakterystyczne, perłowobiałe guzki o średnicy 2-5 mm z centralnym pępkowatym zagłębieniem. Wirus replikuje się w cytoplazmie komórek, tworząc tzw. „fabryki wirusowe” w warstwach kolczystej i ziarnistej naskórka, gdzie powstają charakterystyczne ciałka Hendersona-Patersona – eozynofilne inkluzje cytoplazmatyczne zawierające wiriony. MCV unika odpowiedzi immunologicznej gospodarza poprzez produkcję białek hamujących aktywację NF-κB, interferujących z cytokinami prozapalnymi (np. IL-18) oraz blokujących apoptozę, co sprzyja utrzymaniu zmian skórnych. Okres inkubacji wynosi od 2 do 7 tygodni, a u osób immunokompetentnych zmiany ustępują samoistnie w ciągu 6-18 miesięcy, choć mogą utrzymywać się do 4 lat. U pacjentów z obniżoną odpornością (np. HIV, immunosupresja) infekcja może być rozległa, przewlekła i trudna do leczenia.

Patogeneza Molluscum contagiosum

Molluscum contagiosum to choroba skóry wywołana przez wirusa z rodziny pokswirusów (Poxviridae), nazywanego wirusem mięczaka zakaźnego (molluscum contagiosum virus, MCV). Jest to dwuniciowy wirus DNA, który zakaża wyłącznie keratynocyty naskórka i powoduje charakterystyczne zmiany skórne12. MCV powoduje przewlekłe, zlokalizowane zakażenie, ograniczone do naskórka, bez rozsiewu ogólnoustrojowego1.

Mechanizm zakażenia

Wirus mięczaka zakaźnego wnika do organizmu poprzez uszkodzenia naskórka. Po kontakcie z zakażoną osobą lub zakażonymi przedmiotami, wniknięcie wirusa jest ułatwione przez powierzchowne uszkodzenia naskórka1. W przypadku osób z atopowym zapaleniem skóry, które mają suchą i popękaną skórę, wirus łatwiej wnika do organizmu23.

Po wniknięciu do naskórka, MCV zakaża najpierw warstwę podstawną. Chociaż cząsteczki wirusowe są obecne w warstwie podstawnej, replikacja DNA wirusa i powstawanie nowych cząsteczek wirusowych nie następują, dopóki nie zostaną zaangażowane warstwy kolczysta i ziarnista naskórka1. Okres inkubacji wynosi zazwyczaj od 2 do 7 tygodni, ale może trwać nawet do 6 miesięcy12.

Replikacja wirusa w komórce

Podobnie jak inne pokswirusy, MCV replikuje się całkowicie w cytoplazmie komórki gospodarza, co jest unikatową cechą pokswirusów, ponieważ wszystkie inne wirusy DNA namnażają się w jądrze komórkowym1. Wirus tworzy w cytoplazmie tzw. „fabryki wirusowe”, gdzie zachodzi replikacja DNA, transkrypcja i translacja2.

Zakażenie wirusem powoduje hiperplazję i hipertrofię naskórka. Swobodne rdzenie wirusowe znajdują się we wszystkich warstwach naskórka. Tak zwane fabryki wirusowe są zlokalizowane w warstwach kolczystej i ziarnistej1. Komórki w centrum zmiany wykazują największe zniekształcenie i ostatecznie ulegają zniszczeniu, tworząc duże ciałka hialinowe (ciałka mięczaka, ciałka Hendersona-Patersona) zawierające cytoplazmatyczne masy materiału wirusowego2.

W zakażonych komórkach MCV powoduje powstawanie charakterystycznych ciałek mięczakowych (ciałek Hendersona-Patersona), które są eozynofilnymi, ziarnistymi, wewnątrzcytoplazmatycznymi inkluzjami wypychającymi jądro komórkowe na obwód12. Ciałka mięczakowe zawierają duże ilości dojrzewających wirionów, które są zawarte wewnątrzkomórkowo w bogatej w kolagen i lipidy strukturze workopodobnej, co ma na celu utrudnienie rozpoznania immunologicznego przez gospodarza1.

Zmiany histopatologiczne

Po zakażeniu, proliferacja komórkowa wytwarza płatowe (lobulated) rozrosty naskórka, które uciskają brodawki skórne, podczas gdy włókniste przegrody między płatami tworzą gruszkowate skupiska z wierzchołkiem skierowanym do góry. Warstwa podstawna pozostaje nienaruszona1.

Histologicznie, mięczak zakaźny charakteryzuje się obecnością ciałek mięczakowych w naskórku, powyżej warstwy podstawnej. Składają się one z komórek z obfitymi dużymi ziarnistymi eozynofilnymi cytoplazmatycznymi ciałkami inkluzyjnymi (nagromadzonymi wirionami) i małym jądrem, które zostało przesunięte na obwód1.

Każda pojedyncza zmiana wykazuje hiperplazję naskórka składającą się z wielu płatów, które są podzielone na płaciki zawierające ciałka mięczakowe. Wewnątrzcytoplazmatyczne ciałka inkluzyjne mięczaka zwiększają swoją liczbę i rozmiar w miarę różnicowania się komórek w kierunku powierzchni naskórka, gromadząc się w centralnym punkcie spotkania, odpowiadającym klinicznemu objawowi pępkowania, w którym zakażone komórki ulegają rozpadowi cytotoksycznemu, uwalniając swoją zawartość wirusową na powierzchnię skóry1.

Centralne pępkowanie reprezentuje miejsce przyszłej inwolucji, które zawiera końcową fazę wzrostu zainfekowanych komórek naskórka, gdzie kończy się ona procesem śmierci komórkowej i rozpadu, uwalniając swoją zawartość wirusową na powierzchnię skóry w kraterowym otworze zwanym punktum1.

Mechanizmy unikania odpowiedzi immunologicznej

MCV produkuje białka hamujące ludzką odporność przeciwwirusową, zapobiegając rozwojowi odpowiedzi odporności wrodzonej i przyczyniając się do utrzymywania się zmian skórnych1. Genom MCV zawiera specyficzne geny kodujące białka odpowiedzialne za unikanie rozpoznania przez układ immunologiczny gospodarza1.

Zidentyfikowano kilka kluczowych białek wirusowych zaangażowanych w unikanie odpowiedzi immunologicznej:

  • MC007 – sekwestruje białko retinoblastoma (pRb) na błonie mitochondrialnej, inaktywując je1
  • MC054L – wiąże interleukinę 18, blokując jej dwa miejsca wiązania23
  • MC066 – homolog ludzkiej peroksydazy glutationowej34
  • MC132 – oddziałuje z podjednostką p65 NF-κB i powoduje degradację p6545
  • MC148 – działa jak białko podobne do chemokiny i wypiera rzeczywiste chemokiny z ich receptorów sprzężonych z białkiem G56
  • MC159 – hamuje aktywację NF-κB indukowaną przez TNF-R167
  • MC160 – wiąże białko szoku cieplnego 90, uniemożliwiając stabilizację kinazy I Kappa (IKK)7
  • MC005 – hamuje aktywację kompleksu IKK, wiążąc się z aktywną podjednostką NEMO1
  • MC80R – homolog głównego kompleksu zgodności tkankowej (MHC) klasy I, zakłóca prezentację przez gospodarza peptydów specyficznych dla MCV i hamuje cytotoksyczność komórkową zainfekowanych komórek89

Te białka wirusowe łącznie wpływają na czynnik jądrowy kappa B (NF-κB), który jest kompleksem białkowym obecnym w komórkach dendrytycznych regulującym transkrypcję DNA i ułatwiającym syntezę cytokin prozapalnych (TNF, IL-1, IL-6 i innych) oraz aktywację wrodzonej i nabytej odpowiedzi immunologicznej1.

Ponadto, MC159 oddziałuje z Fas (CD95; członek rodziny receptorów czynnika martwicy nowotworów), czynnikiem martwicy nowotworów (TNF) i ligandem indukującym apoptozę związanym z TNF (TRAIL), aby hamować apoptozę1.

Przebieg infekcji i samoograniczenie

Interesujące jest to, że naciek zapalny nie jest obserwowany aż do chwili poprzedzającej naturalne ustąpienie zmiany1. U osób immunokompetentnych zakażenie ustępuje samoistnie w ciągu 6-18 miesięcy, czasami utrzymując się do 4 lat1.

Ustępujące zmiany mogą towarzyszyć lokalnej reakcji zapalnej (łagodny rumień, podrażnienie), co wskazuje na aktywną odpowiedź immunologiczną komórkową (kliniczny objaw powrotu do zdrowia)1. Nagłe zniknięcie zmian jest konsekwencją silnej odpowiedzi immunologicznej u zdrowych osób2.

Zakażenie MCV powoduje niewielką immunogenność, ponieważ rzadko indukuje tworzenie przeciwciał. Specyficzne przeciwciała zostały znalezione u około 80% pacjentów i u około 15% osób z grupy kontrolnej. Rola odporności humoralnej w cofaniu się zmian nie jest ustalona. Powtórne zakażenie jest częste1.

Czynniki ryzyka i przebieg u osób z immunosupresją

Czynniki ryzyka zakażenia MCV obejmują osłabiony układ odpornościowy, atopowe zapalenie skóry i zatłoczone warunki życia1. Molekularne mechanizmy patogenezy zwiększają podatność na zakażenie u osób z atopowym zapaleniem skóry oraz u osób z zaburzeniami odporności, szczególnie tych, które są predysponowane do przełączania cytokin Th2, jak w przypadku atopowego zapalenia skóry i choroby HIV-11.

U pacjentów z obniżoną odpornością (np. z powodu niekontrolowanego zakażenia HIV, stosowania kortykosteroidów lub chemioterapii) może rozwinąć się bardziej rozległe zakażenie1. U osób z poważnym niedoborem odporności choroba jest przewlekła i wytwarza duże, uogólnione, zlewające się i zniekształcające zmiany, które są trudne do leczenia, o ile nie zostanie przywrócona normalna funkcja immunologiczna1.

