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10.1002/jcp.27155 http://scihub22266oqcxt.onion/10.1002/jcp.27155 30146782!7166610!30146782     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Cell+Physiol 2019 ; 234 (3): 2143-2151 Nephropedia Template TP {{tp|p=30146782|t=2019. Modulation of the immune response by Middle East respiratory syndrome coronavirus |pdf=|usr=}}{{30146782}} gab.com Text Modulation of the immune response by Middle East respiratory syndrome coronavirus JO: J Cell Physiol http://www.kidney.de/pget.php?&tw=1&pmid=30146782 #FOAvip Coronavirus (CoV) infections are commonly associated with respiratory and enteric disease in humans and animals. In 2012, a new human disease called Middle East respiratory syndrome (MERS) emerged in the Middle East. MERS was caused by a virus that was originally called human coronavirus-Erasmus Medical Center/2012 but was later renamed as Middle East respiratory syndrome coronavirus (MERS-CoV). MERS-CoV causes high fever, cough, acute respiratory tract infection, and multiorgan dysfunction that may eventually lead to the death of the infected individuals. The exact origin of MERS-CoV remains unknown, but the transmission pattern and evidence from virological studies suggest that dromedary camels are the major reservoir host, from which human infections may sporadically occur through the zoonotic transmission. Human to human transmission also occurs in healthcare facilities and communities. Recent studies on Middle Eastern respiratory continue to highlight the need for further understanding the virus-host interactions that govern disease severity and infection outcome. In this review, we have highlighted the major mechanisms of immune evasion strategies of MERS-CoV. We have demonstrated that M, 4a, 4b proteins and Plppro of MERS-CoV inhibit the type I interferon (IFN) and nuclear factor-kappaB signaling pathways and therefore facilitate innate immune evasion. In addition, nonstructural protein 4a (NSP4a), NSP4b, and NSP15 inhibit double-stranded RNA sensors. Therefore, the mentioned proteins limit early induction of IFN and cause rapid apoptosis of macrophages. MERS-CoV strongly inhibits the activation of T cells with downregulation of antigen presentation. In addition, uncontrolled secretion of interferon ?-induced protein 10 and monocyte chemoattractant protein-1 can suppress proliferation of human myeloid progenitor cells. Twit Text FOAVip Modulation of the immune response by Middle East respiratory syndrome coronavirus ????J Cell Physiol http://www.kidney.de/pget.php?&tw=1&pmid=30146782 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30146782 #FOAvip English Wikipedia <ref>{{Cite pmid|30146782}}</ref> Modulation of the immune response by Middle East respiratory syndrome coronavirus #MMPMID30146782 Shokri S; Mahmoudvand S; Taherkhani R; Farshadpour F J Cell Physiol 2019[Mar]; 234 (3): 2143-2151 PMID30146782show ga Coronavirus (CoV) infections are commonly associated with respiratory and enteric disease in humans and animals. In 2012, a new human disease called Middle East respiratory syndrome (MERS) emerged in the Middle East. MERS was caused by a virus that was originally called human coronavirus-Erasmus Medical Center/2012 but was later renamed as Middle East respiratory syndrome coronavirus (MERS-CoV). MERS-CoV causes high fever, cough, acute respiratory tract infection, and multiorgan dysfunction that may eventually lead to the death of the infected individuals. The exact origin of MERS-CoV remains unknown, but the transmission pattern and evidence from virological studies suggest that dromedary camels are the major reservoir host, from which human infections may sporadically occur through the zoonotic transmission. Human to human transmission also occurs in healthcare facilities and communities. Recent studies on Middle Eastern respiratory continue to highlight the need for further understanding the virus-host interactions that govern disease severity and infection outcome. In this review, we have highlighted the major mechanisms of immune evasion strategies of MERS-CoV. We have demonstrated that M, 4a, 4b proteins and Plppro of MERS-CoV inhibit the type I interferon (IFN) and nuclear factor-kappaB signaling pathways and therefore facilitate innate immune evasion. In addition, nonstructural protein 4a (NSP4a), NSP4b, and NSP15 inhibit double-stranded RNA sensors. Therefore, the mentioned proteins limit early induction of IFN and cause rapid apoptosis of macrophages. MERS-CoV strongly inhibits the activation of T cells with downregulation of antigen presentation. In addition, uncontrolled secretion of interferon ?-induced protein 10 and monocyte chemoattractant protein-1 can suppress proliferation of human myeloid progenitor cells. |Coronavirus Infections/*immunology/pathology/virology[MESH] |Host-Pathogen Interactions/immunology[MESH] |Humans[MESH] |Immune Evasion/genetics[MESH] |Immunity, Innate/*genetics[MESH]Modulation of the immune response by Middle East respiratory syndrome (epmc).pdf DeepDyve Pubget Overpricing