Effect of Interferon on Experimental Vaccinia and Herpes-Simplex Virus Infections in Rabbits' Eyes

Cantell, Kari; Tommila, V.

doi:10.1016/s0140-6736(60)91751-7

Cited by 72 publications

(17 citation statements)

References 7 publications

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“…For an interferon inducer to be effective against a virus infection in humans, the particu- are generally regarded as relatively insensitive to the effects of interferon (5,11,13). The type 2 strains of HVH have been reported to be more sensitive than type 1 strains to poly(I:C) (24).…”

Section: Discussionmentioning

confidence: 99%

“…Results from a number of laboratories suggest that it may be successful in the prevention or treatment of certain viral infections in vitro as well as in infections of animals and humans (11,12,14,17,20). Although members of the herpesvirus group are relatively insensitive to the action of interferon (5,11,13), evidence suggests that interferon or interferon inducers may be efficacious in certain experimental herpetic infections. The synthetic double-stranded ribonucleic acid inducer of interferon, polyinosinic-polycytidylic acid [poly(I:C)], has been reported to be effective against Herpesvirus hominis (HVH) encephalitis in mice (6,7,15) and HVH keratoconjunctivitis in rabbits (15,26).…”

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confidence: 99%

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Herpesvirus hominis Infection in Newborn Mice: Treatment with Interferon Inducer Polyinosinic-Polycytidylic Acid

Kern

Overall²,

Glasgow³

1975

Antimicrob Agents Chemother

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Intranasal inoculation of newborn mice with Herpesvirus hominis (HVH) type 2 provides a model for disseminated herpesvirus infections of human newborn infants. Treatment of this experimental infection with polyinosinic-polycytidylic acid [poly(I:C)] significantly increased the mean survival time and markedly altered the pathogenesis of the infection. No significant protection against final mortality was observed. Poly(I:C) therapy completely inhibited detectable viral replication in all target organs tested except the brain. In the brain there was a 2-day delay in the onset of viral replication in treated animals, which correlated with the 1- to 2-day increase in mean survival time. In general, the control of HVH replication occurred in those target organs in which poly(I:C)-induced interferon was detectable. The failure of poly(I:C) to alter the final mortality of newborn mice infected with HVH appears to be primarily due to the lack of sufficient levels of interferon induced in brain tissue and the failure to prevent viral replication in this critical target organ.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Herpesvirus hominis Infection in Newborn Mice: Treatment with Interferon Inducer Polyinosinic-Polycytidylic Acid

Kern

Overall²,

Glasgow³

1975

Antimicrob Agents Chemother

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“…The results shown in Table 3 indicate that interferon was effective in modifying peritoneal, dermal and intravenous routes of infection, whereas after infection by intracerebral, corneal and intranasal routes it either had no effect or only a suggestive effect. Difficulty in protection with interferon against infection by the corneal route has been described before (22,23). Intraperitoneal route was previously found to be an effective site of interference with po]yoma virus by herpes simplex virus (24).…”

Section: Passive Trans/er O/inter/eronmentioning

confidence: 99%

The effect of trauma on production of herpes interferon in guinea pigs

Tokumaru

1967

Archiv f Virusforschung

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The adverse effect of trauma on host resistance has been one of the basic concepts in immunology. Recent studies of virus-induced interferons have shown that their production was supressed by trauma-type conditions, such as those produced by X-ray irradiation (1), the administration of steroids (see 2) or antimetabolites (3--5) as well as cold (6--7) and stress (8).It is well known that, among viral infections, those of herpes simplex virus are particularly sensitive to traumatic insults to the hosts, which may elicit an overt infection from a quiescent focus. In view of a possible role of interferon in resistance to this virus, determinations were made of the levels of interferon production in guinea pigs challenged with herpes simplex virus following traumatic insults. The results to be described hereafter seem to suggest both an active role of interferon in resistance to this virus and a marked susceptibility of interferon-producing system to trauma. Materials and MethodsTissue cultures. Two types of cells, primary rabbit and guinea pig kidney cells were used. The procedure for preparing the former has been described previottsly (9--10). The latter cells were prepared from guinea pig embryo kidneys. The minced tissue was first trypsinized with 0.1 ~o Trypsin (Difco 1:250) for 2 hours at room temperature. The cells then were centrifuged at 500 r.p.m, for 20 rain. The sedimented cells were resuspended in the growth medium in a concentration of l0 s cells per ml. and distributed in tissue culture tubes (1 ml./tube) and 4 oz. Sani-prescription bottles (5 ml./bottle)

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“…In addition, activators of CAMP have been reported to enhance the antiviral activity of IFN (t,16). In view of recent observations that herpes simplex virus (HSV) type 1 decreased the intraeeIlular CAMP levels in baby hamster kidney cells (2), and in HF and HEp-2 cell cultures (19), it was of interest to determine whether changes in the intraeellular levels of cyclic nucleotides could account for the relatively low sensitivity of HSV-1 and HSV-2 to the antiviral action of IFN (3,4,9,12,13,17). In this study, the intracellular levels of cyclic nucleotides were monitored in HF cultures that were infected with HSV-1, HSV-2 or VSV and administered IFN.…”

Section: Introductionmentioning

confidence: 99%

Effect of cyclic AMP and cyclic GMP on the activity of interferon against herpes simplex virus types 1 and 2, and vesicular stomatitis virus

Stanwick

Nahmias

1982

Archives of Virology

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The antiviral action of interferon (IFN) on herpes simplex virus (HSV) types 1 and 2, and vesicular stomatitis virus (VSV) was examined with respect to the intracellular levels of cyclic adenosine monophosphate (CAMP) and cyclic guanosine monophosphate (CGMP) in human fibroblast (HF) cultures. Interferon by itself increased the intracellular levels of CAMP, but had no effect on the CGMP levels. Inoculation of HF with HSV, however, decreased the CAMP levels. Also, HSV inoculation elevated the CGMP levels, but VSV did not alter the CGMP levels. When HSV and IFN were added to the HF cultures in various combinations, HSV inhibited the IFN-induced elevation of CAMP and increased the CGMP levels to that characteristically observed with HSV inoculation in the absence of IFN. In contrast, IFN antagonized the VSV-associated decrease in CAMP levels. Although the yields of VSV were unaltered by the presence of CAMP- or CGMP-enhancing compounds, the yields of HSV were decreased with CAMP enhancers and increased with CGMP enhancers. the combination of IFN and CAMP enhancers had an additive effect in reducing the yields of HSV. Neither the CAMP or CGMP enhancers affected the action of IFN on VSV. These studies suggest that the interactions observed between HSV and cyclic nucleotides might account for the relatively refractive nature of HSV, as compared to VSV, toward the antiviral activity of IFN.

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Effect of Interferon on Experimental Vaccinia and Herpes-Simplex Virus Infections in Rabbits' Eyes

Cited by 72 publications

References 7 publications

Herpesvirus hominis Infection in Newborn Mice: Treatment with Interferon Inducer Polyinosinic-Polycytidylic Acid

Herpesvirus hominis Infection in Newborn Mice: Treatment with Interferon Inducer Polyinosinic-Polycytidylic Acid

The effect of trauma on production of herpes interferon in guinea pigs

Effect of cyclic AMP and cyclic GMP on the activity of interferon against herpes simplex virus types 1 and 2, and vesicular stomatitis virus

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