PMID- 11369881
OWN - NLM
STAT- MEDLINE
DCOM- 20010628
LR  - 20200217
IS  - 0022-1317 (Print)
IS  - 0022-1317 (Linking)
VI  - 82
IP  - Pt 6
DP  - 2001 Jun
TI  - The role of the Type I interferon response in the resistance of mice to filovirus 
      infection.
PG  - 1365-1373
LID - 10.1099/0022-1317-82-6-1365 [doi]
AB  - Adult immunocompetent mice inoculated with Ebola (EBO) or Marburg (MBG) virus do 
      not become ill. A suckling-mouse-passaged variant of EBO Zaire '76 
      ('mouse-adapted EBO-Z') causes rapidly lethal infection in adult mice after 
      intraperitoneal (i.p.) inoculation, but does not cause apparent disease when 
      inoculated subcutaneously (s.c.). A series of experiments showed that both forms 
      of resistance to infection are mediated by the Type I interferon response. Mice 
      lacking the cell-surface IFN-alpha/beta receptor died within a week after 
      inoculation of EBO-Z '76, EBO Sudan, MBG Musoke or MBG Ravn, or after s.c. 
      challenge with mouse-adapted EBO-Z. EBO Reston and EBO Ivory Coast did not cause 
      illness, but immunized the mice against subsequent challenge with mouse-adapted 
      EBO-Z. Normal adult mice treated with antibodies against murine IFN-alpha/beta 
      could also be lethally infected with i.p.-inoculated EBO-Z '76 or EBO Sudan and 
      with s.c.-inoculated mouse-adapted EBO-Z. Severe combined immunodeficient (SCID) 
      mice became ill 3-4 weeks after inoculation with EBO-Z '76, EBO Sudan or MBG 
      Ravn, but not the other viruses. Treatment with anti-IFN-alpha/beta antibodies 
      markedly accelerated the course of EBO-Z '76 infection. Antibody treatment 
      blocked the effect of a potent antiviral drug, 3-deazaneplanocin A, indicating 
      that successful filovirus therapy may require the active participation of the 
      Type I IFN response. Mice lacking an IFN-alpha/beta response resemble primates in 
      their susceptibility to rapidly progressive, overwhelming filovirus infection. 
      The outcome of filovirus transfer between animal species appears to be determined 
      by interactions between the virus and the innate immune response.
FAU - Bray, Mike
AU  - Bray M
AD  - Department of Viral Therapeutics, Virology Division, United States Army Medical 
      Research Institute of Infectious Diseases, 1425 Porter Street, Fort Detrick, 
      Frederick, MD 21702-5011, USA1.
LA  - eng
PT  - Journal Article
PL  - England
TA  - J Gen Virol
JT  - The Journal of general virology
JID - 0077340
RN  - 0 (Antibodies)
RN  - 0 (Antiviral Agents)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Interferon Type I)
RN  - 0 (Membrane Proteins)
RN  - 0 (Receptors, Interferon)
RN  - 0 (STAT1 Transcription Factor)
RN  - 0 (Stat1 protein, mouse)
RN  - 0 (Trans-Activators)
RN  - 156986-95-7 (Receptor, Interferon alpha-beta)
RN  - 544SH4020S (3-deazaneplanocin)
RN  - K72T3FS567 (Adenosine)
SB  - IM
MH  - Adenosine/analogs & derivatives/therapeutic use
MH  - Animals
MH  - Animals, Suckling/immunology/virology
MH  - Antibodies/immunology
MH  - Antiviral Agents/therapeutic use
MH  - DNA-Binding Proteins/genetics/metabolism
MH  - Disease Susceptibility/immunology
MH  - Filoviridae/*immunology/pathogenicity
MH  - Filoviridae Infections/drug therapy/*immunology/virology
MH  - Gene Deletion
MH  - Immunization
MH  - Injections, Intraperitoneal
MH  - Injections, Subcutaneous
MH  - Interferon Type I/genetics/*immunology
MH  - Membrane Proteins
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred Strains
MH  - Mice, Knockout
MH  - Mice, SCID
MH  - Receptor, Interferon alpha-beta
MH  - Receptors, Interferon/genetics/immunology/metabolism
MH  - STAT1 Transcription Factor
MH  - Species Specificity
MH  - Survival Rate
MH  - Trans-Activators/genetics/metabolism
MH  - Virulence/genetics
MH  - Weight Loss
EDAT- 2001/05/23 10:00
MHDA- 2001/06/29 10:01
CRDT- 2001/05/23 10:00
PHST- 2001/05/23 10:00 [pubmed]
PHST- 2001/06/29 10:01 [medline]
PHST- 2001/05/23 10:00 [entrez]
AID - 10.1099/0022-1317-82-6-1365 [doi]
PST - ppublish
SO  - J Gen Virol. 2001 Jun;82(Pt 6):1365-1373. doi: 10.1099/0022-1317-82-6-1365.