The Epstein–Barr virus (EBV) is a human gamma-herpesvirus that is impl translation - The Epstein–Barr virus (EBV) is a human gamma-herpesvirus that is impl Russian how to say

The Epstein–Barr virus (EBV) is a h

The Epstein–Barr virus (EBV) is a human gamma-herpesvirus that is implicated in various types of proliferative diseases. Upon infection, it predominantly establishes latency in B cells and cannot ever be eradicated; it persists for the host's lifetime. Reactivation of the virus from latency depends on expression of the viral immediate-early gene, BamHI Z fragment leftward open reading frame 1 (BZLF1). The BZLF1 promoter normally exhibits only low basal activity but is activated in response to chemical or biological inducers, such as 12-O-tetradecanoylphorbol-13-acetate, calcium ionophore, histone deacetylase inhibitor, or anti-Ig. Transcription from the BZLF1 promoter is activated by myocyte enhancer factor 2, specificity protein 1, b-Zip type transcription factors and mediating epigenetic modifications of the promoter, such as histone acetylation and H3K4me3. In contrast, repression of the promoter is mediated by transcriptional suppressors, such as ZEB, ZIIR-BP, and jun dimerization protein 2, causing suppressive histone modifications like histone H3K27me3, H3K9me2/3 and H4K20me3. Interestingly, there is little CpG DNA methylation of the promoter, indicating that DNA methylation is not crucial for suppression of BZLF1. This review will focus on the molecular mechanisms by which the EBV lytic switch is controlled and discuss the physiological significance of this switching for its survival and oncogenesis.
The EBV is a human gamma-herpesvirus with a double-stranded DNA genome. Similar to other herpesviruses, the genome of EBV is long (∼170 kb) and encodes more than 80 genes, indicating that it is a huge virus with a complicated lifecycle. EBV is a ubiquitous virus, infecting more than 90% of the population worldwide. It is transmitted via saliva from close family members, mostly during infancy or childhood. Upon infection, it establishes a latent infection, predominantly in B cells, and remains in the host for their lifetime. Primary infection during infancy is generally asymptomatic; however, primary infection in adolescence or adulthood can cause infectious mononucleosis. In addition, EBV is associated with several human malignancies, including Burkitt lymphoma, Hodgkin disease, nasopharyngeal carcinoma, gastric cancer, T/NK lymphoma, and AIDS- or transplantation-associated lymphomas
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The Epstein–Barr virus (EBV) is a human gamma-herpesvirus that is implicated in various types of proliferative diseases. Upon infection, it predominantly establishes latency in B cells and cannot ever be eradicated; it persists for the host's lifetime. Reactivation of the virus from latency depends on expression of the viral immediate-early gene, BamHI Z fragment leftward open reading frame 1 (BZLF1). The BZLF1 promoter normally exhibits only low basal activity but is activated in response to chemical or biological inducers, such as 12-O-tetradecanoylphorbol-13-acetate, calcium ionophore, histone deacetylase inhibitor, or anti-Ig. Transcription from the BZLF1 promoter is activated by myocyte enhancer factor 2, specificity protein 1, b-Zip type transcription factors and mediating epigenetic modifications of the promoter, such as histone acetylation and H3K4me3. In contrast, repression of the promoter is mediated by transcriptional suppressors, such as ZEB, ZIIR-BP, and jun dimerization protein 2, causing suppressive histone modifications like histone H3K27me3, H3K9me2/3 and H4K20me3. Interestingly, there is little CpG DNA methylation of the promoter, indicating that DNA methylation is not crucial for suppression of BZLF1. This review will focus on the molecular mechanisms by which the EBV lytic switch is controlled and discuss the physiological significance of this switching for its survival and oncogenesis.The EBV is a human gamma-herpesvirus with a double-stranded DNA genome. Similar to other herpesviruses, the genome of EBV is long (∼170 kb) and encodes more than 80 genes, indicating that it is a huge virus with a complicated lifecycle. EBV is a ubiquitous virus, infecting more than 90% of the population worldwide. It is transmitted via saliva from close family members, mostly during infancy or childhood. Upon infection, it establishes a latent infection, predominantly in B cells, and remains in the host for their lifetime. Primary infection during infancy is generally asymptomatic; however, primary infection in adolescence or adulthood can cause infectious mononucleosis. In addition, EBV is associated with several human malignancies, including Burkitt lymphoma, Hodgkin disease, nasopharyngeal carcinoma, gastric cancer, T/NK lymphoma, and AIDS- or transplantation-associated lymphomas
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эпштейн - барра на вирус (ebv) is a human гамма - herpesvirus, причастного к различным видам proliferative заболеваний.от инфекции, то главным образом предусматривает задержки в клетки и никогда не может быть ликвидирована; он по - прежнему хозяина жизни.возобновление этого вируса от латентного зависит от выражения вирусный непосредственно ранние гены, bamhi z фрагмент leftward открытая рамка считывания 1 (bzlf1).в bzlf1 промоутер обычно выставки только низкой основной деятельности, но включается в ответ на химического или биологического inducers, таких, как 12-o-tetradecanoylphorbol-13-acetate, кальций ionophore, деацетилазы гистонов ингибитор, или с ги.транскрипция из bzlf1 промоутер активируется myocyte Enhancer коэффициент 2, специфика белков, 1, b-zip типа факторы транскрипции эпигенетические изменения и посредничеству, промоутером, таких как гистоны acetylation и h3k4me3.в отличие от репрессий в отношении организатора сопровождается transcriptional suppressors, например, зеб, ziir-bp и чжун 3 белка - 2, в результате чего пл гистоны изменения как гистоны h3k27me3, h3k9me2 / 3 и h4k20me3.интересно, что мало цнп метилирование днк от организатора акции, указав, что метилирование днк не решающее значение для пресечения bzlf1.этот обзор будет посвящен молекулярных механизмов, с помощью которых ebv lytic выключатель находится под контролем и обсудить физиологическое значение этого перехода для своего выживания и oncogenesis.в ebv является одним из прав гамма - herpesvirus с двухспиральный генома днк.как и другие herpesviruses, геном ebv давно (∼ 170, что кб) и кодирует более 80 гены, указав, что это огромная вирус со сложной жизни.ebv является повсеместное вирус, заражая более 90% населения во всем мире.он передается через слюну от близких членов семьи, в основном в младенческом возрасте или в детстве.после заражения, она устанавливает скрытые инфекции, главным образом в клетки, и по - прежнему в принимающей их жизни.первичная инфекция в младенческом возрасте, как правило, бессимптомно, однако первичная инфекция в подростковом или во взрослую жизнь, может вызвать инфекционный мононуклеоз.кроме того, ebv ассоциируется с ряда прав онкологические заболевания, в том числе burkitt лимфомы ходжкина - заболевания, назофарингеальная карцинома, рака желудка, т / нк лимфома, и спид - ассоциированных или трансплантации лимфомы
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