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Post. Mikrobiol. 4-2013.Indb POLSKIE TOWARZYSTWO MIKROBIOLOGÓW Kwartalnik Tom 52 Zeszyt 2•2013 KWIECIE¡ – CZERWIEC CODEN: PMKMAV 52 (2) Advances in Microbiology 2013 POLSKIE TOWARZYSTWO MIKROBIOLOGÓW Kwartalnik Tom 52 Zeszyt 3•2013 LIPIEC – WRZESIE¡ CODEN: PMKMAV 52 (3) Advances in Microbiology 2013 POLSKIE TOWARZYSTWO MIKROBIOLOGÓW Kwartalnik Tom 52 Zeszyt 4•2013 PAèDZIERNIK – GRUDZIE¡ CODEN: PMKMAV 52 (4) Advances in Microbiology 2013 Index Copernicus ICV = 9,52 (2012) Impact Factor ISI = 0,151 (2012) Punktacja MNiSW = 15,00 (2012) http://www.pm.microbiology.pl RADA REDAKCYJNA JACEK BIELECKI (Uniwersytet Warszawski), RYSZARD CHRÓST (Uniwersytet Warszawski), JERZY DŁUGOŃSKI (Uniwersytet Łódzki), DANUTA DZIERŻANOWSKA (Centrum Zdrowia Dziecka), EUGENIA GOSPODAREK (Collegium Medicum UMK w Bydgoszczy), JERZY HREBENDA (Uniwersytet Warszawski), WALERIA HRYNIEWICZ (Narodowy Instytut Leków), MAREK JAKÓBISIAK (Warszawski Uniwersytet Medyczny), ANDRZEJ PASZEWSKI (Instytut Biochemii i Biofizyki PAN), ANDRZEJ PIEKAROWICZ (Uniwersytet Warszawski), ANTONI RÓŻALSKI (Uniwersytet Łódzki), ALEKSANDRA SKŁODOWSKA (Uniwersytet Warszawski), BOHDAN STAROŚCIAK (Warszawski Uniwersytet Medyczny), BOGUSŁAW SZEWCZYK (Uniwersytet Gdański), ELŻBIETA TRAFNY (Wojskowy Instytut Higieny i Epidemiologii), STANISŁAWA TYLEWSKA-WIERZBANOWSKA (Państwowy Zakład Higieny), GRZEGORZ WĘGRZYN (Uniwersytet Gdański), PIOTR ZIELENKIEWICZ (Uniwersytet Warszawski) REDAKCJA JACEK BIELECKI (redaktor naczelny), JERZY HREBENDA (zastępca), BOHDAN STAROŚCIAK (sekretarz), MARTA BRZÓSTKOWSKA (korekta tekstów angielskich) ADRESY REDAKCJI Redaktorzy: Instytut Mikrobiologii, Wydział Biologii, Uniwersytet Warszawski ul. Miecznikowa 1, 02-096 Warszawa, tel. (22) 554 13 04, fax (22) 554 14 04 e-mail: [email protected]; [email protected] Sekretarz Zakład Mikrobiologii Farmaceutycznej, Warszawski Uniwersytet Medyczny ul. Oczki 3 (parter), 02-007 Warszawa, tel. (22) 628 08 22, (22) 621 13 51 e-mail: [email protected] PUBLIKACJE METODYCZNE I STANDARDY Redaktor odpowiedzialny: STEFANIA GIEDRYS-KALEMBA (Pomorska Akademia Medyczna w Szczecinie) Adres Redaktora działu Publikacje Metodyczne i Standardy Katedra i Zakład Mikrobiologii i Immunologii Pomorskiej Akademii Medycznej, Al. Powstańców Wlkp. 72, 70-111 Szczecin, tel./fax: (91) 46 616 51, 52, lub fax: (91) 46 616 59, e-mail: [email protected] lub [email protected] Stali recenzenci: JERZY DŁUGOŃSKI (Uniwersytet Łódzki), WALERIA HRYNIEWICZ (Narodowy Instytut Leków), JÓZEF KUR (Politechnika Gdańska), EUGENIUSZ MAŁAFIEJ (Instytut Centrum Zdrowia Matki Polki), ANNA PRZONDO-MORDARSKA (Akademia Medyczna we Wrocławiu) CZASOPISMO WYDAWANE Z FINANSOWĄ POMOCĄ MINISTERSTWA NAUKI I SZKOLNICTWA WYŻSZEGO ISBN 978 - 83 - 923731 - 3 - 1 Informacja o zdjęciu na okładce: Fonsecaea monophora – szczegóły morfologii (widoczny konidiofor i układ konidiów). SEM, pow. 4 000 x. Autor zdjęcia: dr n. med. Tomasz Jagielski; Zakład Mikrobiologii Stosowanej, Instytut Mikrobiologii Wydział Biologii Uniwersytetu Warszawskiego ul. I. Miecznikowa 1; 02-096 Warszawa; e-mail: [email protected]. Szanowni Państwo! Autorzy i Czytelnicy Postępów Mikrobiologii: Informujemy