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1

Manipulation of non-canonical NF-κB signaling by non-oncogenic viruses

100%
Struzik J., Szulc-Dabrowska L.
Archivum Immunologiae et Therapiae Experimentalis
|
2019
|
tom 67
|
nr 1
2

Hamowanie mitochondrialnego szlaku apoptozy przez białka pokswirusów

81%
Gregorczyk K. P., Wyzewski Z., Szulc-Dabrowska L., Niemialtowski M.
Medycyna Weterynaryjna
|
2014
|
tom 70
|
nr 08
Previous studies have shown that mitochondria play a central role in the primary host defense mechanisms against numerous pathogens. These organelles are involved in the intrinsic pathway of apoptosis, which is one of the earliest responses to viral infection. The intrinsic pathway is tightly controlled by cellular Bcl-2 family proteins, which maintain the integrity with the outer mitochondrial membrane. Viruses have evolved multiple strategies to modulate apoptosis for their own purposes. Recent studies have discovered proteins encoded by the poxviruses, such as F1L, N1L, M11L, FPV039, ORF125, DPV022, and SPPV14, which have got a similar structure and/or functions as Bcl-2 family members. Newly identified poxviral proteins localize in mitochondria and interact with mitochondrial proteins to regulate cellular response. They are able to block the intrinsic pathway of apoptosis, and thereby allow the virus to replicate before its host cell dies.
3

Ectromelia virus similarly modulates TH1- and TH2-cytokine polarizing response of conventional dendritic cells from different mouse strains in vitro

71%
Szulc-Dabrowska L., Struzik J., Toka F. N., Nowak Z., Gierynska M.
Postępy Mikrobiologii. Suplement
|
2017
|
tom 56
|
nr 1
4
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In vivo induction of autophagy in splenocytes of C57BL/6 and BALB/c mice infected with ectromelia orthopoxvirus

71%
Martyniszyn L., Szulc-Dabrowska L., Boratynska-Jasinska A., Badowska-Kozakiewicz A. M., Niemialtowski M. G.
Polish Journal of Veterinary Sciences
|
2013
|
tom 16
|
nr 1
Autophagy is a self-degradation process of cellular components. It plays both antiviral and pro-viral roles in the life cycle of different viruses and the pathogenesis of different viral diseases. In this study, we evaluated autophagy induction in splenocytes of ectromelia virus (ECTV)-resistant C57BL/6 and ECTV-susceptible BALB/c mice during infection with the Moscow strain of the ectromelia virus (ECTV-MOS). Autophagy was analyzed using the Western blot method by assessing type II microtubule-associated protein 1 (MAP1) light chain 3 (LC3) and Beclin 1 expression levels relative to β-actin. Results indicated an increased ratio of LC3-II to β-actin in splenocytes of C57BL/6 mice only at 7 day post infection (d.p.i.) compared to uninfected animals. LC3-II/β-actin and Beclin 1/β-actin ratios in splenocytes of BALB/c mice increased at 5 d.p.i. and remained high until day 14 and 7 p.i., respectively. We confirmed the formation of autophagosome structures in the spleen of BALB/c mice by transmission electron microscopy (TEM). Moreover, autophagy accompanied necrosis in the splenocytes of infected animals. Results suggest that ECTV-MOS induced autophagy, especially in the spleen of the susceptible mouse strain, may support viral replication and promote cell necrosis.
5

Changes in the mitochondrial network during ectromelia virus infection of permissive L929 cells

71%
Gregorczyk K. P., Szulc-Dabrowska L., Wyzewski Z., Struzik J., Niemialtowski M.
Acta Biochimica Polonica
|
2014
|
tom 61
|
nr 1
Mitochondria are extremely important organelles in the life of a cell. Recent studies indicate that mitochondria also play a fundamental role in the cellular innate immune mechanisms against viral infections. Moreover, mitochondria are able to alter their shape continuously through fusion and fission. These tightly regulated processes are activated or inhibited under physiological or pathological (e.g. viral infection) conditions to help restore homeostasis. However, many types of viruses, such as orthopoxviruses, have developed various strategies to evade the mitochondrial-mediated antiviral innate immune responses. Moreover, orthopoxviruses exploit the mitochondria for their survival. Such viral activity has been reported during vaccinia virus (VACV) infection. Our study shows that the Moscow strain of ectromelia virus (ECTV-MOS), an orthopoxvirus, alters the mitochondrial network in permissive L929 cells. Upon infection, the branching structure of the mitochondrial network collapses and becomes disorganized followed by destruction of mitochondrial tubules during the late stage of infection. Small, discrete mitochondria co-localize with progeny virions, close to the cell membrane. Furthermore, clustering of mitochondria is observed around viral factories, particularly between the nucleus and viroplasm. Our findings suggest that ECTV-MOS modulates mitochondrial cellular distribution during later stages of the replication cycle, probably enabling viral replication and/or assembly as well as transport of progeny virions inside the cell. However, this requires further investigation.
6

Influence of ectromella virus infection on caphepsins and cystatins gene expression in bone marrow-derived dendritic cells

61%
Bossowska-Nowicka M., Toka F. N., Mielcarska M. B., Romaniewicz M., Kaczmarek M. M., Struzik J., Szulc-Dabrowska L.
Postępy Mikrobiologii. Suplement
|
2017
|
tom 56
|
nr 1
7

Rola mitochondriów w odporności przeciwwirusowej

61%
Gregorczyk K. P., Wyzewski Z., Szulc-Dabrowska L., Struzik J., Szczepanowska J., Niemialtowski M.
Postępy Mikrobiologii
|
2014
|
tom 53
|
nr 3
8

Mitochondrial heat shock response induced by ectromelia virus is accompanied by reduced apoptotic potential in murine L929 fibroblasts

51%
Wyzewski Z., Gregorczyk-Zboroch K. P., Mielcarska M. B., Bossowska-Nowicka M., Struzik J., Szczepanowska J., Toka F. N., Niemialtowski M. G., Szulc-Dabrowska L.
Archivum Immunologiae et Therapiae Experimentalis
|
2019
|
tom 67
|
nr 6
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