Virus growth cycle

This article is restricted to a discussion of experiments with poliovirus RNA and focuses special attention on the steps following the uptake of RNA into a cell, aspects that were not discussed in earlier review articles. The fate of input RNA once inside the cell is determined by the host cell but experimental conditions can be chosen to favor the survival of input RNA and the induction of a virus growth cycle by interfering with host-cell metabolism through events that, in the case of infection with intact virus, might be controlled by viral proteins. 

Naked viral nucleic acid, once inside the cell, is able to initiate a virus growth cycle in a manner similar to intact virus. 

To initiate a virus growth cycle, poliovirus RNA has to act first as mRNA. Since double-stranded RNA is not able to initiate protein synthesis directly (Miura and Muto, 1965), RF-RNA has either to be melted or to be used as a template for the synthesis of new RNA which in turn can serve as mRNA. Therefore the first steps of a virus growth cycle may differ according to whether infection is by viral RNA or RF-RNA. Whereas the initiation of a virus... 

The lytic growth cycle Lysogeny 11 The human immunodeficiency virus... 

In order to study the virus growth curve a one-step growth cycle is performed. A high multiplicity of infection (m.o.i.) is used to ensure every cell is infected — usually 10 plaque forming units (p.f.u.) per cell is adequate. For virus production, however, the infection is prolonged under conditions where secondary infection can occur and a low m.o.i. is recommended especially where there is a tendency for defective virus particles to be produced. 

Detailed laboratory studies showed that the total length of the lytic growth cycles of the Phaeocystis viruses infecting exponentially growing host cells ranged between 25 and 50 h (Jacobsen et al. 1996 Baudoux and Brussaard 2005). For PpV the latent period, the time period from infection until the first increase in the abundance of extracellular free viruses, was around 12-18 h (Jacobsen et al. 1996). The study by Baudoux and Brussaard (2005) showed three different latent periods for the various PgV isolates in culture, i.e., 10,12 and 16 h (Fig. 3). These periods match the range of latent periods for all characterized phytoplankton viruses so far, and are somewhat... 

It is known that RNA oncogenic viruses require DNA synthesis for their replication. As distamycin/A blocks some early steps in the growth cycle of DNA viruses, probably connected with DNA replication32, it was of interest to investigate the effect of distamycin, distamycin-4 and distamycin-5 on MSV (Moloney). 

Once inside the host cell, the vims must replicate its own nucleic acid. To do this, it often uses part of the normal synthesizing machinery of the host cell. If the vims is to continue its growth cycle, viral nucleic acid and viral protein must be propedy transported within the cell, assembled into the infective vims particle, and ultimately released from the cell. All of these fundamental processes involve an intimate utilization of both cellular and viral enzymes. Certain enzymes that are involved in this process are specifically supplied by the invading vims. It is this type of specificity that can provide the best basis for antiviral chemotherapy. Thus an effective antiviral agent should specifically inhibit the viral-encoded or virus-induced enzymes without inhibition of the normal enzymes involved in the biochemical process of the host cell. Virus-associated enzymes have been reviewed (2,3) (Table 1). 

For the purpose of ERA analysis in recent years we have used ERA extracted from fresh virus particles i.e. those produced early in the growth cycle before degradation by heat has occurred and in a recent paper Denoya e al. (11) have drawn attention to the importance of using fresh particles. With these particles homogeneous profiles of ERA can be obtained and treatment with pronase or heating at 60 0 does not produce any alteration in the profile. Benoya (11) also emphasised the value of purifying... 

Schlesinger, R. W., 1950, Incomplete growth cycle of influenza virus in mouse brain, Proc. Soc. Exp. Biol. Med. 74 541. 

It seems only reasonable to suppose that the ability of adenoviruses to induce cellular DNA synthesis and entry into the cell cycle in mammalian cells is of advantage to the virus replication cycle such a property could hardly have evolved for any other purpose. Bellett and colleagues (see, for example, Murray et al., 1982a) have pointed out the particular relevance of this ability to the natural conditions of infection. By contrast to the artificial laboratory situation in which the virus is usually provided with cells that are partially transformed (they are immortal) and undergoing rapid growth and division, most cells encountered by the virus in the natural host are likely to be arrested at the Gl/GO boundary. Thus, it would seem to be of considerable advantage to the virus to possess a mechanism that, soon after an adenovirus enters such a relatively inactive host cell, induces that cell to enter its most active biosynthetic state and, thus, provide maximal quantities of those cellular proteins upon which viral DNA synthesis and gene expression depend. 

Parks, W. P., Melnick, J. L., Rongey, R., Mayor, H. D. Physical assay growth cycle studies of a defective adeno-satellite virus. J. Virol. 1, 171-I8O (1967). 

The first interaction between a virus and a host cell is mediated by specific attachment sites on the host-cell membrane (viral receptors) and by specific structural parts of the viral coat. In 1952 Hershey and Chase demonstrated that in a phage-bacterial system it is almost exclusively the nucleic acid of the virus that enters the cell, while the protein envelope remains on the cell surface and its removal does not affect the subsequent viral growth cycle. Gierer and Schramm (1956) and Fraenkel-Conrat et al. (1957) infected tobacco plants with the isolated RNA of tobacco mosaic virus (TMV). Shortly thereafter several laboratories reported the productive infection of cells by naked nucleic acids from a variety of viruses (see Wecker, 1962 Schaffer, 1962). These findings led to the widespread acceptance of two hypotheses ... 

The clinical importance of these mutations has not been clearly demonstrated. In at least one case a drug-resistant mutant was able to grow in vitro in single-cycle growth experiments as well as wild-type HRV14 [28]. Frequently, however, drug-resistant or acid-stable mutants will not grow as well in cell culture as native virus [93]. 

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