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F F Pindak

Publications and source records attributed to F F Pindak.

At least 37 records · Page 2Linked to original sources
PubMed1971

Interferon-inducing characteristics of MM virus.

Interferon induction by MM virus in mice and in L cells was studied. In mice the virus readily induced interferon. The time of appearance was dose-dependent. A large virus dose induced interferon by 4 hr, whereas a small dose resulted in interferon production which paralleled virus replication 24 hr after infection. In L cells the interferon-inducing capacity of the virus was rapidly destroyed by ultraviolet light irradiation. Heating (56 C) of the virus, on the other hand, greatly increased its ability to induce interferon. Interferon production could also be increased by prior treatment of the cells with homologous interferon (priming). The increase in interferon production after priming was dependent on the concentration of interferon used for priming, the length of interferon treatment, and the multiplicity of infection. It is suggested that MM virus might be useful for the further study of the mechanisms involved in the production and action of interferon.

Animals↗
PubMed1971

Inhibition by estrone of the antiviral protection and interferon elicited by interferon inducers in mice.

The susceptibility of mice to infection with MM virus is markedly increased after treatment with the sex hormone estrone. Studies were undertaken to determine if either suppression of production or interference with the action of interferon was involved in this phenomenon. The protection of mice against MM virus infection by several interferon-inducing agents was partially impeded by estrone treatment either 24 hr before or 24 hr after the administration of the inducing agent. The titers of circulating interferon induced by each of the agents were lower in estrone-pretreated animals than in untreated controls. The protection of mice by exogenous L cell interferon was blocked only when the hormone was given prior to the interferon. It is concluded that the adverse activity of estrone is related to its ability to interfere with the action of interferon.

Journal Article↗
PubMed1971

Effect of progesterone and testosterone on interferon production and on the viral infection-enhancing activity of estrone and hydrocortisone.

The effect of progesterone and testosterone on interferon production and on the viral infection-enhancing (VIE) activity of estrone and hydrocortisone was investigated. Neither hormone interfered with interferon production. Progesterone reduced the VIE activity of estrone but not that of hydrocortisone. Testosterone had no effect on the VIE activity of either hormone. It is concluded that the lack of VIE activity by progesterone and testosterone may be related to their inabilities to suppress interferon production. The interference by progesterone with the VIE activity of estrone suggests that, in this system, the two hormones may affect common target cells.

Animals↗
PubMed1970

Resistance to bacterial infection induced by statolon and pyran.

The antibacterial properties of statolon and pyran were compared with those of bacterial endotoxin and found to be similar. Although high resistance was transient, it was followed by immunity of the same order as in mice infected without pre-treatment with the interferon inducers.

Animals↗
PubMed1970

Protection of mice against bacterial infection by interferon inducers.

Antibacterial effect of known interferon inducers was investigated. Intraperitoneal injection of statolon or pyran markedly enhanced the survival of mice challenged with Klebsiella pneumoniae. The sparing effect of these two interferon inducers resembled that of bacterial endotoxin. Significant protection was obtained when the inducers were administered 24 hr before challenge. Treatments given 6 hr before or at the time of infection were ineffective. The persistence of increased resistance of treated animals to encephalomyocarditis virus strain MM, inoculated 5 days after challenge with K. pneumoniae, indicated that the bacterial infection did not adversely influence the induction or effectiveness of interferon.

Journal Article↗
PubMed1969

Propagation of MM virus in L cells.

MM virus (mouse-brain stock) replicated to a limited extent in L cells without cytopathic effects; the average yield was less than 1 plaque-forming unit/cell. Passage in BHK-21 cells resulted in MM virus [MM(BHK)] which replicated to high titers (200 to 300 plaque-forming units/cell) in L cells with complete cytopathic effects. Appearance of mature MM(BHK) virus in L-cell cultures begins 4 hr after infection and is completed by 8 hr. Release of mature virus was slow (less than 1% at 8 hr) but was completed by 24 hr.

Adaptation, Biological↗
PubMed1969

Propagation of MM virus in continuous cell lines.

