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Selective antiviral activity of human interferons on primate oncogenic and neurotropic herpesviruses
Author(s) -
Daniel Muthiah D.,
Tamulevich Ruth,
Bekesi J. George,
King Norval W.,
Falk Lawrence A.,
Silva Daniel,
Holland James F.
Publication year - 1981
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910270118
Subject(s) - interferon , virus , virology , herpes simplex virus , biology , viral replication , cytopathic effect , neurotropic virus
Human lymphoblastic, leukocytic and fibroblastic interferons were found to have marked antiviral activity on the replication of Herpes virus saimiri and Herpes virus ateles when used at a concentration of 500 IU/ml or greater but only minimal activity against two neurotropic viruses, viz. Herpes‐virus platyrrhine and herpes simplex virus. All three interferons were equally effective as antiviral agents against the oncogenic herpesviruses. Pretreatment of cells with interferons before virus infection was not required as it failed to enhance or retard the antiviral action of interferon, particularly in the case of the oncogenic herpesviruses. The m.o.i. of virus ranging from 100 to 0.0002 did not alter the effectiveness of the antiviral ability of interferon which was maintained at these virus concentrations. Interferon was equally effective in suppressing the replication of the two oncogenic viruses at low and high m.o.i. (20 to 0.00002). Interferon was able to suppress the advancement of virus‐induced cell cytopathic effect of HVS‐ and HVA‐infected cell monolayers. This event could be repeated continuously over a period of several months by addition and withdrawal of interferon. Virus‐infected cell monolayers exhibiting advance (75%) of cell cytopathology could be treated with 10,000 IU/ml interferon to attain cell confluency. These treated cells subsequently could be subcultivated (if maintained on 2000 IU/ml interferon) for over 14 months and 20 subpassages with an absence of virus, viral antigens or virus particles. These same cells, if maintained in the absence of interferon during each subpassage level, will produce virus; however, from the 14th subpassaged cell cultures virus appears to have been repressed or lost in the absence of interferon, suggesting that long‐term application of interferon may have a therapeutic effect in ‘eliminating’ virus infection. Owl monkey kidney cells infected with HVS or HVA at a m.o.i. of > 1 (2 and 20) or m.o.i. < 1 (to induce a multicycle infection) were successfully treated with interferon.