Drogi transmisji mięczaka zakaźnego

Wirus mięczaka zakaźnego szerzy się poprzez bezpośredni kontakt skóry z zakażoną osobą oraz poprzez kontakt z zakażonymi przedmiotami1. Transmisja wirusa mięczaka zakaźnego może następować na kilka sposobów:

Kontakt bezpośredni

  • Kontakt skóra-skóra – bezpośredni kontakt z osobą zakażoną jest główną drogą transmisji12
  • Kontakt seksualny – u nastolatków i dorosłych wirus jest najczęściej przenoszony drogą kontaktów seksualnych12
  • Autoinokulacja – dotykanie, drapanie lub wyskubywanie guzków mięczaka na skórze, a następnie dotykanie obszaru bez mięczaka12

Kontakt pośredni

  • Przedmioty zanieczyszczone wirusem – ręczniki, ubrania, zabawki lub inne przedmioty używane przez osobę zakażoną1
  • Środowisko wodne – transmisja wydaje się występować częściej w wilgotnych środowiskach, jak podczas wspólnych lekcji pływania dla dzieci12

Zakażenie mięczakiem zakaźnym może być również przekazywane drogą wertykalną podczas porodu, co prowadzi do wystąpienia zmian w okresie noworodkowym1.

Czynniki sprzyjające transmisji

Mięczak zakaźny występuje częściej w ciepłym, wilgotnym klimacie oraz wśród dzieci, które pływają1. Ponieważ MCV wnika do organizmu przez uszkodzenia skóry, jest bardziej rozpowszechniony u pacjentów z atopowym zapaleniem skóry, suchą skórą lub jakimkolwiek przerwaniem integralności strukturalnej bariery skórnej1.

Dokładny czas, w którym pacjent jest zakaźny, nie jest znany, ale badania sugerują, że osoba może być zakaźna i rozprzestrzeniać wirusa do momentu, aż guzki znikną z jej skóry1.

Mechanizmy molekularne zakażenia MCV

Genom wirusa i jego ekspresja

MCV jest wirusem DNA należącym do rodziny Poxviridae, podrodziny Chordopoxvirinae1. Podobnie jak inne pokswirusy, MCV jest wirusem DNA, który replikuje się w cytoplazmie zamiast w jądrze. Z tego powodu wirus musi przynieść ze sobą wszystkie niezbędne enzymy do replikacji lub kodować te enzymy w swoim genomie1.

Genom MCV-1 został całkowicie zsekwencjonowany i zidentyfikowano kilka nowatorskich produktów genowych zaangażowanych w jego patogenezę i unikanie układu odpornościowego gospodarza: MC54L, MC148, MC013L, MC159 i peroksydazę glutationową1.

Replikacja i zdolność infekcyjna

Wirus mięczaka zakaźnego, podobnie jak wszystkie pokswirusy, produkuje dwa zakaźne cząsteczki: dojrzałe wiriony (MV) i wiriony pozakomórkowe (EV), przy czym EV różnią się od MV tym, że posiadają dodatkową błonę komórkową1.

Każdy wirion tworzy w cytoplazmie region zwany „fabryką wirusową”, gdzie sekwencyjnie zachodzi replikacja DNA, transkrypcja i translacja1. W zakażonych komórkach wirus MCV powoduje powstawanie charakterystycznych ciałek mięczakowych, które są eozynofilnymi, ziarnistymi, wewnątrzcytoplazmatycznymi inkluzjami wypychającymi jądro komórkowe na obwód1.

Molekularne interakcje z komórką gospodarza

MCV koduje homolog ciężkiego łańcucha głównego kompleksu zgodności tkankowej (MHC) I, któremu brakuje zachowanych aminokwasów istotnych dla wiązania peptydów1. Białko MC80 zaburza prezentację antygenu MHC-I w komórkach ludzkich i mysich1.

Ekspresja MC80 prowadzi do retencji w siateczce śródplazmatycznej (ER) i w konsekwencji zmniejszonej ekspresji powierzchniowej klasycznego MHC-I w komórkach ludzkich i mysich1. Mechanistycznie, MC80 oddziałuje z tapasyną za pośrednictwem swojej domeny luminalnej i kieruje ją do degradacji związanej z siateczką śródplazmatyczną w sposób zależny od regionu transbłonowego (TM) i ogona cytoplazmatycznego1.

Utrata tapasyny zbiega się z utratą TAP, co dodatkowo utrudnia gromadzenie się MHC-I z peptydami o wysokim powinowactwie1.

Wpływ na cykl komórkowy i apoptozę

Białko MC007 sekwestruje białko retinoblastoma (pRb) na błonie mitochondrialnej, inaktywując je1. MC148 promuje replikację wirusową, zapobiegając różnicowaniu się zakażonych keratynocytów1.

MC159 oddziałuje z Fas (CD95; członek rodziny receptorów czynnika martwicy nowotworów), czynnikiem martwicy nowotworów (TNF) i ligandem indukującym apoptozę związanym z TNF (TRAIL), aby hamować apoptozę1.

Molekularne mechanizmy unikania odpowiedzi immunologicznej

MCV wykorzystuje kilka różnych metod, aby uniknąć wykrycia przez ludzki układ odpornościowy1. Białka wirusowe zakłócają aktywację czynnika jądrowego kappa B (NF-κB), który jest kluczowym regulatorem odpowiedzi immunologicznej1.

MC054L zapobiega zapaleniu, wiążąc się z prozapalną cytokiną ludzką interleukiną-181. MC148 działa jak białko podobne do chemokiny i wypiera rzeczywiste chemokiny z ich receptorów sprzężonych z białkiem G1.

MC132 oddziałuje z podjednostką p65 NF-κB i powoduje degradację p651. MC160 wiąże białko szoku cieplnego 90, uniemożliwiając stabilizację kinazy I Kappa (IKK)2.

Ponadto, zakażone komórki wykazują ekspresję peroksydazy glutationowej, aby zapobiec uszkodzeniom oksydacyjnym wywołanym przez leukocyty1.

Przebieg kliniczny zakażenia

Objawy kliniczne

Mięczak zakaźny objawia się małymi, wyniosłymi guzkami (brodawkami) na skórze, które mogą być różowe, perłowobiałe lub przeźroczyste, kopulaste, o gładkiej powierzchni, o średnicy 2-5 mm, z charakterystycznym pępkowatym zagłębieniem w środku12.

Guzki mięczaka pojawiają się zwykle 2-8 tygodni po zakażeniu wirusem1. Typowo, każdy guzek (mięczak) utrzymuje się przez kilka tygodni lub miesięcy, pokrywa się strupem, a następnie znika1.

Jednak nowe guzki mają tendencję do pojawiania się, gdy stare znikają, ponieważ wirus rozprzestrzenia się na inne obszary skóry. Dlatego grupy mięczaków mogą wydawać się pojawiać i znikać przez kilka miesięcy2.

Przebieg naturalny i samoograniczenie

U osób immunokompetentnych zakażenie ustępuje samoistnie w ciągu 6-18 miesięcy, czasami utrzymując się do 4 lat12. Bez leczenia, guzki mięczaka zazwyczaj znikają w ciągu 6 miesięcy do 2 lat1.

Ustępujące zmiany mogą towarzyszyć lokalnej reakcji zapalnej (łagodny rumień, podrażnienie), co wskazuje na aktywną odpowiedź immunologiczną komórkową (kliniczny objaw powrotu do zdrowia)1. Ten objaw jest nazywany objawem BOTE (beginning of the end), czyli początkiem końca1.

Po epizodzie mięczaka zakaźnego, osoby są zwykle odporne na wirusa, co oznacza, że jest bardzo mało prawdopodobne, aby choroba powróciła1.

Powikłania

Najczęstszym powikłaniem mięczaka zakaźnego jest wtórne zakażenie bakteryjne, jeśli guzki są drapane lub uszkodzone12. Takie wtórne zakażenia mogą powodować poważne problemy zdrowotne u osób z obniżoną odpornością, takich jak osoby z HIV lub AIDS, lub osoby przyjmujące leki immunosupresyjne1.

Autoinokulacja, wtórne zakażenie bakteryjne (szczególnie jeśli zmiany są drapane) i powstawanie blizn mogą powikłać przebieg choroby1.

Przebieg u osób z immunosupresją

U pacjentów z obniżoną odpornością (np. z powodu niekontrolowanego zakażenia HIV, stosowania kortykosteroidów lub chemioterapii) może rozwinąć się bardziej rozległe zakażenie1.

U osób z poważnym niedoborem odporności choroba jest przewlekła i wytwarza duże, uogólnione, zlewające się i zniekształcające zmiany, które są trudne do leczenia, o ile nie zostanie przywrócona normalna funkcja immunologiczna1.

U pacjentów z HIV mięczak zakaźny może nie ustąpić samoistnie bez leczenia1. Terapia antyretrowirusowa (ARV) jest głównym leczeniem u pacjentów z HIV12.

Rozległe i utrzymujące się zakażenie skóry wirusem mięczaka zakaźnego może wskazywać na podstawowy niedobór odporności1.

Specyficzne aspekty zakażenia u dzieci i dorosłych

Mięczak zakaźny jest częstą infekcją u dzieci i młodych dorosłych, najczęściej występuje u dzieci w wieku 1-4 lat1. U dzieci zakażenie jest zwykle nabywane poprzez bezpośredni kontakt skóra-skóra, natomiast u dorosłych często poprzez kontakt seksualny1.

U nastolatków i dorosłych, zmiany częściej występują w okolicy narządów płciowych1. W przypadku zakażeń okołopłciowych u dzieci należy rozważyć możliwość molestowania seksualnego1.

U pacjentów z HIV większość zmian mięczaka zakaźnego znajduje się na twarzy i szyi1.

Nowe perspektywy w leczeniu

Leczenie oparte na patogenezie

Zrozumienie mechanizmów molekularnych patogenezy mięczaka zakaźnego prowadzi do opracowania nowych podejść terapeutycznych1.

Leczenie mięczaka zakaźnego może obejmować metody destrukcyjne (np. łyżeczkowanie, krioterapię, terapię laserową, elektrokoagulację) lub środki miejscowe (np. kwas trichlorooctowy, kantarydyna, tretynoina, tazaroten, podofilotoksyna, berdazimer)1.

Inne metody leczenia obejmują wstrzyknięcie antygenu Candida do guzka i terapię fotodynamiczną1. Antygeny Candida to białka pochodzące z drożdży Candida. Po wstrzyknięciu do guzka wywołują odpowiedź immunologiczną, która zwalcza wirusa1.

Innowacyjne terapie

Zelsuvmi (natrowy) to lek do stosowania miejscowego zaprojektowany do leczenia mięczaka zakaźnego. Sformułowany z 10,3% NO, żel wykorzystuje innowacyjną platformę NITRICIL™ firmy Novan do uwalniania NO w miejscu aplikacji poprzez duże polimery. Zelsuvmi to substancja polimeryczna, która posiada szkielet polisiloksanowy i kowalencyjnie związane donory NO N-diazeniumdiolatu1.

