Macrophage (MO) and natural killer (NK) cell mediated cytotoxicity to K562 target cells were strikingly decreased in patients with systemic lupus erythematosus (SLE). SLE NK cells failed to release soluble factor(s) for lysing the targets. IFN-induced enhancement of both types of cytotoxicity was impaired. NK cells from healthy subjects kept their activity in culture with or without IFN for more than six days whereas SLE NK cell activity declined to zero at day 3. So, the increased IFN level of many SLE patients and a possible prior IFN priming effect seemed unrelated to the insensitivity to exogenous IFN in vitro. Inhibition factor(s) of SLE serum suppressed NK cytotoxicity in the presence of IFN whereas IFN sensitivity of MO remained unaffected indicating the complex regulation by serum components of immune reactions.

Several reports indicate that, in addition to disturbances found in the specific immune reactions, also the broader interferon /IFN/ system, including the NK-cells and IL-2 etc, shows misregulation in autoimmune disorders /Hooks et al., 1981, Waschke and Diezel, 1984, Rovenský et al., 1984, Lange et al., 1984 etc./.

Comparison of two starting materials for actin purification has shown that preparation of actin from aceton-dried cytoskeleton was more effective than from native chick embryos (CE). The isolated actin formed a single band of Mr = 42-43000 in SDS-PAGE; less purified samples revealed additional faint bands. G form of actin (non-polymerized) inhibited the activity of DNase I, electron microscopy showed actin filaments and bundles formed upon its polymerization. The freshly purified homogeneous actin has not lost its DNase I-inhibiting activity when incubated for 60 min at 35 degrees or 45 degrees C. Older or less purified actin samples kept under similar conditions showed 18-25% decrease of their DNase I-inhibiting activity and a loss of their polymerization ability. Digestion with trypsin caused a decrease of DNase I-inhibiting activity of fresh as well as for older actin samples.

Relatively high levels of interferon were achieved in rat sera by intracardial inoculation with Sindbis virus followed 15 min later by intraperitoneal application of dimethylsulfoxide. At intervals when interferon titres reached the maximum, the levels of complement were decreased as compared with the control group of rats. Single administration of dimethylsulfoxide did neither induce interferon nor influence the complement levels in sera of rats of the Dobrá Voda breed tested. Similar results were obtained with concentrated Newcastle disease virus inoculated intraperitoneally. Of interest is the finding that properdin levels seem to increase at the same time as interferon.

Further data were obtained in support of the finding that the levels of interferon and complement show a negative correlation after induction of interferon in vivo. Experiments with selective chelating agents showed that the activation of complement occurs by the by-pass mechanism. Preliminary results indicate that interferon itself can reduce the level of complement in vivo. Experiments are underway to verify in rats the results obtained in mice.

The consumption of complement observed during the induction of interferon by various inducers may proceed via the alternate pathway. The alternate pathway requires the presence of Mg ions in the medium while Ca ions may be absent.

The amounts of released soluble (s) antigen of influenza A/WSN virus were increased when the virus was allowed to interact with isolated plasma membranes in a medium containing substances enhancing the level of adenosine 3',5' cyclic monophosphate (c'AMP) or activating the enzyme adenylate cyclase. By contrast, less s-antigen was released upon addition to the incubation medium of foetal calf serum or calf serum proteins which activate c'AMP phosphodiesterase and thus decrease the level of c'AMP. Changes in the amount of released s-antigen were parallelled by changes in the activities of membrane Ca-adenosine triphosphatase and creatine phosphokinase.

A modified micromethod of complement fixation (CF) reaction for quantitive assay of Influenzavirus soluble (s) antigen was elaborated. The method makes it possible to determine microquantities of s-antigen with an accuracy of +/- 15%. The accuracy of the method was checked by theoretical calculations.

Intraperitoneal administration of Newcastle disease virus (NDV) resulted in enhanced serum levels of complement not accompanied by an increase of interferon levels, when measured at 24 hours' intervals. On the other hand, intravenous injection of NDV caused a drop of complement levels of short duration with an accompanying increase of interferon levels. Hyporeactivity to induction of serum interferon could not be achieved by intraperitoneal administration of NDV, but an incomplete hyporeactivity could be achieved by intravenous administration of NDV. It might be assumed that production of interferon in mice occurs in different separated compartments depending on the route of inoculation of the inducer.

Naturally occurring swine influenza is caused by a strain of virus closely related to influenza strains isolated from man in 1918 and later. Information is lacking on certain aspects of the epidemiology of swine influenza that, if obtained, might shed some light on the epidemiology of human influenza, particularly with respect to inter-epidemic reservoirs and shedders of the virus. In a first series of experiments undertaken by the authors pigs were experimentally infected intranasally with swine influenza virus and the course of clinical infection, spread by contact, and the serological response of infected animals were studied. Observations were also made on persons in contact with the infected swine to determine whether cross-transmission occurred. Respiratory and feverish clinical signs of the disease were observed in infected animals. Contact infection of several animals in the same piggery occurred, as revealed by serological tests, although the contact-infected pigs showed no clinical signs. There was some but not highly significant serological evidence of human infection in laboratory workers and animal handlers exposed to swine influenza virus. Some pigs infected as weanlings developed specific antibodies that lasted for 1(1/2) years of observation. Antibody titres decreased markedly towards the end of 1 year in animals of a lower age at the time of infection (42 days old), as compared with older animals (52-77 days) in which there were lesser decreases in titre.

As part of a study described in a previous paper observations were made to determine whether and for how long experimentally infected young pigs would transmit their infection to new groups of weanlings maintained in contact with them. When groups of 4 or 5 susceptible weanlings 2-3 months old were placed in contact for a month with infected pigs 42 days or 3, 6, 9 or 12 months after experimental infection, no antibody rises were observed in the contact pigs. However, a strain of virus identical with the infecting strain was isolated from lung suspensions from 2 of the 5 contact pigs exposed to pigs infected 3 months previously. Possible sources of technical error such as laboratory contamination could be almost certainly excluded. It is considered that a shedder state of virus had occurred some time during the fourth month following experimental infection. There was suggestive serological evidence that the shed virus acted as a booster dose to previously infected pigs.