Antiviral activity of carboxyethylgermanium sesquioxide (Ge-132) in mice infected with influenza virus

H. Aso, Fujio Suzuki, T. Ebina, N. Ishida

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Abstract

The protective effect of carboxyethylgermanium sesquioxide (Ge-132) in mice infected with a mouse-adapted strain of influenza virus (H2N2) was investigated. When mice were exposed to a 10 LD50 dose influenza virus via aerosol and were treated orally with 20 or 100 mg/kg of Ge-132 daily for 6 consecutive days, a significant protective effect was demonstrated. The antiviral effect of Ge-132 was indicated by an increase of survivors, a prolongation of mean survival days, an inhibition of the development of lung consolidation, and a decrease of virus titer in lung tissues, as compared to infected control mice treated with phosphate-buffered saline. Natural killer (NK) cell activity in the spleens and lungs of the infected mice was also significantly augmented after the oral administration of Ge-132. In addition, NK cells stimulated with Ge-132 in vivo showed killing activity against NK-insensitive Meth-A cells infected with influenza virus. Because no virucidal or virustatic activities of Ge-132 on the virus were found in vitro, this protective effect in mice against influenza virus infection may be displayed through immunomodulating activities of this compound such as the augmentation of NK cell activity.

Original languageEnglish (US)
Pages (from-to)180-189
Number of pages10
JournalJournal of Biological Response Modifiers
Volume8
Issue number2
StatePublished - 1989
Externally publishedYes

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Orthomyxoviridae
Antiviral Agents
Natural Killer Cells
Lung
Lethal Dose 50
Virus Diseases
proxigermanium
Aerosols
Viral Load
Oral Administration
Spleen
Phosphates
Viruses

ASJC Scopus subject areas

  • Cancer Research
  • Immunology
  • Pharmacology

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Antiviral activity of carboxyethylgermanium sesquioxide (Ge-132) in mice infected with influenza virus. / Aso, H.; Suzuki, Fujio; Ebina, T.; Ishida, N.

In: Journal of Biological Response Modifiers, Vol. 8, No. 2, 1989, p. 180-189.

Research output: Contribution to journalArticle

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