Zelsuvmi jest immunomodulatorem, co oznacza, że może regulować odpowiedź układu odpornościowego na zakażenia, a także wykazuje szerokie spektrum działania przeciwdrobnoustrojowego i przeciwwirusowego, prawdopodobnie z powodu S-nitrozylacji białek i cytotoksyczności dla replikacji wirusowej z reaktywnych form tlenu, co czyni go skutecznym leczeniem szerokiego zakresu zakażeń1.

Zelsuvmi skutecznie zmniejsza ładunek wirusowy pokswirusów i hamuje ekspresję białka immunomodulacyjnego MC160 mięczaka zakaźnego, bezpośrednio atakując wiriony MC. Sugeruje to, że przeciwwirusowe działanie Zelsuvmi wynika z jego bezpośredniego działania na sam wirus, a nie na układ odpornościowy gospodarza1.

Nowe kierunki badań

Lepsze zrozumienie dokładnej patogenezy mięczaka zakaźnego było utrudnione z powodu braku możliwości replikacji wirusa w hodowlach tkankowych (z powodu defektu w ekspresji genomu), a także braku odpowiednich modeli zwierzęcych1.

Dalsze badania nad unikalnymi cechami zakażenia wirusem mięczaka zakaźnego mogą dać fundamentalny wgląd w naturę odporności skóry1.

Postępy w badaniach stwarzają perspektywę nowych podejść do leczenia opartych na biologii wirusa1.

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  1. 10.04.2026
  2. www.leksykon.com.pl

