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2017 ; 8
(ä): 1220
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Induction of Apoptosis and Subsequent Phagocytosis of Virus-Infected Cells As an
Antiviral Mechanism
#MMPMID29033939
Nainu F
; Shiratsuchi A
; Nakanishi Y
Front Immunol
2017[]; 8
(ä): 1220
PMID29033939
show ga
Viruses are infectious entities that hijack host replication machineries to
produce their progeny, resulting, in most cases, in disease and, sometimes, in
death in infected host organisms. Hosts are equipped with an array of defense
mechanisms that span from innate to adaptive as well as from humoral to cellular
immune responses. We previously demonstrated that mouse cells underwent apoptosis
in response to influenza virus infection. These apoptotic, virus-infected cells
were then targeted for engulfment by macrophages and neutrophils. We more
recently reported similar findings in the fruit fly Drosophila melanogaster,
which lacks adaptive immunity, after an infection with Drosophila C virus. In
these experiments, the inhibition of phagocytosis led to severe influenza
pathologies in mice and early death in Drosophila. Therefore, the induction of
apoptosis and subsequent phagocytosis of virus-infected cells appear to be an
antiviral innate immune mechanism that is conserved among multicellular
organisms. We herein discuss the underlying mechanisms and significance of the
apoptosis-dependent phagocytosis of virus-infected cells. Investigations on the
molecular and cellular features responsible for this underrepresented virus-host
interaction may provide a promising avenue for the discovery of novel substances
that are targeted in medical treatments against virus-induced intractable
diseases.