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2015 ; 12
(ä): 218
Nephropedia Template TP
gab.com Text
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English Wikipedia
Middle East respiratory syndrome coronavirus infection: virus-host cell
interactions and implications on pathogenesis
#MMPMID26690369
Zhou J
; Chu H
; Chan JF
; Yuen KY
Virol J
2015[Dec]; 12
(ä): 218
PMID26690369
show ga
Middle-East Respiratory Syndrome coronavirus (MERS-CoV) was identified to cause
severe respiratory infection in humans since 2012. The continuing MERS epidemic
with a case-fatality of more than 30% poses a major threat to public health
worldwide. Currently, the pathogenesis of human MERS-CoV infection remains poorly
understood. We reviewed experimental findings from human primary cells and ex
vivo human lung tissues, as well as those from animal studies, so as to
understand the pathogenesis and high case-fatality of MERS. Human respiratory
epithelial cells are highly susceptible to MERS-CoV and can support productive
viral replication. However, the induction of antiviral cytokines and
proinflammatory cytokines/chemokines are substantially dampened in the infected
epithelial cells, due to the antagonistic mechanisms evolved by the virus.
MERS-CoV can readily infect and robustly replicate in human macrophages and
dendritic cells, triggering the aberrant production of proinflammatory
cytokines/chemokines. MERS-CoV can also effectively infect human primary T cells
and induce massive apoptosis in these cells. Although data from clinical, in
vitro and ex vivo studies suggested the potential for virus dissemination,
extrapulmonary involvement in MERS patients has not been ascertained due to the
lack of autopsy study. In MERS-CoV permissive animal models, although viral RNA
can be detected from multiple organs of the affected animals, the brain of human
DPP4-transgenic mouse was the only extrapulmonary organ from which the infectious
virus can be recovered. More research findings on the pathogenesis of MERS and
the tissue tropisms of MERS-CoV may help to improve the treatment and infection
control of MERS.