Defective interfering virus (DI) particles represent a major controlling element of virus replication. They are constantly generated at low levels by infectious virus and only amplify to interfering levels when the parent helper vims is abundant. This autointerference phenomenon, as it was called when first discovered, is achieved by rearrangements and deletions of the standard virus genome such that the resulting “incomplete form” of the virus can preferentially replicate.

Origin and replication of defective interfering particles.

The paramyxovirus group is a large one which includes the parainfluenza viruses types 1–5, Newcastle disease, and mumps viruses. Measles, canine distemper, and rinderpest viruses form a distinct subgroup on the basis of antigenicity, hemagglutinating characteristics, and lack of evidence for a virion-associated neuraminidase or neuraminic acid-containing cellular receptors. However, it is now generally accepted that these viruses should also be included in the paramyxovirus group because of their similar structural properties. Other more recently isolated viruses which have been classified as paramyxoviruses on the basis of morphological and biological properties are Yucaipa (Dinter et al., 1964) and Nariva (Walder, 1971) viruses. Table 1 lists paramyxoviruses and their primary hosts.

Reproduction of Paramyxoviruses

Several mechanisms have been put forward to explain how persistently infected virus-carrier cell cultures are maintained. In this report, information is summarized which suggests that selection of temperature-sensitive mutants may be involved in either establishment or maintenance of persistent infections both in cell cultures and in animals. The possible relation of this mechanism to other mechanisms of regulation of persistent infections is also discussed. Finally, a practical suggestion is offered to researchers and clinicians seeking endogenous viruses from cultured cells and tissues that may harbor temperature-sensitive variants.

Temperature-sensitive viruses and the etiology of chronic and inapparent infections.

There is an extensive literature dealing with persistent infections established by a wide variety of animal viruses. Several mechanisms have been suggested that may be involved in the establishment and maintenance of persistent infection by a normally virulent, cytolytic virus. One of these mechanisms, which involves defective-interfering (DI) virus particles in the initiation and regulation of some persistent infections, is discussed in Chapter 3 of this volume. This chapter will concentrate on another aspect of persistent viral infection, namely, the evolution of virus populations in infections initiated by virulent viruses in cell culture model systems or in immunologically competent animals. A comprehensive survey of the findings with many different groups of viruses will be followed by a discussion of the patterns of virus evolution during persistent infection and the implications of these changes in systems in which cytolytic viral infections are converted to more temperate host-virus interactions. Persistent infections in which the evolution of the virus population has not been studied will be mentioned but are outside the main focus of this review.

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Viral Persistence: Evolution of Viral Populations

https://mmbr.asm.org/content/mmbr/41/3/636.full.pdf

Measles virus and its associated diseases.

RNA-dependent DNA polymerase activity was found in peparations of a mutant of Newcastle disease virus. The enzyme activity was not found in wild-type virus preparations.

Phillip A. Furman

Papers

RNA-Dependent DNA Polymerase Activity in Preparations of a Mutant of Newcastle Disease Virus Arising from Persistently Infected L Cells