Materiały źródłowe

  • #1 Molluscum Contagiosum – StatPearls – NCBI Bookshelf
    https://www.ncbi.nlm.nih.gov/books/NBK441898/
    Molluscum contagiosum is caused by a double-stranded DNA poxvirus called molluscum contagiosum virus (MCV). […] Molluscum contagiosum virus infects only keratinocytes, and skin lesions are limited to the epidermis and do not have systemic dissemination. […] Molluscum contagiosum virus produces proteins inhibiting human antiviral immunity, thus preventing the development of innate immunity response, and contributing to the persistence of skin lesions.
  • #1 Azthena logo with the word Azthena
    https://www.news-medical.net/health/What-is-Molluscum-Contagiosum.aspx
    After direct skin contact with an infected individual, viral entrance is facilitated by superficial damage to the epithelium. […] The molluscum contagiosum virus encodes specific molecules that are used to control host defenses by utilizing several different methods to evade detection by the human immune system. […] Better insights in the exact pathogenesis of molluscum contagiosum have been hindered by the lack of ability to replicate the virus in tissue cultures (due to a defect in the genome expression), as well as the absence of appropriate animal models.
  • #1 Molluscum Contagiosum: Background, Etiology, Epidemiology
    https://emedicine.medscape.com/article/910570-overview
    Molluscum contagiosum virus is an unclassified member of the Poxviridae family. It cannot be grown in tissue culture or eggs; it has been grown in human foreskin grafted to athymic mice but has not been transmitted to other laboratory animals. […] The molluscum contagiosum virus replicates in the cytoplasm of epithelial cells, producing cytoplasmic inclusions and enlargement of infected cells. This virus infects only the epidermis. Infection follows contact with infected persons or contaminated objects, but the extent of necessary epidermal injury is unknown. The initial infection seems to occur in the basal layer, and the incubation period is usually 2-7 weeks. This is suggested by the fact that, although viral particles are noted in the basal layer, viral deoxyribonucleic acid (DNA) replication and the formation of new viral particles do not occur until the spindle and granular layers of the epidermis are involved. Infection may be accompanied by a latent period of as long as 6 months.
  • #1 Molluscum contagiosum virus – Wikipedia
    https://en.wikipedia.org/wiki/Molluscum_contagiosum_virus
    Molluscum contagiosum virus (MCV) is a species of DNA poxvirus that causes the human skin infection molluscum contagiosum. […] MCV is a member of the subfamily Chordopoxvirinae of family Poxviridae. […] Like other poxviruses, MCV is a DNA virus that replicates in the cytoplasm instead of the nucleus. Because of this, the virus must bring all necessary enzymes for replication with it or encode the enzymes in its genome. […] Molluscum contagiosum virus, similar to all poxviruses, produces two infectious particles: mature virions (MV) and extracellular virions (EV), with the EV differing from the MV in that they possess an extra cellular membrane. […] Molluscum contagiosum virus, like other poxviruses, replicates entirely in the cytoplasm of the host cell. This is a property unique to poxviruses, as all other DNA viruses replicate in the nucleus.
  • #1 Molluscum contagiosum
    https://escholarship.org/uc/item/6z11d13p
    Molluscum contagiosum is a disease caused by a poxvirus of the Molluscipox virus genus that produces a benign self-limited papular eruption of multiple umbilicated cutaneous tumors. […] This disease is transmitted primarily through direct skin contact with an infected individual. Fomites have been suggested as another source of infection, with molluscum contagiosum reportedly acquired from bath towels, tattoo instruments, and in beauty parlors and Turkish baths. […] Infection with the virus causes hyperplasia and hypertrophy of the epidermis. Free virus cores have been found in all layers of the epidermis. So-called viral factories are located in the malpighian and granular cell layers. […] The molluscum bodies contain large numbers of maturing virions. These are contained intracellularly in a collagen-lipid-rich saclike structure that is thought to deter immunological recognition by the host. […] Rupture and discharge of the infectious virus-packed cells occur in the center of the lesion. MCV induces a benign tumor instead of the usual necrotic pox lesion associated with other poxviruses.
  • #1 Congenital Molluscum Contagiosum | Actas Dermo-Sifiliográficas
    https://www.actasdermo.org/es-congenital-molluscum-contagiosum-articulo-S1578219013002217
    Molluscum contagiosum infection is very common in children and is one of the most frequent reasons for consultation in outpatient and hospital pediatric care. Infection occurs as a result of direct person-to-person contact through infected skin, contact with fomites, or autoinoculation. In adolescence and adulthood, infection may occur through sexual contact. Occurrence during the neonatal period is rare. […] Molluscum contagiosum is caused by a member of the poxvirus family, and manifests clinically as a flesh-colored or translucent, pearl-like papule with an umbilicated center measuring 1 to 5 mm in diameter. The most frequently affected areas are the trunk, the limbs, and the scalp. The diagnosis of this disorder is clinical. A pathology study is performed only occasionally, when the diagnosis is uncertain. Histology reveals a well-defined hyperplastic lesion of the epidermis sometimes with a central crater, and, commonly, eosinophilic inclusion bodies within the keratinocytes that later become basophilic inclusion bodies as they rise in the epithelium.
  • #1 Molluscum Contagiosum: Background, Etiology, Epidemiology
    https://emedicine.medscape.com/article/910570-overview
    Following infection, cellular proliferation produces lobulated epidermal growths that compress epidermal papillae, while fibrous septa between the lobules produce pear-shaped clumps with the apex upwards. The basal layer remains intact. […] Cells at the core of the lesion show the greatest distortion and are ultimately destroyed, resulting in large hyaline bodies (ie, molluscum bodies, Henderson-Paterson bodies) containing cytoplasmic masses of virus material. These bodies are present in large numbers and appear as a white depression at the center of fully developed lesions. […] As with other poxviruses, molluscum contagiosum virus does not appear to develop latency but evades the immune system through the production of virus-specific proteins. Cell-mediated immunity is most important in modulating and controlling the infection. […] The virus is not strongly immunogenic, as it infrequently induces antibody formation. Specific antibodies have been found in approximately 80% of patients and in about 15% of control subjects. A role for humoral immunity in regression of lesions is not established. Reinfection is common.
  • #1 Molluscum contagiosum – Wikipedia
    https://en.wikipedia.org/wiki/Molluscum_contagiosum
    The infection is caused by a poxvirus called the molluscum contagiosum virus (MCV). The virus is spread either by direct contact, including sexual activity, or via contaminated objects such as towels. […] Risk factors include a weak immune system, atopic dermatitis, and crowded living conditions. […] Histologically, molluscum contagiosum is characterized by molluscum bodies (also known as Henderson-Patterson bodies) in the epidermis, above the stratum basale, which consist of cells with abundant large granular eosinophilic cytoplasmic inclusion bodies (accumulated virions) and a small nucleus that has been pushed to the periphery. […] The viral infection is limited to a localized area on the topmost layer of the superficial layer of the skin.
  • #1 Pathogenesis of Molluscum Contagiosum&58; A new concept for the s…: Ingenta Connect
    https://www.ingentaconnect.com/content/10.7241/ourd.20153.72
    Molluscum contagiosum is a common viral skin disease that usually has a self-clearing course. […] to study the process of involution of molluscum contagiosum through utilizing histological examination. […] Each individual lesion showed an epidermal hyperplasia consisting of many lobes which subdivided into lobules that contain the molluscum bodies. The intra-cytoplasmic molluscum inclusion bodies increase in the number and size as the cells differentiate toward the surface of the epidermis to accumulate at a central meeting point equivalent to the clinical sign of umblication at which the infected cells undergo cytocidal disintegration releasing its viral contents into the skin surface. […] The central umblication represent the site of the future involution that contains the final growth phase of the infected epidermal cells where it ends by a process of cellular death and disintegration releasing its viral contents into the surface of the skin at the craterform opening which is called punctum. This process of self-involution may resemble that of keratoacanthoma where there are many similar pathological features in both conditions.
  • #1 Update on Clinical Management of Cutaneous Molluscum Contagiosum
    https://www.skintherapyletter.com/dermatology/molluscum-contagiosum/
    Molluscum contagiosum is a poxvirus infection of the skin that is commonly observed in children. The molluscum contagiosum virus (MCV) expresses several gene-products that are involved in its pathogenesis and evasion of the host immune system. […] The genome of MCV-1 has been completely sequenced and several novel gene products involved in its pathogenesis and evasion of the immune system have been identified: MC54L, MC148, MC013L, MC159, and glutathione peroxidase. […] The protein MC54L prevents inflammation by binding the pro-inflammatory cytokine human interleukin-18. MC148 promotes viral replication by preventing infected keratinocytes from differentiating. MC159 interacts with Fas (CD95; a member of the tumor necrosis factor receptor family), tumor necrosis factor (TNF), and TNF-related apoptosis-inducing ligand (TRAIL) to inhibit apoptosis. MC80R, a major histocompatibility complex (MHC) class I homolog, interferes with the host presentation of peptides specific to MCV and inhibits cell-mediated cytotoxicity of infected cells. Finally, infected cells express glutathione peroxidase to prevent leukocyte-mediated oxidative damage. Together, these viral gene products are able to maintain active infection until the host immune system gradually prevails.
  • #1 Molluscum contagiosum virus – Wikipedia
    https://en.wikipedia.org/wiki/Molluscum_contagiosum_virus
    Each virion sets up a region in the cytoplasm, called a 'viral factory’ where DNA replication, transcription, and translation all occur sequentially. […] The MC007 protein sequesters retinoblastoma protein (pRb) on the mitochondria membrane, inactivating it. […] The MC054 long protein binds Interleukin 18 which blocks its two binding sites. […] The MC066 protein is homologous to human glutathione peroxidase. […] The MC132 protein interacts with the NF-B subunit p65 and causes p65 degradation. […] The MC148 protein acts like a chemokine-like protein and displaces actual chemokines from their G-protein coupled receptors. […] The MC159 protein inhibits TNF-R1 induced NF-B activation. […] The MC160 protein binds heat shock protein 90, keeping it from stabilizing I Kappa Kinase (IKK).
  • #1 Molluscum contagiosum: an update and review of new perspectives in etiology, diagnosis, and treatment
    https://pmc.ncbi.nlm.nih.gov/articles/PMC6553952/
    Brady et al have seen that MC132 and MC005 proteins would alter the activation of NF-kB by inhibiting pattern recognition receptors (PRRs). […] Added to this, MC132 would bind and stimulate the degradation of the p65 subunit of NF-kB and MC005 would inhibit the activation of the IKK complex (IkB kinase) binding to active NEMO subunit (essential modulator of NF-kB).
  • #1 Molluscum contagiosum: an update and review of new perspectives in etiology, diagnosis, and treatment
    https://pmc.ncbi.nlm.nih.gov/articles/PMC6553952/
    Molluscum contagiosum (MC) is caused by molluscum contagiosum virus (MCV), a double-strand DNA virus which belongs to the Poxviridae family; humans are MCV only host. […] MCV infects the epidermis and replicates in the cytoplasm of cells with a variable incubation period between two and six weeks. […] Different studies have been developed to sequence the genome of this virus and determine possible genes involved in the evasion of the host immune response, a hypothesis that arose based on the absence of inflammation observed in histopathological samples of infected skin. […] To date, four viral genes have been identified that code proteins that would alter the activation of the nuclear factor kB (NF-kB): MC159, MC160, MC132, and MC005. […] NF-kB is a nuclear protein complex present in dendritic cells that regulate the transcription of DNA and facilitate the synthesis of pro-inflammatory cytokines (TNF, IL-1, IL-6, among others) and activation of innate and acquired immune response.
  • #1 Update on Clinical Management of Cutaneous Molluscum Contagiosum
    https://www.skintherapyletter.com/dermatology/molluscum-contagiosum/
    MCV likely enters the skin through small abrasions; this explains why eczema-prone and atopic individuals, who typically scratch inflamed areas on their skin, are more susceptible. Once MCV has penetrated the lower layers of the epidermis it begins to replicate, extending upwards, in the lower layers of the epidermis. The estimated incubation period varies from 14 days to 6 months. When active infection commences, the epidermis hypertrophies, extending into the underlying dermis, and characteristic molluscum bodies (also known as Henderson-Paterson bodies) form inside cells of the stratum spinosum. As infection progresses, the molluscum bodies enlarge, causing the spinosa cells to migrate upwards while hyperplasia of the basal cell layer simultaneously replaces the migrating spinosa cells. […] Interestingly, an inflammatory infiltrate is not observed until shortly before natural resolution of the lesion.
