Poxvirus virions

Most poxvirus virions appear to enter cells by pinocytosis, and then to uncoat within cytoplasmic vesicles. Poxvirus replication occurs in these discrete cytoplasmic inclusions, independent of the cell nucleus. Host biosynthetic processes are inhibited soon after poxvirus infection occurs. Virus transcription initiates almost immediately after entry, as DNA transcription is initiated by core enzymes while the genome is still in the core. Early gene products have to do with DNA synthesis, ensuring adequate levels of precursors for DNA synthesis and inhibition of host defense mechanisms.26 This... 

Poxvirus promoters are not recognized by eukaryotic transcription machinery. Transcription of poxviral genes is initiated only by virally encoded RNA polymerase, normally packaged alongside the DNA in the virion particles. Purified poxvirus DNA is, therefore, non-infectious. 

The virion (the complete infective virus, such as exists extracellularly) consists of a core of either DNA or RNA (but not both) surrounded by a protective capsid (= shell) of one, or sometimes two, proteins. These two components are arranged in a highly ordered fashion that is characteristic of the particular kind of virus. Most of the viruses that infect animals are icosahedral (20-sided) and hence roughly spherical. But the viruses of measles and influenza are spirals. In the latter virus two kinds of protein (neuraminidase and haemagglutinin) form the capsid which is embedded in lipid, and this lipoprotein envelope encloses a coiled ribonucleoprotein tube. Poxviruses (which include the herpesviruses) are the largest known, brick-shaped and of very complicated structure. Many types of virus have a protein core around which the nucleic acid is arranged. 

Rifampicin is also an inhibitor of the synthesis of a number of phages and viruses. It has been demonstrated that the RNA polymerase, which transcribes phage p 22 following infection of Bacillus subtilis, retains the rifampicin sensitivity of the host cell enzyme , Rifampicin also inhibits the formation of infectious vaccinia virus and viral particles. Whereas virion formation is completely inhibited neither the synthesis of RNA and protein nor the activity of in vitro RNA polymerase associated to the virion is affected lt>, Rifampicin inhibits the multiplication of poxvirus in vitro and in vivo. The side chain of this antibiotic derivative appears to be essential for the anti-viral effect and anti-trachomal activity found in... 

The feature common to the cytotoxic effects brought on by nonreplicating influenza virus, poxvirus, and defective-interfering vesicular stomatitis virus is the high multiplicity of infection required. This has led to the assumption that the toxic effect is caused by one or more components of the parental input virion, most likely protein in origin. However, Cordell-Stewart and Taylor (1971, 1973) have provided evidence that the double-stranded viral RNA isolated from cells infected with bovine enterovirus causes a rapid cytopathic effect as determined by trypan-blue uptake or Cr release from affected Ehrlich ascites tumor cells or L1210 cells toxic effects are reduced or do not occur in cells exposed to single-stranded or heat-denatured double-stranded viral RNA and the toxic effect of bovine enteroviral double-stranded RNA is not abolished by inhibitors of protein synthesis such as puromycin or cycloheximide. 

Several excellent reviews on the reproduction of poxviruses are available (Moss, 1974, 1978). A brief synopsis of the morphology of the virus and its mode of replication is included in this chapter to point out virion components and events in virus replication likely to be associated with virus cytopathology. Poxviruses are the largest in size and most complex of all animal viruses. Vaccinia virus, the prototype of these viruses, has been widely used to study the molecular biology of this major group. 

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