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Influenza, mumps and measles viruses were examined for their ability to induce in guinea pigs homologous and cross-reactive delayed hypersensitivity. A majority of the animals skin tested with homologous and a portion of the animals skin tested with heterologous viruses and vaccines developed positive reactions. Findings with the heterologous preparations suggest that the observed cross-reactive hypersensitivity might be due to shared antigens of viral or substrate origin in the influenza, mumps and measles preparations. The present findings in guinea pigs suggest that the adverse effects, attributed in whole or in part to induced hypersensitivity, observed in man following injection of killed influenza, mumps and measles vaccines could be due to cross-reactive delayed hypersensitivity resulting from the use of these preparations.
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In previous reports of this series, it was shown that persistent infection of MCN cultures with certain myxoviruses rendered the cells insusceptible to superinfection by several cytopathogenic viruses. It was thought that production of an interferon might be the cause of this resistance and efforts to confirm this suggestion have been presented. Addition of ultraviolet-inactivated myxoviruses (mumps, Newcastle disease, influenza A, and Sendai) to MCN cultures for periods of 2 to 3 hours, followed by washing and refeeding of the cells, led to the subsequent release into the media of a substance which induced in fresh MCN cells a transitory resistance to infection by vesicular stomatitis virus, and prevented incomplete reproductive cycles of influenza A and Sendai viruses. Media containing this substance were free of detectable hemagglutinating activity and viral complement-fixing antigens. The substance was not neutralized by specific antiviral sera; it was not sedimentable by high speed centrifugation; it was not adsorbed onto red cells; but it was inactivated by trypsin. Thus, its properties matched those of the interferon described by Isaacs and his associates. A comparison of the extent of resistance induced in MCN cells by decreasing doses of ultraviolet-inactivated myxoviruses (interference test) and the protection afforded by the media removed from the cultures prior to challenge and transferred to fresh MCN tubes (interferon test) revealed that wherever interference became detectable in the cells, the media of the corresponding cultures contained some interferon. Interferon was obtained by inactivated myxoviruses also from primary cell cultures by the same techniques, but not from HeLa cells. Interferons derived from one type of culture may protect others equally well or show a certain degree of host specificity in that resistance in homologous cells may be somewhat more pronounced than in heterologous cultures. No resistance could be induced in HeLa cells by the interferon preparations employed. Interferon was detected also in MCN cultures, persistently infected with mumps virus. Its concentration was apparently too small in carrier cultures maintained as routine to be measurable. However, when the cells were grown in heavy sheets in roller bottles, and especially when the volume of medium was reduced for several days prior to harvest, interferon became readily detectable. These results strengthen the suggestion that interferon may play a decisive role in the establishment and maintenance of persistent infections in the system under study. Its nature, source, mode of action, and exact role in persistent infection remains to be elucidated.
A study of the mechanism of myxovirus and paramyxovirus inactivattion by hydroxylamine, O-methylhydroxylamine and N-methylhydroxylamine was conducted. Influenza A (WSN) was used as the sensitive myxovirus and Newcastle disease virus (NDV-L) was used as the relatively resistant paramyxovirus in certain experiments. Inactivation was found to be rapid (15 minutes) and mose effective at high concentrations (2M). All three compounds significantly decreased the hemagglutination titer of WSN treated at pH smaller than or equal to 5.0. There was no detectable change in NDV hemagglutination titer. Adsorption of hydroxylamine (pH 7.0) inactivated WSN appeared normal; however, the rate of adsorption was decreased when virus was inactivated by (pH 5.0) O-methylhydroxylamine. Equilibrium density gradient centrifugation in potassium tartrate showed no density changes in inactivated virus. WSN inactivated virus. WSN inactivated with 14C-O-methylhydroxylamine and subjected to RNA extraction showed greater than or equal to 35 percent of the 14C in the phenol phases and 21 per cent in the RNA. The 14C-O-methylhydroxylamine associated with the RNA of insensitive NDV was about 3 per cent of that associated with sensitive WSN-RNA. Hydroxylamine has no apparent effect on paramyxovirus (NDV) hemagglutination titer and less 14C-O-methylhydroxylamine is associated with the RNA of this virus. The results suggest these compounds may affect both the RNA and the envelope portion of myxoviruses (WSN) to produce inactivation.
Sulfated polysaccharides (i.e., dextran sulfate) and sulfated polymers (i.e., sulfated polyvinylalcohol and sulfated copolymers of acrylic acid with vinylalcohol) were found to be potent and selective inhibitors of the replication of respiratory syncytial virus (RSV) and influenza virus type A (influenza A virus) but not of other myxoviruses (parainfluenza 3, measles, and influenza B viruses). The compounds were also inhibitory to human immunodeficiency virus type 1 (HIV-1) and HIV-2 and simian immunodeficiency virus but not simian AIDS-related virus. The mode of antiviral action of the sulfated polysaccharides and polymers can be attributed to an inhibition of virus binding to the cells (HIV-1), inhibition of virus-cell fusion (influenza A virus), or inhibition of both virus-cell binding and fusion (RSV). The fact that the sulfated polysaccharides and polymers are inhibitory to some myxoviruses and retroviruses but not to others seems to depend on the composition of the amino acid sequences of the viral envelope glycoproteins that are involved in virus-cell binding and fusion. All myxoviruses and retroviruses that are sensitive to the sulfated polysaccharides and polymers share a tripeptide segment (Phe-Leu-Gly). This tripeptide segment may be involved either directly (as a target sequence) or indirectly in the inhibitory effects of the compounds on virus-cell binding and fusion.