Państwa, że uległ zmianie numer konta bankowego Zarządu Głównego Polskiego Towarzystwa Mikrobiologów. Aktualny numer konta: BGŻ SA 57 2030 0045 1110 0000 0261 2550 POLSKIE TOWARZYSTWO MIKROBIOLOGÓW Nakład 1150, Objętość 15 arkuszy wyd., Papier offset 80 g Skład i druk: Zakład Wydawniczy Letter Quality, tel. 22 115 38 10, 607 217 879 e-mail: [email protected]; projekt okładki: Jerzy Grzegorkiewicz POST. MIKROBIOL., US3 – WIELOFUNKCYJNA KINAZA SERYNOWO-TREONINOWA 2013, 52, 4, 329–341 http://www.pm.microbiology.pl ALFAHERPESWIRUSÓW Dorota Lesiak1, Agnieszka Brzozowska1, Krystyna Bieńkowska-Szewczyk1, Andrea D. Lipińska1* Zakład Biologii Molekularnej Wirusów, Międzyuczelniany Wydział Biotechnologii Uniwersytetu Gdańskiego i Gdańskiego Uniwersytetu Medycznego, ul. Kładki 24, 80-822 Gdańsk Wpłynęło w maju 2013 r. 1. Wstęp. 2. US3 a uwalnianie kapsydów z jądra komórkowego. 3. Wpływ US3 na ekspresję genów. 4. Wpływ kinazy US3 na cytoszkielet komórki. 5. Rola kinazy US3 w blokowaniu apoptozy. 6. Właściwości immunomodulacyjne białka US3. 6.1. Oddziaływanie z systemami interferonów. 6.2. Wpływ na prezentację antygenów w kontekście cząsteczek MHC klasy I i inaktywacja limfocytów T cytotoksycznych. 6.3. Redukcja ekspresji antygenów wirusowych na powierzchni komórki. 6.4. Wpływ na aktywację limfocytów NKT. 7. Inne funkcje kinazy US3. 8. Podsumowanie US3 – a multifunctional serine-threonine kinase of alphaherpesviruses Abstract: Phosphorylation by protein kinases modulates the function of target proteins by interfering with their enzymatic activity, cellular location and/or association with other proteins. Viruses have evolved complex interactions with their hosts and often mimic cellular proteins in order to usurp the cellular machinery for their own benefit, so it is not surprising that vast number of viruses encode protein kinases. Alphaherpesvirus kinase US3 is a conserved multifunctional protein, regulating the egress of viral particles, but also responsible for alterations in cell morphology resulting from the breakdown of actin stress fibers and formation of cell projections. US3 homologs control the trafficking of viral and cellular proteins and inhibit apoptosis. The current review provides an overview of the properties and functions of alphaherpesvirus US3 protein kinase orthologues. 1. Introduction. 2. US3 and the virus egress from the cell nucleus. 3. Effect of US3 on gene expression. 4. Effect of US3 on cytoskeleton. 5. Role of US3 in the blocking of apoptosis. 6. Immunomodulatory properties of US3. 6.1. Interactions with the interferon systems. 6.2. Effect on the MHC class I-restricted antigen presentation and inactivation of cytotoxic T lymphocytes. 6.3. Reduction in the cell surface expression of viral antigens. 6.4. Effect on the activation of NKT lymphocytes. 7. Other functions of US3 kinase. 