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African Swine Fever Virus: a new old enemy of Europe

100%
Cisek A. A., Dabrowska I., Gregorczyk K. P., Wyzewski Z.
Annals of Parasitology
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2016
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tom 62
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nr 3
African swine fever (ASF) is a highly contagious viral disease of swine with a mortality rate approaching 100 percent. African Swine Fever Virus (ASFV) is a double-stranded DNA virus with a complex molecular structure. Its large genome, encoding multiple virulence factors, allows for efficient replication, which takes place predominantly in the cytoplasm of monocytes and macrophages. Also, ASFV has the ability to interfere with cell signalling pathways, which leads to various modulations in the synthesis profiles of interferon and other cytokines. Sustained viremia favours the persistence of virions in blood and tissues of the convalescents, and the extended circulation of ASFV within the herd. ASFV has been spreading in the Caucasus since 2007, and in 2014 reached the eastern territory of the European Union. Outbreaks pose an economical threat to native pig rearing, especially since a single point source may easily develop into an epizootic event. There is currently no effective vaccine nor treatment for ASF, and eradication is possible only by prevention or the slaughter of diseased animals. This review paper summarizes the current state of knowledge about ASFV.
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Strategie hamowania apoptozy przez wirusy zapalenia wątroby typu E i C

100%
Wyzewski Z., Gregorczyk K. P., Niemialtowski M.
Medycyna Weterynaryjna
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2014
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tom 70
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nr 06
Apoptosis is one of the processes of programmed cell death (PCD) in multicellular organism, and it is mediated by an intracellular proteolytic cascade. During viral infections, the host cell is the environment of the pathogen replication cycle. HEV and HCV encode proteins that prevent apoptosis. The ORF2 protein of HEV is responsible for overexpression of antiapoptotic Hsp72 in cells. Envelope glycoproteins E1 and E2 inhibit apoptosis induced by the Fas/Fas-L system. They block the activity of caspase-8 – the enzyme whose inactive form is part of DISC. The core protein HCV is a positive regulator of protein c-FLIP expression. c-FLIP prevents the conversion of caspase-8 zymogen into the mature, active form of the enzyme. NS5A inhibits the activity of p38MAPK, prevents the efflux of potassium ions from the cell, and thereby counteracts apoptosis.
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Hamowanie mitochondrialnego szlaku apoptozy przez białka pokswirusów

100%
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.
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Changes in the mitochondrial network during ectromelia virus infection of permissive L929 cells

88%
Gregorczyk K. P., Szulc-Dabrowska L., Wyzewski Z., Struzik J., Niemialtowski M.
Acta Biochimica Polonica
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2014
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tom 61
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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.
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Rola mitochondriów w odporności przeciwwirusowej

76%
Gregorczyk K. P., Wyzewski Z., Szulc-Dabrowska L., Struzik J., Szczepanowska J., Niemialtowski M.
Postępy Mikrobiologii
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2014
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tom 53
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nr 3
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