Journal of General Virology - Volume 19, Issue 3, 1973

Chicks inoculated in the wing web with fixed rabies virus (RV) were protected against subsequent challenge injections of Rous sarcoma virus (RSV). The protection was transient, generalized and was not elicited in birds treated with actinomycin D or hydrocortisone. Chick serum was shown to possess a factor induced by RV, which inhibited RSV in vivo, and its presence in the serum at different times after RV administration was closely correlated with the RV-RSV blockade. This serum factor (SF), probably protein in nature, was heat and pH-labile. The inhibition of RSV by RV or the serum factor was affected by flock changes in a manner suggesting the occasional presence of interfering contaminating agent(s).

Reciprocal complementation experiments in mouse L cells and BHK-21 cells show that the complementing temperature-sensitive (ts) mutants of vesicular stomatitis virus (VSV), Indiana serotype, isolated from the hr wild-type strain, belong to groups I, III and IV (Flamand & Pringle, 1971). Since the homologies of ts mutants isolated from three different wild-type strains growing in different host cells can be established by cross-complementation, proposals are made for a uniform nomenclature of ts mutants of VSV Indiana.

The Rivers ‘revived’ strain of vaccinia virus (cvi), a population of virus particles produced in chorioallantoic membrane of eggs, is shown to be physically heterogeneous. Some cloned subpopulations isolated on RK cells interfere and others complement each other in mixed infection. Some are physically different, as shown by sedimentation velocity spectra, but none produce plaques on L cells. Yet pulse-inoculation (by centrifuging) at an input multiplicity of 20 virus particles per L cell produces progeny that make more plaques on L cells than on the RK cells from which they were selected. High multiplicity is essential to this process and the frequency of emerging L+ virus particles may be increased up to 400-fold if the recipient L cells are starved prior to inoculation. One cloned L+RK− virus, isolated from these progeny, is suppressed in plaque formation by antiserum to the original cvi virus but it no longer produces the characteristic necrotic lesions in rabbit skin.

The sudden emergence of these large numbers of host-range variants in the absence of a mutagenic agent is similar in some respects to ‘symmetrical host-controlled modification’ observed with certain bacterial viruses.

Proteus mirabilis strains 13 and 5006 on rare occasions liberate temperate phages, 13M and 5006M, which may reinfect parent strains. These prophages are not inducible but the probability of phage liberation may be increased by growth in nitrosoguanidine. P. mirabilis strain 34 liberates a phage, φ34, spontaneously. Strain 34 is doubly lysogenic for this phage. Phages 13M, 5006M and 34 are serologically identical and convert their hosts. The cryptic lysogeny of these strains may be due to the mode of integration of the prophages in the bacterial chromosome.

Infection by N- or B-tropic murine sarcoma virus (MSV) ‘pseudotypes’ in the presence of murine leukaemia virus (MLV) of the opposite tropism to non-permissive cells of the MSV resulted in about a 100- to 1000-fold increase of focus formation in comparison with MSV solitary infection. The culture fluid of such mixedly infected cells contained MSV ‘pseudotypes’ whose tropism was identical to that of MLV.

Peritoneal exudate cells transferred from adult to suckling BALB/c mice before infection of the recipients with Coxsackie B-3 virus protected them against the lethal effects of the virus. Undiluted antibody alone also prevented lethal virus infections in suckling mice but diluted antibody conferred protection only when transferred together with syngeneic adult peritoneal exudate cells. Impairment of macrophage function by intravenous injection of silica increased the susceptibility to virus infection of adult mice. Peritoneal exudate cells inactivated the virus in vitro, and this property may be related to their protective effect in vivo. It is suggested that antibody and host cells collaborate to provide effective resistance against the spread of Coxsackie virus.

Young adult CBA mice developed lethal infections with Coxsackie B-3 virus when immunosuppressed with cyclophosphamide. In the immunosuppressed mice high titres of virus and severe lesions were found in target organs, including the heart and pancreas, as well as persistent viraemia. Immunosuppressed animals showed transient production of IgM but no IgG virus neutralizing antibody; levels of interferon in peripheral blood were higher than in controls. Immunosuppressed mice could be passively protected by administration of serum antibody after infection. The results suggest that circulating antibody plays a critical role in limiting infection of young adult mice by Coxsackie B-3 virus.

There is no correlation between virulence in experimental animals and such physical properties of Semliki Forest virus (SFV) as rates of inactivation or electrophoretic and chromatographic distribution patterns. Changes in the surface properties of the virus can be induced in most strains of SFV by addition of polysaccharide derivatives during virus growth in chick embryo cells; these changes cause a variation in the pattern of infection in both chick embryo cells and mice.

Glucosamine and DEAE-dextran both inhibit a function involved in the release of virus from chick embryo cells. It is suggested that one or more of at least five sites may be used during the ‘budding’ of virus from the cell depending on the strain of SFV.

In sugar-free media, mannosamine inhibits transfer of infective material across the cell membrane; both glucose and mannose relieve this inhibition, but relief by galactose is variable, indicating that more than one mechanism may be used. Transfer of infective material across the cell membrane is not always a corollary of attachment of virus to the cell.

The polypeptides of several strains of the seven serotypes of foot-and-mouth disease virus have been examined by polyacrylamide gel electrophoresis. Most strains gave a distinctive pattern of separation in urea-polyacrylamide gels but all the viruses contained one polypeptide which migrated to the same position. The mol. wt. of this polypeptide (VP 4) was shown by co-electrophoresis in sodium dodecyl sulphate-polyacrylamide gels to be the same, 13.5 × 103, for all seven serotypes. Since VP 4 aggregates when it is dissociated from the virus, it can be separated readily from acid-disrupted virus particles by centrifuging. It has the properties of a group antigen since it reacts in complement fixation tests with both homotypic and heterotypic antisera. The reaction between VP 4 and heterotypic antisera has also been demonstrated by using [125I]-Fab fragments. The antigenic site of VP 4 is not located on the surface of virus particles since there is no reaction between intact particles and [125I]-labelled heterotypic IgG or its Fab fragments.

We have assigned mutations in cowpea chlorotic mottle virus and the related brome mosaic virus to specific RNA components. Coat protein changes, as well as associated ‘maturation faults’ and systemic symptom changes, are located on RNA species 3; local and primary lesion alterations are found on either RNA species 2 or 3. Changes in nucleoprotein component ratio are associated either with the coat protein changes on RNA species 3 or with primary lesion alterations on species 2. Local lesion temperature sensitivity is found on RNA species 1.