Viral growth cycle

Lytic Viral Growth Cycles Lead to Death of Host Cells... 

Viral DNA Is Integrated into the Host-Cell Genome in Some Nonlytic Viral Growth Cycles... 

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 ... 

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). 

HIV replication is strongly influenced by the cellular environment in which the virus finds itself. Host factors, particularly cytokines, can exercise either positive or negative effects on viral growth, which together are brought to bear on viral infection in vivo (8). Many different cytokines affect the viral life cycle at various steps and, in some instances, at multiple steps (Table 1). Chemokines have been implicated chiefly as inhibitors of viral entry, an effect related to HIV s use of chemokine receptors to enter its target cells. The details of this inhibitory function of chemokines, as well as additional stimulatory functions of these same chemokines and other chemokine family members, will be discussed below. 

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. 

Fig. I3a-c. Infection by viral RNA of untreated and polycation-exposed HeLa cells during different stages of the growth cycle. Suspended HeLa cells were synchronized by a double thymidine block (Tobia et al.,1970). Synchrony was measured by following...

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... 

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