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10.1128/JVI.01172-20

http://scihub22266oqcxt.onion/10.1128/JVI.01172-20
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33144319!7925085!33144319
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suck abstract from ncbi


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pmid33144319      J+Virol 2021 ; 95 (3): ä
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  • Middle East Respiratory Syndrome Coronavirus Gene 5 Modulates Pathogenesis in Mice #MMPMID33144319
  • Gutierrez-Alvarez J; Wang L; Fernandez-Delgado R; Li K; McCray PB Jr; Perlman S; Sola I; Zuniga S; Enjuanes L
  • J Virol 2021[Jan]; 95 (3): ä PMID33144319show ga
  • Middle East respiratory syndrome coronavirus (MERS-CoV) causes a highly lethal pneumonia that emerged in 2012. There is limited information on MERS-CoV pathogenesis, as data from patients are scarce and the generation of animal models reproducing MERS clinical manifestations has been challenging. Human dipeptidyl peptidase 4 knock-in (hDPP4-KI) mice and a mouse-adapted MERS-CoV strain (MERS(MA)-6-1-2) were recently described. hDPP4-KI mice infected with MERS(MA)-6-1-2 show pathological signs of respiratory disease, high viral titers in the lung, and death. In this work, a mouse-adapted MERS-CoV infectious cDNA was engineered by introducing nonsynonymous mutations contained in the MERS(MA)-6-1-2 genome into a MERS-CoV infectious cDNA, leading to a recombinant mouse-adapted virus (rMERS-MA) that was virulent in hDDP4-KI mice. MERS-CoV adaptation to cell culture or mouse lungs led to mutations and deletions in genus-specific gene 5 that prevented full-length protein expression. In contrast, analysis of 476 MERS-CoV field isolates showed that gene 5 is highly stable in vivo in both humans and camels. To study the role of protein 5, two additional viruses were engineered expressing a full-length gene 5 (rMERS-MA-5FL) or containing a complete gene 5 deletion (rMERS-MA-Delta5). rMERS-MA-5FL virus was unstable, as deletions appeared during passage in different tissue culture cells, highlighting MERS-CoV instability. The virulence of rMERS-MA-Delta5 was analyzed in a sublethal hDPP4-KI mouse model. Unexpectedly, all mice died after infection with rMERS-MA-Delta5, in contrast to those infected with the parental virus, which contains a 17-nucleotide (nt) deletion and a stop codon in protein 5 at position 108. Expression of interferon and proinflammatory cytokines was delayed and dysregulated in the lungs of rMERS-MA-Delta5-infected mice. Overall, these data indicated that the rMERS-MA-Delta5 virus was more virulent than the parental one and suggest that the residual gene 5 sequence present in the mouse-adapted parental virus had a function in ameliorating severe MERS-CoV pathogenesis.IMPORTANCE Middle East respiratory syndrome coronavirus (MERS-CoV) is a zoonotic virus causing human infections with high mortality rate ( approximately 35%). Animal models together with reverse-genetics systems are essential to understand MERS-CoV pathogenesis. We developed a reverse-genetics system for a mouse-adapted MERS-CoV that reproduces the virus behavior observed in humans. This system is highly useful to investigate the role of specific viral genes in pathogenesis. In addition, we described a virus lacking gene 5 expression that is more virulent than the parental one. The data provide novel functions in IFN modulation for gene 5 in the context of viral infection and will help to develop novel antiviral strategies.
  • |*Disease Models, Animal[MESH]
  • |Animals[MESH]
  • |Cell Line[MESH]
  • |Coronavirus Infections/immunology/pathology/*virology[MESH]
  • |Cytokines/metabolism[MESH]
  • |DNA, Complementary/genetics[MESH]
  • |Dipeptidyl Peptidase 4/genetics[MESH]
  • |Genome, Viral/genetics[MESH]
  • |Humans[MESH]
  • |Immunity, Innate[MESH]
  • |Lung/immunology/pathology/virology[MESH]
  • |Mice[MESH]
  • |Mice, Transgenic[MESH]
  • |Middle East Respiratory Syndrome Coronavirus/genetics/*pathogenicity[MESH]
  • |Mutation[MESH]
  • |Viral Load[MESH]
  • |Viral Nonstructural Proteins/genetics/*metabolism[MESH]


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