  • #1 Molluscum Contagiosum – Viral Diseases – Infectious Diseases – Diseases – McMaster Textbook of Internal Medicine
    https://empendium.com/mcmtextbook/chapter/B31.II.18.1.11.
    Molluscum contagiosum is a chronic inflammatory viral skin disease that causes characteristic papular epidermal lesions. […] The etiologic agent is the Molluscum contagiosum virus (MCV), which replicates exclusively in squamous epithelial cells, does not spread into the deeper layers of skin, and does not cause viremia. […] Autoinoculation is frequent; this causes the lesions to spread to unaffected areas and leads to the persistent course of the disease. […] In immunocompetent individuals, the infection resolves spontaneously over 6 to 18 months, occasionally persisting for up to 4 years. […] Receding lesions may be accompanied by a local inflammatory reaction (mild erythema, irritation), which indicates an active cell-mediated immune response (the clinical manifestation of recovery).
  • #1
    https://link.springer.com/article/10.2165/00128071-200203080-00004
    MCV also encodes a major histocompatibility complex (MHC) Ilike heavy chain homolog that lacks conserved amino acids important for peptide binding. […] Other mechanisms by which MCV evades host mechanisms for killing virally infected cells, include its viral FLICE-like inhibitory protein (FLIP) and a selenocysteine-containing glutathione peroxidase. […] The combined effects of Th1 cytokine switching, along with increased antigen presentation, may be particularly helpful in patients with underlying immune deficits, especially those that are predisposed to a Th2 cytokine switching pattern as is seen in atopic dermatitis and HIV-1 disease. […] MCV is a poxvirus that exists worldwide and causes disease almost exclusively limited to the skin. Although MCV does not develop latency, it has many mechanisms to evade and subvert the immune responses of the host.
  • #1 Molluscum Contagiosum – Dermatologic Disorders – Merck Manual Professional Edition
    https://www.merckmanuals.com/professional/dermatologic-disorders/viral-skin-diseases/molluscum-contagiosum
    Molluscum contagiosum is characterized by clusters of pink, dome-shaped, smooth, waxy, or pearly and umbilicated papules 2 to 5 mm in diameter caused by the molluscum contagiosum virus, a poxvirus. […] Molluscum contagiosum virus commonly causes a localized chronic infection. […] Immunocompromised patients (eg, due to HIV/late-stage HIV, corticosteroid use, or chemotherapy) may develop a more widespread infection (1, 2). […] The latter suggests that the etiology may be sexually transmitted. […] Diagnosis of molluscum contagiosum is usually based on clinical appearance. […] Treatments can include destructive methods (eg, curettage, cryosurgery, laser therapy, electrocautery) or topical agents (eg, trichloroacetic acid, cantharidin, tretinoin, tazarotene, podophyllotoxin, berdazimer).
  • #1 Molluscum Contagiosum – Viral Diseases – Infectious Diseases – Diseases – McMaster Textbook of Internal Medicine
    https://empendium.com/mcmtextbook/chapter/B31.II.18.1.11.
    Autoinoculation, secondary bacterial infection (in particular if the lesions are being scratched), and scarring may complicate the course of the disease. […] Invasive treatment (according to authors of the Cochrane review, the evidence for effectiveness of physical destruction of molluscum is very limited and, until this changes, awaiting spontaneous resolution of molluscum lesions remains a strong option): […] Prognosis: In immunocompetent individuals the lesions resolve spontaneously. In severely immunocompromised patients the disease is protracted and produces giant, generalized, confluent, and disfiguring lesions, which are difficult to treat unless a normal immune function is restored.
  • #1 Molluscum contagiosum – Symptoms & causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/molluscum-contagiosum/symptoms-causes/syc-20375226
    Molluscum contagiosum (mo-LUS-kum kun-tay-jee-OH-sum) is a fairly common skin infection caused by a virus. It causes round, firm, painless bumps ranging in size from a pinhead to a pencil eraser. […] Molluscum contagiosum also spreads through person-to-person contact and contact with infected objects. […] Left untreated, the bumps usually disappear in 6 months to 2 years. […] The virus that causes molluscum contagiosum spreads easily through skin-to-skin contact. […] Scratching or rubbing the bumps, which spreads the virus to nearby skin. […] The bumps and the skin around them may become inflamed. This is thought to be an immune system response to the infection. […] If scratched, these bumps can become infected and heal with scarring.
  • #1 About Molluscum Contagiosum | Molluscum Contagiosum | CDC
    https://www.cdc.gov/molluscum-contagiosum/about/index.html
    Molluscum contagiosum is an infection caused by a poxvirus that causes lesions (growths) that can appear on the body, either alone or in groups. […] The infection is usually mild and goes away without any treatment. […] Molluscum contagiosum causes small, raised bumps called Mollusca, which: […] The sores may be itchy, sore, red, or swollen. […] The most common complication is a bacterial infection if lesions are scratched or broken. […] You can get molluscum if you touch someone who has it. […] If you have molluscum, you can spread it to other areas of your body. […] Healthy people usually recover from molluscum without treatment. […] One exception is if you have sores around your genitals (penis, vulva, vagina, or anus). […] Do not try to remove the sores or the fluid inside them yourself.
  • #1 What Is Molluscum Contagiosum? Symptoms, Causes, Diagnosis, Treatment, and Prevention
    https://www.everydayhealth.com/molluscum-contagiosum/guide/
    Molluscum contagiosum is caused by the molluscum contagiosum virus, a type of poxvirus. Poxviruses are a family of viruses thats responsible for smallpox, among other diseases. […] The virus lives solely in the epidermis, or top layer of skin. Anywhere from two to six weeks after being exposed to the virus, the dome-shaped mollusca begin to form on the skin. […] Molluscum contagiosum thrives in warm, humid environments, so youre more likely to get the condition if you live in a tropical climate. […] Having atopic dermatitis (the most common type of eczema) or a weakened immune system, such as from HIV or AIDS, also increases your risk of getting the condition. […] In teenagers and adults, the virus is most often spread through sexual contact. […] A secondary infection caused by bacteria is the most common complication of molluscum contagiosum. Such secondary infections may cause serious health problems in people who are immunocompromised, such as those with HIV or AIDS, or those taking immunosuppressing drug therapies.
  • #1 Molluscum contagiosum: Who gets and causes
    https://www.aad.org/public/diseases/a-z/molluscum-contagiosum-causes
    A virus called molluscum contagiosum causes this skin infection. […] People catch molluscum contagiosum when they get the virus on their skin. […] Its believed that children who are 1 to 10 years old are most likely to get this skin infection because they have the most skin-to-skin contact. They seem especially vulnerable if they have eczema. The extremely dry, cracked skin of eczema may make it easier for the virus to infect the skin. […] No. The virus that causes molluscum contagiosum stays in the top layer of the skin. […] Because it never gets inside the body, you cannot catch the virus when someone sneezes or coughs. […] You can spread the virus from one part of your body to another by: Touching, scratching, or picking at a molluscum bumps on your skin and then touching an area without molluscum. […] When the virus spreads, you won’t see new bumps right away. The bumps usually appear 2 to 6 weeks later.
  • #1 Molluscum contagiosum: MedlinePlus Medical EncyclopediaLock
    https://medlineplus.gov/ency/article/000826.htm
    Molluscum contagiosum is a viral skin infection that causes raised, pearl-like papules or nodules on the skin. […] Molluscum contagiosum is caused by a virus that is a member of the poxvirus family. […] The virus can spread through contact with contaminated objects, such as towels, clothing, or toys. […] The virus also spreads by sexual contact. […] People with a weakened immune system (due to conditions such as HIV/AIDS) or severe eczema may have a rapidly spreading case of molluscum contagiosum. […] The infection on the skin begins as a small, painless papule, or bump. […] Scratching or other irritation causes the virus to spread in a line or in groups, called crops. […] In people with a healthy immune system, the disorder usually goes away on its own over months to years. […] The disorder may persist in people with a weakened immune system.
  • #1 Molluscum Contagiosum: Causes, Symptoms, and More
    https://www.healthline.com/health/molluscum-contagiosum
    Molluscum contagiosum is a skin infection caused by a virus of the same name. It produces benign, raised bumps, or lesions, on the upper layers of your skin. […] Molluscum contagiosum occurs when you acquire the M. contagiosum virus, a type of poxvirus. […] This virus can transmit between people while lesions are visible. Its also possible to transmit the virus from one area of skin on your own body to another part. […] There are a number of ways that M. contagiosum passes between people, including: Skin contact with a person who carries the infection. You can get molluscum contagiosum by touching the lesions on the skin of a person who has this infection. […] Transmission seems to take place more in wet environments, like during childrens shared swimming classes. […] Antiretroviral therapy (ART) is the most effective treatment for people who live with HIV if they contract molluscum contagiosum. It can help strengthen the immune system and fight the virus.
  • #1 Congenital Molluscum Contagiosum | Actas Dermo-Sifiliográficas
    https://www.actasdermo.org/es-congenital-molluscum-contagiosum-articulo-S1578219013002217
    The authors of the previous cases all agree that the infection may have occurred through vertical transmission during delivery. This same mechanism is behind other viral infections such as those caused by the herpes virus and the human papillomavirus. The human papillomavirus has a long latency period from infection to clinical manifestation, potentially leading to laryngeal papillomatosis or common warts appearing years after infection; the incubation period of molluscum contagiosum, on the other hand, is quite short (2-8 weeks), thus causing the lesions to appear in the neonatal period. […] These histological findings provide firm support for the theory of vertical transmission of the virus during delivery. In the second case, the lesions appeared on the shoulder, a location not described previously. In cases where the mother’s genitals are not identified as infected, transmission probably occurs through undiagnosed vaginal infection, as the poxvirus causing molluscum contagiosum may also affect the mucous membranes. […] It is important to consider congenital molluscum contagiosum as a possible diagnosis in neonatal patients with one or more umbilicated papules.
  • #1 Molluscum Contagiosum: Epidemiology, Considerations, Treatment Options, and Therapeutic Gaps | JCAD – The Journal of Clinical and Aesthetic Dermatology
    https://jcadonline.com/molluscum-contagiosum-epidemiology-considerations-treatment-options/
    Molluscum contagiosum (MC) virus is an unclassified member of the Poxviridae family, encompassing Types I to IV viruses. This virus causes a benign, cutaneous-manifested infection that occurs only in humans. MC papules are produced by a double-stranded DNA virus in humans. After invading the host, MC infects the epidermis and replicates itself in the cytoplasm of cells. The incubation period for the virus is variable and generally ranges from 2 to 6 weeks. Since the MC enters the body through a break in the skin, it is more prevalent in patients with atopic dermatitis, dry skin, or any interrupted structural integrity of the skin barrier. MC is more prevalent in hot, humid climates and among children who go swimming. Currently, it is not clear if MC transmission occurs in water, although the condition has been referred to as water warts. Infectious transmission seems to occur through direct contact with infected skin, by sexual or nonsexual means, or by autoinoculation.
  • #1 Molluscum Contagiosum: What it is, Symptoms & Treatment
    https://my.clevelandclinic.org/health/diseases/12175-molluscum-contagiosum
    Molluscum contagiosum is a skin infection caused by a virus. The molluscum contagiosum virus, which is a virus of the poxvirus family, causes molluscum contagiosum. When this virus enters your body, bumps or spots (papules) appear on your skin. These papules can spread to other areas of your skin and other people (contagious). […] Molluscum contagiosum is an infection caused by a virus. The virus (poxvirus) spreads from person to person through physical contact or contaminated surfaces or objects. This infection begins with a single bump that can spread and increase in number when you itch your skin. […] The exact time that you’re contagious is unknown, but studies suggest you could be contagious and spread the virus until the papules leave your skin. […] Molluscum contagiosum can clear up on its own, but treatment reduces your infection time and decreases the spread of the infection to other parts of your skin.
  • #1 Unmasking molluscum contagiosum: Navigating atypical presentations in a clinical mosaic – Annals of National Academy of Medical Sciences