Calcium elenolate inactivates all myxoviruses so far tested. The pH of the reaction mixture is less critical for myxovirus inactivation than that required for coxsackie A-21 virus; the myxoviruses are inactivated at a broad spectrum of pH with the maximum activity occurring at a pH below 7.0. The infectivity of the virus is more susceptible to the action of calcium elenolate than is either the neuraminidase activity or the hemagglutinin. The inactivation of Newcastle disease virus by calcium elenolate also destroys the ability of the virus to induce interferon formation in cell culture and in mice.
Using the kinetics of neutralization, it was established that two strains of Myxovirus Parainfluenza 3 of cattle and sheep origin which are immunologicaly identical have a different sensitivity to early neutralizing antibodies of reconvalescent calf sera. Complement-dependent neutralizing antibodies, supplied by adding 5% guinea pig serum to the calf serum, appear earlier than the usual neutralizing antibodies. Goat anti-cattle gammaglobulin serum decreases the neutralizing activity of early reconvalescent serum and release some of the neutralizing virus from the virus-antibody complex. It is believed that the lability of the virus-antibody complex depends not only on the activity of the antibody, but also on some properties of the strains. The addition of complement stabilizes this complex. The previous addition of adenovirus antigen to bivalent cattle serum against Myxovirus Parainfluenza 3 and cattle adenovirus, decreases the complement-dependent neutralizing antibody of the serum against Myxovirus Parainfluenza 3. It is suggested that this is the possible mechanism for the mutual activation of mixed virus infections.
Dawson, C. R. (The Middlesex Hospital Medical School, London, England), M. A. Epstein, and K. Hummeler. Cytochemical and electron microscopical observations on the presence and origin of adenosine triphosphatase-like activity at the surface of two myxoviruses. J. Bacteriol. 89:1526-1532. 1965.-HeLa cells infected with either fowl plague virus (FPV) or Newcastle disease virus (NDV) were examined in thin sections by electron microscopy. Preparations were studied both after direct fixation and embedding and after the application of cytochemical staining for enzymes splitting adenosine triphosphate. Viral particles were identified by their size and characteristic structure, and were found to form at the cell surface by budding out through structurally altered plasmalemma. After cytochemical staining for adenosine triphosphatase activity, extracellular FPV or NDV particles lying close against cell membranes with enzyme activity likewise carried this function, whereas those particles which were associated with cell surfaces without reaction product were themselves free from it. This correspondence between enzyme function in cell membranes and the outer viral membranes of newly formed particles adjacent to them indicates that surface enzymatic capability of the host cell survives even when the cell membrane undergoes morphological and antigenic alteration into myxovirus outer membrane.
Craighead, J. E. (Harvard Medical School, Boston, Mass.). Growth of Myxovirus parainfluenza type 3 in organ cultures of guinea pig tissue. J. Bacteriol. 92:751-761. 1966.-Organ cultures of adult guinea pig nasal mucosa, lung, and pleura were infected with Myxovirus parainfluenza type 3. Observations were made on the growth of virus at intervals after inoculation. An inoculum of 10(2.5) tissue culture infectious doses (tcid(50)) initiated infection in each of the tissues. Cultures of nasal mucosa yielded up to 10(6.0)tcid(50) per 6 hr for periods of as long as 2 weeks. Virus production was not affected by the "immune" status of the animal used as a source of tissue. Introduction of antiserum into the medium appeared to suppress virus release but failed to "cure" the infection. Interferon was not detected in fluids bathing the nasal mucosa. Cultured fragments of lung produced virus for 28 days after inoculation. As much as 10(5.0)tcid(50) per 6 hr was released by the tissue. Pleural mesothelial cells lining the diaphragm yielded up to 10(6.0)tcid(50) per 6 hr over a 14-day period. Histological sections showed that the tissues retained differentiated morphological features during maintenance in vitro. Cytological changes unequivocally associated with infection were not recognized. The techniques described give reproducible, quantitative results. Organ cultures are feasible for the study of virus growth and cytopathology in differentiated tissues.
Myxoviruses were disrupted with Tween 20 at high pH, and the major surface antigens were separated in biologically active form. The neuraminidase had a sedimentation coefficient of 10.8S, and the hemagglutinin had a sedimentation coefficient of 8.1S. Electron microscopic examination of negatively stained preparations revealed structures identical in size and morphology to the neuraminidase and hemagglutinin subunits described by others. Inhibition of neuraminidase activity by antibody to the hemagglutinin which occurred with intact viruses (probably for "steric" reasons) did not occur after the viruses were disrupted with Tween 20. Serological assays for neuraminidase were possible in the presence of the mild surfactant, whereas serological assays for hemagglutinin were possible after removal of the reagent. Disruption of myxoviruses with Tween 20 therefore provides a method for the independent study of these antigens during antigenic drift.
Electron spin resonance (ESR) spectra of the spin probes C5 and C16, the iminoxyl derivatives of stearic acids, have been investigated after their incorporation into lipid membranes of influenza and Sendai viruses. At room temperature the spectra of both probes coincided indicating the similar composition and origin of lipid viral membranes. Similar to influenza virus, Sendai virus was shown to possess the external lipid bilayer. Investigation of the rigidity of the lipid phase of myxoviruses as a function temperature has shown that the structure of the lipid external layer (no less than 8 A in thickness) is due to surface glycoproteins incorporated into the viral membrane. The structural transition of the lipid phase of influenza and Sendai viruses 8 A apart from the viral surface was observed at 50 degrees C. The surface glycoproteins do not probably penetrate deep in the lipid membrane of myxoviruses and do not condition its structure at long distances (22 A) from the viral surface. The completely reversible structural transition of lipid phase at this distance was observed at temperatures 17--20 degrees C.