Baby hamster kidney (BHK), McCoy, and L cell lines were found to be suitable for isolation of MM virus from infected mouse brain tissue. The virus was recovered in high titer in the first passage in BHK and McCoy cells, with concomitant cytopathic effect (CPE). In L cells, virus yield was lower than in the other two cell lines and CPE was incomplete. Adaptation of the virus to BHK and McCoy cells by serial passages was evidenced by accelerated development of the CPE and increase in the virus titer. Plaques were obtained in all three cell lines when inoculated with infected mouse brain or with the tissue culture-propagated virus. In the BHK cells, the virus release preceded the appearance of CPE and maximal yield of virus was obtained after 1 to 3 days of incubation, depending on the size of inoculum. The BHK-propagated virus had the same lethality for mice as did the mouse brain-propagated stock, and there was no difference in the course of the disease caused by the two preparations.

Adaptation, Biological↗
PubMed1969

Influence of statolon on resistance of mice to influenza.

Various interferon inducers are known to elicit protection against lethal or infecting doses of certain viral agents. Because of the relatively high morbidity rate of influenza and its seasonal occurrence, we wished to determine whether statolon-induced interferon might be effective in controlling this disease. Mice were treated intraperitoneally with statolon and challenged with influenza A(2) virus by the intranasal route. Although interferon was present in the serum at the time of virus administration, no change in mortality rate was observed. There was, however, a significant increase in the mean survival time of treated animals. Similar results were obtained when Newcastle disease virus was used as the interferon inducer. To determine the effect of the route of challenge, other mice were treated with statolon or Newcastle disease virus and inoculated with mengovirus by the intranasal or intraperitoneal route. The results demonstrated that the treated mice were protected to similar degree against challenge by either route. It is suggested that the relative ineffectiveness of interferon in protecting mice against influenza is due to an intrinsic characteristic of the virus itself rather than the type of interferon induced or the route of virus challenge.

Animals↗
PubMed1968

Duration of prophylactic effect of statolon against mengovirus in mice.

Intraperitoneal injection of statolon into mice is known to exert a protective effect against a subsequent infection with a variety of viruses owing to stimulation of production of interferon. To study the duration of such protection, groups of mice were treated with 350 mug of statolon at 69, 55, 41, 27, 13, 6, or 1 day prior to a challenge with mengovirus. Other groups were treated with 760 mug at 1 to 6 days before challenge. Ten days after inoculation with the virus, LD(50) determinations were made for each group. Mice which received statolon 1 to 5 days before infection were significantly more resistant to the virus than nontreated controls; no protection could be demonstrated in the other groups.

Animals↗
PubMed1968

Effect of statolon-induced interferon on antibody formation.

The effect of statolon-induced interferon on immune response was investigated. Young adult Swiss albino mice were immunized with chicken red blood cells or infectious mengovirus. The red blood cells were injected three times and the virus twice at 2-week intervals, with or without treatment with statolon 24 hr before the inoculations. The effect of interferon on antibody formation was measured by determinations of hemagglutinating, hemolytic, and virus-neutralizing antibodies in the sera of treated and nontreated groups. The hemagglutinin and hemolysin titers after each successive inoculation were equal in both groups, indicating that interferon had no effect on their production. A decrease in the primary response to the viral antigen was associated with interferon induction; the booster response was unaffected. The possible use of interferon inducers as attenuants for immunization with live virulent viruses is discussed.

Animals↗
PubMed1967

Statolon-induced resistance of mice to mengovirus.

Mice receiving statolon intraperitoneally were 1,000 times more resistant to intraperitoneal challenge with mengovirus than were untreated controls. Protection was afforded when statolon was administered 1 day before or 1 day after intraperitoneal inoculation with the virus. No therapeutic effect was observed when treatment with statolon was delayed for 2 days or more after virus infection. Exposure of mice to a simulated space cabin environment did not increase their susceptibility to the lethal effects of mengovirus infection or eliminate the protective effect of statolon.

Animals↗
PubMed1967

Treatment of mengovirus infection in mice with statolon.

A single intraperitoneal injection of statolon was shown to exert a therapeutic effect on mice previously injected with the large plaque-forming variant of mengovirus. The ld(50) and survival time data demonstrated that such treatment was effective when given 2 to 48 hr after infection. No protective effect was apparent when statolon was administered 3, 4, or 5 days after the viral challenge. It was concluded that statolon, or other similar interferon inducers, may be of therapeutic value in instances of accidental or other known exposure to hazardous viral agents.

Animals↗