    https://nams-annals.in/unmasking-molluscum-contagiosum-navigating-atypical-presentations-in-a-clinical-mosaic/
    MCV causes epithelial lobules to develop after infecting epidermal keratinocytes. Molluscum bodies are found in these downward-growing lobules of epithelial proliferation. […] Diagnosis is mostly made by clinical evaluation; however, biopsy or cytology is required for a definitive diagnosis, especially in cases of unusual presentations. The lesions are confirmed by the demonstration of molluscum bodies. […] The latter also known as Henderson-Patterson bodies, are cytoplasmic, faintly granular eosinophilic inclusions that displace nuclei in the cells of the stratum malpighi. […] Treatment can be in the form of curettage, laser, cryotherapy, or salicylic acid.
  • #1 Molluscum contagiosum virus MC80 sabotages MHC-I antigen presentation by targeting tapasin for ER-associated degradation | PLOS Pathogens
    https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1007711
    The human specific poxvirus molluscum contagiosum virus (MCV) produces skin lesions that can persist with minimal inflammation, suggesting that the virus has developed robust immune evasion strategies. […] Herein we demonstrate that MCV-encoded MC80 can disrupt MHC-I antigen presentation in human and mouse cells. […] Expression of MC80 results in ER-retention of host MHC-I and thereby reduced cell surface presentation. […] MC80 accomplishes this by engaging tapasin via its luminal domain, targeting it for ubiquitination and ER-associated degradation in a process dependent on the MC80 transmembrane region and cytoplasmic tail. […] Our findings reveal a unique mechanism by which MCV undermines adaptive immune surveillance. […] Here we demonstrate that expression of MC80 results in ER-retention and consequent surface downregulation of classical MHC-I in human and mouse cells.
  • #1 Molluscum contagiosum virus MC80 sabotages MHC-I antigen presentation by targeting tapasin for ER-associated degradation | PLOS Pathogens
    https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1007711
    Mechanistically, we found that MC80 interacts with Tpn via its luminal domain and targets Tpn for ER-associated degradation in a transmembrane (TM)- and cytoplasmic tail-dependent manner. […] The loss of Tpn coincides with a loss of TAP, further impeding the assembly of MHC-I with high-affinity peptides. […] Our findings reveal a strategy employed by MCV to disrupt antigen presentation and thereby CTL responses by exploiting MHC-I fold recognition by the PLC.
  • #1 Molluscum Contagiosum: Pathogenesis and Clinical Findings | Calgary Guide
    https://calgaryguide.ucalgary.ca/molluscum-contagiosum-pathogenesis-and-clinical-findings/molluscum-contagiosum-pathogenesis-and-clinical-findings/
    Molluscum contagiosum: Pathogenesis and clinical findings […] Molluscipox virus infection of epidermal keratinocytes […] Virus replicates in cytoplasm of epithelial cells […] Cytoplasmic inclusion bodies form, multiply push nucleus to edge of cell […] Rupture and discharge of virus-packed inclusion bodies […] MCV-released proteins inhibit NF-KB activation […] Suppress host immune response to infection […] Immunosuppression […] Impaired T-cell immunity fails to defend against MCV infection.
  • #1 Molluscum Contagiosum: Causes, Symptoms, and Treatment
    https://patient.info/childrens-health/viral-skin-infections-leaflet/molluscum-contagiosum
    The small lumps (mollusca) on the skin usually develop 2-8 weeks after becoming infected with the virus. Typically, each lump (molluscum) lasts a few weeks or months, crusts over and then goes. […] However, new ones tend to appear as old ones are going, as the virus spreads to other areas of skin. Therefore, crops of mollusca may appear to come and go for several months. […] Molluscum contagiosum is usually harmless. […] After an episode of molluscum contagiosum has cleared away, people are normally then immune to the virus, meaning it’s very unlikely to come back. […] If you develop a very large number of mollusca (hundreds) or the mollusca are larger than normal, it could be a marker of an underlying problem with your immune system, which might require further tests.
  • #1 Molluscum Contagiosum: Epidemiology, Considerations, Treatment Options, and Therapeutic Gaps | JCAD – The Journal of Clinical and Aesthetic Dermatology
    https://jcadonline.com/molluscum-contagiosum-epidemiology-considerations-treatment-options/
    Infection with MC appears to modulate host immunologic response in a variety of patterns as evidenced by the elicitation of molluscum dermatitis and also by the presence of spontaneous visible inflammation of individual MC papules that leads to resolution of these lesions. This latter response to some MC lesions is referred to as the BOTE sign (beginning of the end). The common persistence of MC may be explained at least partially by one report showing that MC, via specific gene-induced mechanisms, can inhibit activation of antigen-specific T lymphocytes, affect natural killer (NK) cell recognition, and promote evasion of cytotoxic (CD8+) T lymphocytes.
  • #1 Molluscum contagiosum treated with topical glycolic acid | CCID
    https://www.dovepress.com/molluscum-contagiosum-in-hiv-patient-treated-with-20-topical-glycolic–peer-reviewed-fulltext-article-CCID
    In HIV patients, the majority of MC lesions are found on the face and neck. […] The diagnosis of MC can be made based on the typical characteristics of the lesion. […] The discovery of molluscum bodies (Henderson-Paterson bodies) on cytological examination of Tzanck smear with Giemsa staining is pathognomonic in MC. […] In HIV patients, MC may not undergo spontaneous resolution without treatment. […] Overall, topical 20% glycolic acid can be used for MK therapy with minimal side effects, easy to apply and safe.
  • #1 Molluscum contagiosum treated with topical glycolic acid | CCID
    https://www.dovepress.com/molluscum-contagiosum-in-hiv-patient-treated-with-20-topical-glycolic–peer-reviewed-fulltext-article-CCID
    Molluscum contagiosum (MC) is a benign papular skin infection caused by Molluscum contagiosum virus (MCV). […] The incidence of MC in HIV patients is quite high at 5-8%. […] In HIV patients, anti retro viral therapy (ARV) is the main therapy with several other additional therapies such as cantaridin, chemical peeling agents such as glycolic acid (20-70%) and trichloroacetic acid (20-100%), cryosurgery, electrosurgery, incision, lactic acid, laser surgery, podophyllin, retinoic acid, and urea. […] The virus will enter the host epithelial cells by endocytosis or cell fusion and will replicate in the stratum spinosum of the epidermis. […] The virus replicates in the cytoplasm of the cell producing cytoplasmic inclusion bodies (Henderson-Paterson bodies). […] The clinical picture of MC is a skin-colored papule, pearly or pink, dome-shaped, has a smooth surface, spongy consistency, with umbilication in the central part, contains a white mass containing molluscum bodies and can be seen when removed with pressure.
  • #1 Molluscum Contagiosum – Verrica Pharmaceuticals
    https://verrica.com/keypublication_groups/molluscum-contagiosum/
    Molluscum contagiosum virus is an important human skin pathogen: it can cause disfigurement and suffering in children, in adults it is less common and often sexually transmitted. Extensive and persistent skin infection with the virus can indicate underlying immunodeficiency. Traditional ablative therapies have not been compared directly with newer immune-modulating and specific antiviral therapies. Advances in research raise the prospect of new approaches to treatment informed by the biology of the virus; in human skin, the infection is localized in the epidermal layers, where it induces a typical, complex hyperproliferative lesion with an abundance of virus particles but a conspicuous absence of immune effectors. Functional studies of the viral genome have revealed effects on cellular pathways involved in the cell cycle, innate immunity, inflammation, and cell death. Extensive lesions caused by molluscum contagiosum can occur in patients with DOCK8 deficiency-a genetic disorder affecting migration of dendritic and specialized T cells in skin. Sudden disappearance of lesions is the consequence of a vigorous immune response in healthy people. Further study of the unique features of infection with molluscum contagiosum virus could give fundamental insight into the nature of skin immunity.
  • #1 Molluscum contagiosum – Symptoms, diagnosis and treatment | BMJ Best Practice
    https://bestpractice.bmj.com/topics/en-gb/310
    Molluscum contagiosum is a common infection in children and young adults and is usually acquired through direct skin-to-skin contact. […] Immunocompromise and underlying skin disease, particularly atopic dermatitis, increase the risk of molluscum infection. […] This condition is caused by the molluscum contagiosum virus, a ubiquitous poxvirus that escapes immune destruction for months to years. […] Molluscum lesions display characteristic intracytoplasmic inclusion bodies (referred to as molluscum bodies or Henderson-Patterson bodies) on histology. […] Lesions are generally caused via skin-to-skin or fomite contact in children, and often by sexual transmission in adults.
  • #1 Molluscum contagiosum Made Extremely Simple | PPT
    https://www.slideshare.net/slideshow/molluscum-contagiosum-made-extremely-simple/183090987
    Molluscum contagiosum virus is classified within the poxvirus family in a specific genus, the Molluscipox Molluscum contagiosum virus causes a benign viral infection characterized by single or multiple, rounded, dome-shaped, pink, waxy papules that are 2-5 mm in diameter. The papules are umbilicated and contain a caseous plug. […] Infection follows contact with infected persons or contaminated objects. In young adults sexual transmission causes lesions that are more common in the genital area. It is not known if epidermal injury is important for establishment of infection. […] The virus enters the basal epidermis causing an increase in cell division extending into the suprabasal layer. The cellular proliferation produces lobulated epidermal growths which compress the papillae until they appear as fibrous septa between the lobules, which are pear shaped with the apex upwards. Basal layer remains intact. Cells at the core of the lesion show the greatest distortion and are ultimately destroyed, and appear as large hyaline bodies (Molluscum bodies/ Henderson-Patterson Bodies) containing cytoplasmic masses of virus material. […] Cell-mediated immunity is significant in controlling and eliminating the infection.
  • #1 Comprehensive Management of Molluscum Contagiosum: Assessment of Clinical Associations, Comorbidities, and Management Principles | JCAD – The Journal of Clinical and Aesthetic Dermatology
    https://jcadonline.com/comprehensive-management-of-molluscum-contagiosum/
    The possibility of sexual abuse in pediatric cases of MC is important to consider, especially when the lesions only appear in the anogenital region. […] Some underlying health conditions may increase the risk of contracting MC and contribute to intraindividual spread of lesions. […] Immunosuppression predisposes patients to emergence of multiple MC lesions, which are often more difficult to treat effectively and may be atypical in appearance. […] There is now strong consensus among the experts that benign neglect is not a recommended treatment approach in the majority of cases of MC.
  • #1 Molluscum Contagiosum – Skin Disorders – Merck Manual Consumer Version
    https://www.merckmanuals.com/home/skin-disorders/viral-skin-infections/molluscum-contagiosum
    Other treatments include injection of Candida antigen into a bump and photodynamic therapy. Candida antigens are proteins that come from the Candida yeast. When injected into the bump, they cause an immune response that fights against the virus. Similarly, interferons are proteins that trigger immune cells to attack the virus. In photodynamic therapy, a chemical preparation is applied to the skin and then artificial light is applied to the bumps. The light activates the chemical to produce a form of oxygen that kills the virus causing the bumps. […] In people with HIV infection who develop molluscum contagiosum, treatment of the HIV infection with antiviral medications is often necessary to allow the molluscum contagiosum to resolve.
  • #1 Zelsuvmi: a promising treatment for molluscum contagiosum
    https://www.explorationpub.com/Journals/em/Article/1001266
    Molluscum contagiosum (MC) is a common skin infection caused by a poxvirus, primarily affecting children and immunocompromised adults. […] MCV is distinctive in evading immune surveillance by inhibiting or dampening several immune pathways via the production of viral proteins. This results in decreasing local inflammatory response which contributes to the prolonged survival of MCV in the epidermis. […] Zelsuvmi topical gel, marketed as ZELSUVMITM by Novan Inc., is a medication designed for the treatment of MC. Formulated with 10.3% NO, the gel leverages Novans innovative NITRICILTM platform to release NO at the site of application through large polymers. Zelsuvmi is a polymeric substance that features a polysiloxane backbone and covalently bound N-diazeniumdiolate NO donors. Upon exposure to proton donors such as water, Zelsuvmi releases NO, facilitated by the degradation of the N-diazeniumdiolate entity. Zelsuvmi is an immunomodulator, which means it can regulate the immune systems response to infections, and it also exhibits broad-spectrum antimicrobial and antiviral activity, likely due to the S-nitrosylation of proteins and cytotoxicity to viral replication from reactive oxygen species, making it an effective treatment for a wide range of infections.
  • #1 Zelsuvmi: a promising treatment for molluscum contagiosum
