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Development of mouse models for analysis of human virus infections.

Abstract Viruses usually exhibit strict species-specificity as a result of co-evolution with the host. Thus, in mouse models, a great barrier exists for analysis of infections with human-tropic viruses. Mouse models are unlikely to faithfully reproduce the human immune response to viruses or viral compounds and it is difficult to evaluate human therapeutic efficacy with antiviral reagents in mouse models. Humans and mice essentially have different immune systems, which makes it difficult to extrapolate mouse results to humans. In addition, apart from immunological reasons, viruses causing human diseases do not always infect mice because of species tropism. One way to determine tropism would be a virus receptor that is expressed on affected cells. The development of gene-disrupted mice and Tg mice, which express human receptor genes, enables us to analyze several viral infections in mice. Mice are, indeed, susceptible to human viruses when artificially infected in receptor-supplemented mice. Although the mouse cells less efficiently permit viral replication than do human cells, the models for analysis of human viruses have been established in vivo as well as in vitro, and explain viral pathogenesis in the mouse systems. In most systems, however, nucleic acid sensors and type I interferon suppress viral propagation to block the appearance of infectious manifestation. We herein review recent insight into in vivo antiviral responses induced in mouse infection models for typical human viruses.
PMID
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Authors

Mayor MeshTerms

Disease Models, Animal

Mice

Keywords

animal model

type I IFN

viral infection

Journal Title microbiology and immunology
Publication Year Start




PMID- 28370181
OWN - NLM
STAT- MEDLINE
DA  - 20170403
DCOM- 20170418
LR  - 20170418
IS  - 1348-0421 (Electronic)
IS  - 0385-5600 (Linking)
VI  - 61
IP  - 3-4
DP  - 2017 Apr
TI  - Development of mouse models for analysis of human virus infections.
PG  - 107-113
LID - 10.1111/1348-0421.12477 [doi]
AB  - Viruses usually exhibit strict species-specificity as a result of co-evolution
      with the host. Thus, in mouse models, a great barrier exists for analysis of
      infections with human-tropic viruses. Mouse models are unlikely to faithfully
      reproduce the human immune response to viruses or viral compounds and it is
      difficult to evaluate human therapeutic efficacy with antiviral reagents in mouse
      models. Humans and mice essentially have different immune systems, which makes it
      difficult to extrapolate mouse results to humans. In addition, apart from
      immunological reasons, viruses causing human diseases do not always infect mice
      because of species tropism. One way to determine tropism would be a virus
      receptor that is expressed on affected cells. The development of gene-disrupted
      mice and Tg mice, which express human receptor genes, enables us to analyze
      several viral infections in mice. Mice are, indeed, susceptible to human viruses 
      when artificially infected in receptor-supplemented mice. Although the mouse
      cells less efficiently permit viral replication than do human cells, the models
      for analysis of human viruses have been established in vivo as well as in vitro, 
      and explain viral pathogenesis in the mouse systems. In most systems, however,
      nucleic acid sensors and type I interferon suppress viral propagation to block
      the appearance of infectious manifestation. We herein review recent insight into 
      in vivo antiviral responses induced in mouse infection models for typical human
      viruses.
CI  - (c) 2017 The Societies and John Wiley & Sons Australia, Ltd.
FAU - Takaki, Hiromi
AU  - Takaki H
AD  - Department of Microbiology and Immunology, Graduate School of Medicine, Hokkaido 
      University, Sapporo.
FAU - Oshiumi, Hiroyuki
AU  - Oshiumi H
AD  - Department of Immunology, Graduate School of Medical Sciences, Kumamoto
      University, Kumamoto.
FAU - Shingai, Masashi
AU  - Shingai M
AD  - Laboratory for Biologics Development, Research Center for Zoonosis Control,
      GI-CoRE Global Station for Zoonosis Control, Hokkaido University, Sapporo, Japan.
FAU - Matsumoto, Misako
AU  - Matsumoto M
AD  - Department of Microbiology and Immunology, Graduate School of Medicine, Hokkaido 
      University, Sapporo.
FAU - Seya, Tsukasa
AU  - Seya T
AD  - Department of Microbiology and Immunology, Graduate School of Medicine, Hokkaido 
      University, Sapporo.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - Australia
TA  - Microbiol Immunol
JT  - Microbiology and immunology
JID - 7703966
SB  - IM
MH  - Animals
MH  - Animals, Genetically Modified
MH  - *Disease Models, Animal
MH  - Humans
MH  - Immunity, Innate
MH  - *Mice
MH  - Viral Tropism
MH  - Virus Diseases/*pathology/*virology
OTO - NOTNLM
OT  - animal model
OT  - type I IFN
OT  - viral infection
EDAT- 2017/04/04 06:00
MHDA- 2017/04/19 06:00
CRDT- 2017/04/04 06:00
PHST- 2017/03/20 [received]
PHST- 2017/03/23 [accepted]
AID - 10.1111/1348-0421.12477 [doi]
PST - ppublish
SO  - Microbiol Immunol. 2017 Apr;61(3-4):107-113. doi: 10.1111/1348-0421.12477.

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