Abnormal macrophages and NK cell cytotoxicity in human systemic lupus erythematosus and the role of interferon and serum factors.

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.

Actin organization in chick embryo fibroblasts after influenza virus infection. I. Isolation and characterization of actin from chick embryo cells.

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 effect of interferon induction on complement level in rat.

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.

Levels of complement during interferon induction.

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.

Quantitative assay of influenza virus soluble antigen by complement-fixation micromethod.

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.

Interaction of plasma membranes with influenza virus. VI. The possible role of the adenylate cyclase system.

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.

Consumption of complement in chelated and nonchelated guinea pig serum after challenge with some viral and nonviral interferon inducers.

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.

Interferon-hyporesponsiveness in mice in connection with dose interval and site of administration of Newcastle disease virus. Reflexion in serum complement levels.

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.

Experimental infection of weanling pigs with A-swine influenza virus. 3. Immunity in piglets farrowed by antibody-bearing dams experimentally infected a year earlier.

Pigs experimentally infected as weanlings with swine influenza virus, as described in previous papers, were bred from when mature. Attempts to isolate virus at parturition from the placenta and from different organs of some of the piglets immediately after birth gave negative results. Antibody levels were determined in the sows and remaining piglets at different times after birth, and the clinical course, immunity and antibody formation were studied in some of the piglets challenged with swine influenza virus 10 days after birth.

Experimental infection of weanling pigs with A-swine influenza virus. 2. The shedding of virus by infected animals.

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.

Experimental infection of weanling pigs with A-swine influenza virus. I. Epidemiology and serological response.

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.