    https://www.explorationpub.com/Journals/em/Article/1001266
    Zelsuvmi sodium has been found to effectively reduce the viral load of poxvirus and suppress the expression of the MC immunomodulation protein MC160 by directly targeting MC virions. This suggests that Zelsuvmis antiviral effects are due to its direct action on the virus itself, rather than the hosts immune system.
  • #2 Molluscum contagiosum – UpToDate
    https://www.uptodate.com/contents/molluscum-contagiosum
    Molluscum contagiosum virus (MCV) is a poxvirus that causes a chronic, localized infection, consisting of skin-colored, dome-shaped papules on the skin of an infected individual. […] MCV is a double-stranded deoxyribonucleic acid (dsDNA) virus and member of the poxvirus family. […] MCV causes a chronic, localized infection with small papules on the skin. […] Molluscum contagiosum contains many unique genes that encode proteins responsible for novel viral defense mechanisms; these mechanisms inhibit the host inflammatory and immune responses to the infection.
  • #2 Molluscum Contagiosum: Epidemiology, Considerations, Treatment Options, and Therapeutic Gaps | JCAD – The Journal of Clinical and Aesthetic Dermatology
    https://jcadonline.com/molluscum-contagiosum-epidemiology-considerations-treatment-options/
    Molluscum contagiosum (MC) virus is an unclassified member of the Poxviridae family, encompassing Types I to IV viruses. This virus causes a benign, cutaneous-manifested infection that occurs only in humans. MC papules are produced by a double-stranded DNA virus in humans. After invading the host, MC infects the epidermis and replicates itself in the cytoplasm of cells. The incubation period for the virus is variable and generally ranges from 2 to 6 weeks. Since the MC enters the body through a break in the skin, it is more prevalent in patients with atopic dermatitis, dry skin, or any interrupted structural integrity of the skin barrier. MC is more prevalent in hot, humid climates and among children who go swimming. Currently, it is not clear if MC transmission occurs in water, although the condition has been referred to as water warts. Infectious transmission seems to occur through direct contact with infected skin, by sexual or nonsexual means, or by autoinoculation.
  • #2 Molluscum contagiosum: Causes and treatment — DermNet
    https://dermnetnz.org/topics/molluscum-contagiosum
    Molluscum contagiosum is caused by a poxvirus, the molluscum contagiosum virus. There are at least 4 viral subtypes. […] Transmission of molluscum contagiosum appears to be more likely in wet conditions, such as when children bathe or swim together. The incubation period is usually about 2 weeks but can be as long as 6 months. […] Molluscum contagiosum frequently induces dermatitis around them and affected skin becomes pink, dry and itchy. As the papules resolve, they may become inflamed, crusted, or scabby for a week or two. […] Numerous and widespread molluscum contagiosum that are larger than usual may occur in immune-deficient patients (such as uncontrolled HIV infection or in patients on immune suppressing drugs), and often affect the face. […] Molluscum contagiosum is infectious while active. However, affected children and adults should continue to attend daycare, school, and work.
  • #2 Molluscum contagiosum virus – Wikipedia
    https://en.wikipedia.org/wiki/Molluscum_contagiosum_virus
    Each virion sets up a region in the cytoplasm, called a 'viral factory’ where DNA replication, transcription, and translation all occur sequentially. […] The MC007 protein sequesters retinoblastoma protein (pRb) on the mitochondria membrane, inactivating it. […] The MC054 long protein binds Interleukin 18 which blocks its two binding sites. […] The MC066 protein is homologous to human glutathione peroxidase. […] The MC132 protein interacts with the NF-B subunit p65 and causes p65 degradation. […] The MC148 protein acts like a chemokine-like protein and displaces actual chemokines from their G-protein coupled receptors. […] The MC159 protein inhibits TNF-R1 induced NF-B activation. […] The MC160 protein binds heat shock protein 90, keeping it from stabilizing I Kappa Kinase (IKK).
  • #2 Molluscum Contagiosum: Background, Etiology, Epidemiology
    https://emedicine.medscape.com/article/910570-overview
    Following infection, cellular proliferation produces lobulated epidermal growths that compress epidermal papillae, while fibrous septa between the lobules produce pear-shaped clumps with the apex upwards. The basal layer remains intact. […] Cells at the core of the lesion show the greatest distortion and are ultimately destroyed, resulting in large hyaline bodies (ie, molluscum bodies, Henderson-Paterson bodies) containing cytoplasmic masses of virus material. These bodies are present in large numbers and appear as a white depression at the center of fully developed lesions. […] As with other poxviruses, molluscum contagiosum virus does not appear to develop latency but evades the immune system through the production of virus-specific proteins. Cell-mediated immunity is most important in modulating and controlling the infection. […] The virus is not strongly immunogenic, as it infrequently induces antibody formation. Specific antibodies have been found in approximately 80% of patients and in about 15% of control subjects. A role for humoral immunity in regression of lesions is not established. Reinfection is common.
  • #2 Molluscum contagiosum Made Extremely Simple | PPT
    https://www.slideshare.net/slideshow/molluscum-contagiosum-made-extremely-simple/183090987
    Molluscum contagiosum virus is classified within the poxvirus family in a specific genus, the Molluscipox Molluscum contagiosum virus causes a benign viral infection characterized by single or multiple, rounded, dome-shaped, pink, waxy papules that are 2-5 mm in diameter. The papules are umbilicated and contain a caseous plug. […] Infection follows contact with infected persons or contaminated objects. In young adults sexual transmission causes lesions that are more common in the genital area. It is not known if epidermal injury is important for establishment of infection. […] The virus enters the basal epidermis causing an increase in cell division extending into the suprabasal layer. The cellular proliferation produces lobulated epidermal growths which compress the papillae until they appear as fibrous septa between the lobules, which are pear shaped with the apex upwards. Basal layer remains intact. Cells at the core of the lesion show the greatest distortion and are ultimately destroyed, and appear as large hyaline bodies (Molluscum bodies/ Henderson-Patterson Bodies) containing cytoplasmic masses of virus material. […] Cell-mediated immunity is significant in controlling and eliminating the infection.
  • #2 Molluscum Contagiosum – Verrica Pharmaceuticals
    https://verrica.com/keypublication_groups/molluscum-contagiosum/
    Molluscum contagiosum virus is an important human skin pathogen: it can cause disfigurement and suffering in children, in adults it is less common and often sexually transmitted. Extensive and persistent skin infection with the virus can indicate underlying immunodeficiency. Traditional ablative therapies have not been compared directly with newer immune-modulating and specific antiviral therapies. Advances in research raise the prospect of new approaches to treatment informed by the biology of the virus; in human skin, the infection is localized in the epidermal layers, where it induces a typical, complex hyperproliferative lesion with an abundance of virus particles but a conspicuous absence of immune effectors. Functional studies of the viral genome have revealed effects on cellular pathways involved in the cell cycle, innate immunity, inflammation, and cell death. Extensive lesions caused by molluscum contagiosum can occur in patients with DOCK8 deficiency-a genetic disorder affecting migration of dendritic and specialized T cells in skin. Sudden disappearance of lesions is the consequence of a vigorous immune response in healthy people. Further study of the unique features of infection with molluscum contagiosum virus could give fundamental insight into the nature of skin immunity.
  • #2 Molluscum Contagiosum: Causes, Symptoms, and More
    https://www.healthline.com/health/molluscum-contagiosum
    Molluscum contagiosum is a skin infection caused by a virus of the same name. It produces benign, raised bumps, or lesions, on the upper layers of your skin. […] Molluscum contagiosum occurs when you acquire the M. contagiosum virus, a type of poxvirus. […] This virus can transmit between people while lesions are visible. Its also possible to transmit the virus from one area of skin on your own body to another part. […] There are a number of ways that M. contagiosum passes between people, including: Skin contact with a person who carries the infection. You can get molluscum contagiosum by touching the lesions on the skin of a person who has this infection. […] Transmission seems to take place more in wet environments, like during childrens shared swimming classes. […] Antiretroviral therapy (ART) is the most effective treatment for people who live with HIV if they contract molluscum contagiosum. It can help strengthen the immune system and fight the virus.
  • #2 Molluscum Contagiosum
    https://www.ashasexualhealth.org/molluscum-contagiosum/
    Molluscum contagiosum is a skin disease caused by the molluscum contagiosum virus (MCV) […] Molluscum contagiosum virus (MCV) may be sexually transmitted by skin-to-skin contact (does not have to be mucous membranes) and/or lesions. Transmission through sexual contact is the most common form of transmission for adults. […] MCV also may be transmitted by autoinoculation, such as touching a lesion and then touching another part of the body. […] Most symptoms eventually resolve on their own, so treatment may not be necessary. But lesions can also be removed. This helps reduce the risk of further spreading the lesions on your own body of passing on MCV to others. […] Lesions may come back, but it is not clear whether this is due to reinfection or reactivation of a dormant infection. […] The most common complication from molluscum is a secondary infection caused by bacteria. This can be more of a problem for people with compromised immune systems. […] Because transmission through sexual contact is the most common form of transmission for adults, preventing skin-to-skin contact with an infected partner will be most effective in preventing MCV.
  • #2 Molluscum Contagiosum: Causes, Symptoms, and Treatment
    https://patient.info/childrens-health/viral-skin-infections-leaflet/molluscum-contagiosum
    The small lumps (mollusca) on the skin usually develop 2-8 weeks after becoming infected with the virus. Typically, each lump (molluscum) lasts a few weeks or months, crusts over and then goes. […] However, new ones tend to appear as old ones are going, as the virus spreads to other areas of skin. Therefore, crops of mollusca may appear to come and go for several months. […] Molluscum contagiosum is usually harmless. […] After an episode of molluscum contagiosum has cleared away, people are normally then immune to the virus, meaning it’s very unlikely to come back. […] If you develop a very large number of mollusca (hundreds) or the mollusca are larger than normal, it could be a marker of an underlying problem with your immune system, which might require further tests.
  • #2 Molluscum contagiosum: Causes and treatment — DermNet
    https://dermnetnz.org/topics/molluscum-contagiosum
    In immune competent hosts, molluscum contagiosum is a relatively harmless. The papules may persist for up to 2 years or longer. In children, about half of cases have cleared by 12 months, and two-thirds by 18 months, with or without treatment. Contact with another infected individual later on can lead to a new crop. […] Infection can be very persistent in the presence of significant immune deficiency.
  • #2 Molluscum contagiosum – Symptoms & causes – Mayo Clinic
    https://www.mayoclinic.org/diseases-conditions/molluscum-contagiosum/symptoms-causes/syc-20375226
    Molluscum contagiosum (mo-LUS-kum kun-tay-jee-OH-sum) is a fairly common skin infection caused by a virus. It causes round, firm, painless bumps ranging in size from a pinhead to a pencil eraser. […] Molluscum contagiosum also spreads through person-to-person contact and contact with infected objects. […] Left untreated, the bumps usually disappear in 6 months to 2 years. […] The virus that causes molluscum contagiosum spreads easily through skin-to-skin contact. […] Scratching or rubbing the bumps, which spreads the virus to nearby skin. […] The bumps and the skin around them may become inflamed. This is thought to be an immune system response to the infection. […] If scratched, these bumps can become infected and heal with scarring.
  • #3 Molluscum contagiosum – BAD Patient Hub
    https://www.skinhealthinfo.org.uk/condition/molluscum-contagiosum/
    Molluscum contagiosum is caused by a virus known as the Molluscum contagiosum virus. It is infectious and can spread to other people if the bumps are in direct contact with someone, or by sharing the same items such as towels, flannels, bedding, etc. […] This is because people with eczema have dry, cracked skin, which allows the virus to enter the body more easily, leading to infection. […] Most individuals develop few or no molluscum contagiosum bumps. However, people with a weakened or suppressed immune system may experience more bumps. This can happen due to various reasons, such as underlying health conditions like HIV or treatments that affect the immune system. […] There are a range of topical therapies used which include salicylic acid and potassium hydroxide. These work by irritating the bumps and causing them to become inflamed. The immune system then detects the virus and clears the bumps. […] Sometimes it may take a few years for the body to clear the virus and for the bumps to disappear.
