2011
DOI: 10.1099/vir.0.030346-0
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Cytokine production by primary human macrophages infected with highly pathogenic H5N1 or pandemic H1N1 2009 influenza viruses

Abstract: Highly pathogenic H5N1 avian influenza viruses have caused infection in humans, with a high mortality rate, since 1997. While the pathogenesis of this infection is not completely understood, hypercytokinaemia and alveolar macrophages are thought to play a role. To gain further insight into the cytokine-mediated pathogenesis of this infection in humans, we measured various cytokines produced by primary human macrophages infected with H5N1, pandemic H1N1 or seasonal influenza viruses. We found that many cytokine… Show more

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Cited by 59 publications
(89 citation statements)
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References 23 publications
(33 reference statements)
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“…The induction of proinflammatory cytokines in response to HPAI H5 infection of human MDMs was inhibited by b-propiolactone-inactivation of the virus [36]. Although this result suggests that replication is required for the induction of proinflammatory cytokines following H5N1 IAV infection of macrophages, b-propiolactone was shown to cause a 16-fold reduction in viral HA activity [61].…”
Section: Iav Replication and Hypercytokinemiamentioning
confidence: 75%
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“…The induction of proinflammatory cytokines in response to HPAI H5 infection of human MDMs was inhibited by b-propiolactone-inactivation of the virus [36]. Although this result suggests that replication is required for the induction of proinflammatory cytokines following H5N1 IAV infection of macrophages, b-propiolactone was shown to cause a 16-fold reduction in viral HA activity [61].…”
Section: Iav Replication and Hypercytokinemiamentioning
confidence: 75%
“…The majority of studies addressing the replication of HPAI H5N1 viruses in human MDMs demonstrate productive virus replication [32,33,[35][36][37]. Moreover, a direct comparison of human MDMs and AMs suggested that, while AMs did not support productive replication of IAV, an HPAI H5N1 virus was more efficient at infecting AMs than seasonal viruses were [37].…”
Section: Replication Of Iav In Macrophagesmentioning
confidence: 99%
“…К ним добавлена питатель-ная среда RPMI-1640, содержащая 40 нг/мл GM-CSF, на 7 дней. Не обнаружено существенных из-менений в морфологии моноцитов 2-х доноров, Полученный результат подтверждает резистент-ность альвеолярных макрофагов c фенотипом М1 к пандемическому и сезонным вирусам гриппа А H1N1 [27]. Влияние GM-CSF на экспрессию генов сигналь-ных иммунных рецепторов TLR7 и RIG1 в моно-цитах GM-CSF является членом семейства цито-кинов, которые регулируют рост, дифференциа-цию, миграцию и эффекторные функции гемо-поэтических клеток и иммуноцитов [10].…”
Section: дифференцировка моноцитов периферической крови доноров в макunclassified
“…Имеет значение источник получения и способ активации Мф, достигаемый Мф уровень диф-ференцировки. Со стороны вируса влияют осо-бенности углеводной структуры гликопротеинов вирусной оболочки, прежде всего ГА и NA, и сте-пень патогенности штаммов и изолятов вирусов гриппа А [14,27]. На поверхности Мф присут-ствуют α-2,3-и α-2,6-связанные сиаловые кис-лоты, с которыми взаимодействуют ГА вирусов гриппа [31].…”
Section: Introductionunclassified
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