8. Summary Słowa kluczowe: US3, herpeswirus, kinaza serynowo-treoninowa Key words: US3, herpesvirus, serine-threonine kinase 1. Wstęp Największą podrodziną herpeswirusów są alfaherpes - wirusy. Tak jak inne wirusy z tej rodziny, są one zdolne Rodzina Herpesviridae obejmuje ponad dwieście do przechodzenia w stan latencji, czyli infekcji utajonej gatunków wirusów o bardzo szerokim spektrum gospo- w organizmie swojego naturalnego gospodarza. Reak- darzy, głównie kręgowców. Według najnowszej systema- tywacja ze stanu latencji pod wpływem specyficznego tyki herpeswirusów rodzina Herpesviridae współtworzy czynnika, często związanego ze stresem oraz/lub osła- rząd Herpesvirales wraz z dwiema innymi rodzinami: bieniem systemu odpornościowego, może doprowadzić Alloherpesviridae, która skupia wirusy zakażające ryby do nawrotu objawów chorobowych [3]. Zidentyfiko- i płazy, oraz Malacoherpesviridae, skupiającą wirusy wano trzy alfaherpeswirusy ludzkie: ludzki herpeswi- infekujące mięczaki [17]. Osiem spośród zidentyfiko- rus 1 (HHV-1; nazwa zwyczajowa: wirus opryszczki wanych dotychczas gatunków herpeswirusów stanowią typu 1, herpes simplex virus type 1, HSV-1), ludzki wirusy patogenne dla ludzi. Herpeswirusy mają wiele herpeswirus 2 (HHV-2; nazwa zwyczajowa: wirus cech wspólnych. Są to duże wirusy posiadające osłonkę, opryszczki typu 2, herpes simplex virus type 2, HSV-2) tegument i ikozaedralny kapsyd, a ich materiał gene- oraz ludzki herpeswirus 3 (HHV-3; nazwa zwyczajowa: tyczny występuje w formie dwuniciowego DNA o wiel- wirus ospy wietrznej i półpaśca, varicella zoster virus, kości 125–290 tysięcy par zasad [79]. Na podstawie VZV) [17]. Wirusy HSV-1 i HSV-2 są kojarzone głów- istniejących różnic w tropizmie, składzie i organizacji nie z opryszczką wargową i narządów płciowych, ale genomu rodzina Herpesviridae została podzielona na czasem mogą również prowadzić do powikłań, w tym trzy podrodziny: Alphaherpesvirinae, Betaherpesvirinae zapalenia mózgu, zapalenia rogówki i ślepoty. Wirus i Gammaherpesvirinae [17]. VZV jest czynnikiem wywołującym ospę wietrzną, * Autor korespondencyjny: Zakład Biologii Molekularnej Wirusów, Międzyuczelniany Wydział Biotechnologii Uniwersytetu Gdań- skiego i Gdańskiego Uniwersytetu Medycznego, ul. Kładki 24, 80-822 Gdańsk; tel. (58) 5236382; e-mail: [email protected] 330 DOROTA LESIAK, AGNIESZKA BRZOZOWSKA, KRYSTYNA BIEŃKOWSKA-SZEWCZYK, ANDREA D. LIPIŃSKA Tabela I Ogólne cechy budowy ortologów kinazy US3 alfaherpeswirusów [na podstawie sekwencji białek z bazy NCBI, http://www.ncbi.nlm.nih.gov/pubmed/]. Cecha Pozycja domeny Liczba izoform, Numer Liczba reszt katalitycznej w których referencyjny NCBI aminokwasowych Wirus w sekwencji aa występuje białko HSV-1 NP_044665.1 481 200–374 2 HSV-2 NP_044533.1 481 200–398 1 PRV YP_068384.2 390 59–233 2 VZV NP_040188.1 393 102–275 1 BHV-1 NP_045368.1 468 165–463 1 BHV-5 YP_003662531.1 444 153–325 1 MDV YP_001034009.1 402 108–318 1 a podczas reaktywacji ze stanu latencji może powodo- cytomegalovirus, HCMV), BGLF4 u należącego do wać pół paśca. Do podrodziny alfaherpeswirusów należy gammaherpeswirusów wirusa Epsteina-Barr (EBV). również kilka patogenów o znaczeniu weterynaryjnym, Oprócz tej kinazy w poszczególnych podrodzinach Her­ bardzo ważnych z ekonomicznego punktu widzenia. pesviridae występują inne enzymy wirusowe o aktyw- Wirus pseudowścieklizny (pseudorabies virus, PRV) ności kinazowej. W latach osiemdziesiątych XX wieku jest czynnikiem zakaźnym wywołującym u świń cho- w genomach różnych alfaherpeswirusów zidentyfiko- robę Aujeszkyego.
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