  • #3 Update on Clinical Management of Cutaneous Molluscum Contagiosum
    https://www.skintherapyletter.com/dermatology/molluscum-contagiosum/
    Molluscum contagiosum is a poxvirus infection of the skin that is commonly observed in children. The molluscum contagiosum virus (MCV) expresses several gene-products that are involved in its pathogenesis and evasion of the host immune system. […] The genome of MCV-1 has been completely sequenced and several novel gene products involved in its pathogenesis and evasion of the immune system have been identified: MC54L, MC148, MC013L, MC159, and glutathione peroxidase. […] The protein MC54L prevents inflammation by binding the pro-inflammatory cytokine human interleukin-18. MC148 promotes viral replication by preventing infected keratinocytes from differentiating. MC159 interacts with Fas (CD95; a member of the tumor necrosis factor receptor family), tumor necrosis factor (TNF), and TNF-related apoptosis-inducing ligand (TRAIL) to inhibit apoptosis. MC80R, a major histocompatibility complex (MHC) class I homolog, interferes with the host presentation of peptides specific to MCV and inhibits cell-mediated cytotoxicity of infected cells. Finally, infected cells express glutathione peroxidase to prevent leukocyte-mediated oxidative damage. Together, these viral gene products are able to maintain active infection until the host immune system gradually prevails.
  • #3 Molluscum contagiosum virus – Wikipedia
    https://en.wikipedia.org/wiki/Molluscum_contagiosum_virus
    Each virion sets up a region in the cytoplasm, called a 'viral factory’ where DNA replication, transcription, and translation all occur sequentially. […] The MC007 protein sequesters retinoblastoma protein (pRb) on the mitochondria membrane, inactivating it. […] The MC054 long protein binds Interleukin 18 which blocks its two binding sites. […] The MC066 protein is homologous to human glutathione peroxidase. […] The MC132 protein interacts with the NF-B subunit p65 and causes p65 degradation. […] The MC148 protein acts like a chemokine-like protein and displaces actual chemokines from their G-protein coupled receptors. […] The MC159 protein inhibits TNF-R1 induced NF-B activation. […] The MC160 protein binds heat shock protein 90, keeping it from stabilizing I Kappa Kinase (IKK).
  • #4 Update on Clinical Management of Cutaneous Molluscum Contagiosum
    https://www.skintherapyletter.com/dermatology/molluscum-contagiosum/
    Molluscum contagiosum is a poxvirus infection of the skin that is commonly observed in children. The molluscum contagiosum virus (MCV) expresses several gene-products that are involved in its pathogenesis and evasion of the host immune system. […] The genome of MCV-1 has been completely sequenced and several novel gene products involved in its pathogenesis and evasion of the immune system have been identified: MC54L, MC148, MC013L, MC159, and glutathione peroxidase. […] The protein MC54L prevents inflammation by binding the pro-inflammatory cytokine human interleukin-18. MC148 promotes viral replication by preventing infected keratinocytes from differentiating. MC159 interacts with Fas (CD95; a member of the tumor necrosis factor receptor family), tumor necrosis factor (TNF), and TNF-related apoptosis-inducing ligand (TRAIL) to inhibit apoptosis. MC80R, a major histocompatibility complex (MHC) class I homolog, interferes with the host presentation of peptides specific to MCV and inhibits cell-mediated cytotoxicity of infected cells. Finally, infected cells express glutathione peroxidase to prevent leukocyte-mediated oxidative damage. Together, these viral gene products are able to maintain active infection until the host immune system gradually prevails.
  • #4 Molluscum contagiosum virus – Wikipedia
    https://en.wikipedia.org/wiki/Molluscum_contagiosum_virus
    Each virion sets up a region in the cytoplasm, called a 'viral factory’ where DNA replication, transcription, and translation all occur sequentially. […] The MC007 protein sequesters retinoblastoma protein (pRb) on the mitochondria membrane, inactivating it. […] The MC054 long protein binds Interleukin 18 which blocks its two binding sites. […] The MC066 protein is homologous to human glutathione peroxidase. […] The MC132 protein interacts with the NF-B subunit p65 and causes p65 degradation. […] The MC148 protein acts like a chemokine-like protein and displaces actual chemokines from their G-protein coupled receptors. […] The MC159 protein inhibits TNF-R1 induced NF-B activation. […] The MC160 protein binds heat shock protein 90, keeping it from stabilizing I Kappa Kinase (IKK).
  • #5 Molluscum contagiosum: an update and review of new perspectives in etiology, diagnosis, and treatment
    https://pmc.ncbi.nlm.nih.gov/articles/PMC6553952/
    Molluscum contagiosum (MC) is caused by molluscum contagiosum virus (MCV), a double-strand DNA virus which belongs to the Poxviridae family; humans are MCV only host. […] MCV infects the epidermis and replicates in the cytoplasm of cells with a variable incubation period between two and six weeks. […] Different studies have been developed to sequence the genome of this virus and determine possible genes involved in the evasion of the host immune response, a hypothesis that arose based on the absence of inflammation observed in histopathological samples of infected skin. […] To date, four viral genes have been identified that code proteins that would alter the activation of the nuclear factor kB (NF-kB): MC159, MC160, MC132, and MC005. […] NF-kB is a nuclear protein complex present in dendritic cells that regulate the transcription of DNA and facilitate the synthesis of pro-inflammatory cytokines (TNF, IL-1, IL-6, among others) and activation of innate and acquired immune response.
  • #5 Molluscum contagiosum virus – Wikipedia
    https://en.wikipedia.org/wiki/Molluscum_contagiosum_virus
    Each virion sets up a region in the cytoplasm, called a 'viral factory’ where DNA replication, transcription, and translation all occur sequentially. […] The MC007 protein sequesters retinoblastoma protein (pRb) on the mitochondria membrane, inactivating it. […] The MC054 long protein binds Interleukin 18 which blocks its two binding sites. […] The MC066 protein is homologous to human glutathione peroxidase. […] The MC132 protein interacts with the NF-B subunit p65 and causes p65 degradation. […] The MC148 protein acts like a chemokine-like protein and displaces actual chemokines from their G-protein coupled receptors. […] The MC159 protein inhibits TNF-R1 induced NF-B activation. […] The MC160 protein binds heat shock protein 90, keeping it from stabilizing I Kappa Kinase (IKK).
  • #6 Update on Clinical Management of Cutaneous Molluscum Contagiosum
    https://www.skintherapyletter.com/dermatology/molluscum-contagiosum/
    Molluscum contagiosum is a poxvirus infection of the skin that is commonly observed in children. The molluscum contagiosum virus (MCV) expresses several gene-products that are involved in its pathogenesis and evasion of the host immune system. […] The genome of MCV-1 has been completely sequenced and several novel gene products involved in its pathogenesis and evasion of the immune system have been identified: MC54L, MC148, MC013L, MC159, and glutathione peroxidase. […] The protein MC54L prevents inflammation by binding the pro-inflammatory cytokine human interleukin-18. MC148 promotes viral replication by preventing infected keratinocytes from differentiating. MC159 interacts with Fas (CD95; a member of the tumor necrosis factor receptor family), tumor necrosis factor (TNF), and TNF-related apoptosis-inducing ligand (TRAIL) to inhibit apoptosis. MC80R, a major histocompatibility complex (MHC) class I homolog, interferes with the host presentation of peptides specific to MCV and inhibits cell-mediated cytotoxicity of infected cells. Finally, infected cells express glutathione peroxidase to prevent leukocyte-mediated oxidative damage. Together, these viral gene products are able to maintain active infection until the host immune system gradually prevails.
  • #6 Molluscum contagiosum virus – Wikipedia
    https://en.wikipedia.org/wiki/Molluscum_contagiosum_virus
    Each virion sets up a region in the cytoplasm, called a 'viral factory’ where DNA replication, transcription, and translation all occur sequentially. […] The MC007 protein sequesters retinoblastoma protein (pRb) on the mitochondria membrane, inactivating it. […] The MC054 long protein binds Interleukin 18 which blocks its two binding sites. […] The MC066 protein is homologous to human glutathione peroxidase. […] The MC132 protein interacts with the NF-B subunit p65 and causes p65 degradation. […] The MC148 protein acts like a chemokine-like protein and displaces actual chemokines from their G-protein coupled receptors. […] The MC159 protein inhibits TNF-R1 induced NF-B activation. […] The MC160 protein binds heat shock protein 90, keeping it from stabilizing I Kappa Kinase (IKK).
  • #7 Update on Clinical Management of Cutaneous Molluscum Contagiosum
    https://www.skintherapyletter.com/dermatology/molluscum-contagiosum/
    Molluscum contagiosum is a poxvirus infection of the skin that is commonly observed in children. The molluscum contagiosum virus (MCV) expresses several gene-products that are involved in its pathogenesis and evasion of the host immune system. […] The genome of MCV-1 has been completely sequenced and several novel gene products involved in its pathogenesis and evasion of the immune system have been identified: MC54L, MC148, MC013L, MC159, and glutathione peroxidase. […] The protein MC54L prevents inflammation by binding the pro-inflammatory cytokine human interleukin-18. MC148 promotes viral replication by preventing infected keratinocytes from differentiating. MC159 interacts with Fas (CD95; a member of the tumor necrosis factor receptor family), tumor necrosis factor (TNF), and TNF-related apoptosis-inducing ligand (TRAIL) to inhibit apoptosis. MC80R, a major histocompatibility complex (MHC) class I homolog, interferes with the host presentation of peptides specific to MCV and inhibits cell-mediated cytotoxicity of infected cells. Finally, infected cells express glutathione peroxidase to prevent leukocyte-mediated oxidative damage. Together, these viral gene products are able to maintain active infection until the host immune system gradually prevails.
  • #7 Molluscum contagiosum virus – Wikipedia
    https://en.wikipedia.org/wiki/Molluscum_contagiosum_virus
    Each virion sets up a region in the cytoplasm, called a 'viral factory’ where DNA replication, transcription, and translation all occur sequentially. […] The MC007 protein sequesters retinoblastoma protein (pRb) on the mitochondria membrane, inactivating it. […] The MC054 long protein binds Interleukin 18 which blocks its two binding sites. […] The MC066 protein is homologous to human glutathione peroxidase. […] The MC132 protein interacts with the NF-B subunit p65 and causes p65 degradation. […] The MC148 protein acts like a chemokine-like protein and displaces actual chemokines from their G-protein coupled receptors. […] The MC159 protein inhibits TNF-R1 induced NF-B activation. […] The MC160 protein binds heat shock protein 90, keeping it from stabilizing I Kappa Kinase (IKK).
  • #8 Update on Clinical Management of Cutaneous Molluscum Contagiosum
    https://www.skintherapyletter.com/dermatology/molluscum-contagiosum/
    Molluscum contagiosum is a poxvirus infection of the skin that is commonly observed in children. The molluscum contagiosum virus (MCV) expresses several gene-products that are involved in its pathogenesis and evasion of the host immune system. […] The genome of MCV-1 has been completely sequenced and several novel gene products involved in its pathogenesis and evasion of the immune system have been identified: MC54L, MC148, MC013L, MC159, and glutathione peroxidase. […] The protein MC54L prevents inflammation by binding the pro-inflammatory cytokine human interleukin-18. MC148 promotes viral replication by preventing infected keratinocytes from differentiating. MC159 interacts with Fas (CD95; a member of the tumor necrosis factor receptor family), tumor necrosis factor (TNF), and TNF-related apoptosis-inducing ligand (TRAIL) to inhibit apoptosis. MC80R, a major histocompatibility complex (MHC) class I homolog, interferes with the host presentation of peptides specific to MCV and inhibits cell-mediated cytotoxicity of infected cells. Finally, infected cells express glutathione peroxidase to prevent leukocyte-mediated oxidative damage. Together, these viral gene products are able to maintain active infection until the host immune system gradually prevails.
  • #9 Molluscum contagiosum virus MC80 sabotages MHC-I antigen presentation by targeting tapasin for ER-associated degradation | PLOS Pathogens
    https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1007711
    The human specific poxvirus molluscum contagiosum virus (MCV) produces skin lesions that can persist with minimal inflammation, suggesting that the virus has developed robust immune evasion strategies. […] Herein we demonstrate that MCV-encoded MC80 can disrupt MHC-I antigen presentation in human and mouse cells. […] Expression of MC80 results in ER-retention of host MHC-I and thereby reduced cell surface presentation. […] MC80 accomplishes this by engaging tapasin via its luminal domain, targeting it for ubiquitination and ER-associated degradation in a process dependent on the MC80 transmembrane region and cytoplasmic tail. […] Our findings reveal a unique mechanism by which MCV undermines adaptive immune surveillance. […] Here we demonstrate that expression of MC80 results in ER-retention and consequent surface downregulation of classical MHC-I in human and mouse cells.