Viral replication cycle

Recently, it has been found that NO donors inhibit HIV-1 replication in acutely infected human peripheral blood mononuclear cells (PBMCs), and have an additive inhibitory effect on HIV-1 replication in combination with 3 -azido-3 -deoxythymisylate (AZT) [139, 140]. S-nitrosothiols (RSNOs) inhibit HIV-1 replication at a step in the viral replicative cycle after reverse transcription, but before or during viral protein expression through a cGMP-independent mechanism. In the latently infected U1 cell line, NO donors and intracellular NO production stimulate HIV-1 reactivation. These studies suggest that NO both inhibits HIV-1 replication in acutely infected cells and stimulates HIV-1 reactivation in chronically infected cells. Thus, NO donors may be useful in the treatment of HIV-1 disease by inhibiting acute infection, or reactivating a latent virus. 

The chemotherapy of viral infections may involve interference with any or all of the steps in the viral replication cycle. Because viral replication and host cell processes are so intimately linked, the main problem in... 

Mechanism of Action An antiviral that appears to exert an inhibitory effect early in the viral replication cycle. May inhibit uncoating of the virus. Therapeutic Effect Prevents replication of influenza A virus. 

An important advantage of using heterologous expression systems is the ability to separate the assembly process from other events of the viral replication cycle such as transcription and replication, which may complicate the investigation and make interpretation of results difficult. Heterologous expression systems also allow for a more refined analysis of the assembly pathway on the basis of the possibility to express the components required for formation of the particle separately or in various combinations. As described in more detail below, this approach has been particularly useful in analyzing the assembly of large, multicomponent... 

Viral capsid proteins, in E. coli, 5 Viral genome organization, 219 Viral phylogeny, 185-186 Viral protein structural folds, 125-186 determination of, 125-126 four-helix bundle, 132 immunoglobulin fold, 131 jelly-roll /3 barrel, 128-131, 129 serine protease fold, 132 terminology, 125 virus families and, 125 Viral replication cycle, 8... 

The progress made in cell culture techniques has provided a better understanding of viral replication cycles. Human viruses generally have a slow multiplication cycle requiring from 4 to more than 40 hours (in some herpesviruses) for completion this contrasts with bacterial viruses (bacteriophages) with a replication cycle as fast as 30 minutes. Certain viruses exhibit low infectivity for example, pi-cornavirus infectivity can be as low as 0.1% and rotavirus about 0.2%, and this makes the study of viral replication difficult. 

In general, viral replication cycles, whatever the differences in detail, comprise events that can be separated into six discrete stages (Fig. 5.8) ... 

Moebes A, Enssle J, Bieniasz PD, Hein-kelein M, Lindemann D, et al. 1997. Human foamy virus reverse transcription that occurs late in the viral replication cycle. J. Virol. 71 7305-11... 

The model NPV system is an isolate from the alfalfa looper, Autographa californica and, in conjunction with Lepidopteran cell culture, makes an excellent laboratory system. In cell culture, the NOV is he exclusive infectious form PIBs play no role. After infection, the nucleocapsid makes its way to the nucleus, where replication begins. The initial steps in the viral replication cycle are performed by cellular factors,... 

An understanding of the viral replicative cycle can give us some insight into possible areas of selective chemical interference that leads to successful chemotherapy. 

In summary, HCMV blocks IFN-y-stimulated MHC class II transcription through two means with distinct mechanisms and kinetics. At relatively early times after infection, there is an HCMV-mediated repression of CIITA expression or function (Heise et al. 1998 LeRoy et al. 1999). At later times after infection, HCMV blocks IFN-y-stimulated transcription factor activation, CIITA expression, and class II transcription (Miller et al. 1998). The HCMV gene products mediating these effects remain to be identified however, experiments have shown that immediate-early and/or early gene products are involved (Heise et al. 1998 LeRoy et al. 1999 Miller et al. 1998). This represents a critical HCMV immunoevasive strategy as the virus has evolved two mechanisms, operative over distinct stages of the viral replication cycle, for blocking the IFN-y-inducible MHC class II transcription system. 

Enzymatic Synthesis. DNA and RNA are biosynthesized by polymerase enzymes. RNA is synthesized from a DNA strand with the assistance of an RNA polymerase enzyme. Inversely, DNA can be synthesized from an RNA strand with a reverse transcriptase (RT) enzyme. This mechanism is important because of retroviruses (such as HIV) in which RT makes up part of the viral replication cycle. (HIV-RT is an important target for anti-HIV therapy.) In any enzymatic synthesis of DNA or RNA, it is critical to the life of the organism that these enzymes synthesize their respective polynucleotides in a specific sequence of monomer units. The enzymes are able to accomplish this by utilizing a template strand to direct the synthesis. By reading the sequence of nucleobases on the template, the enzymes select the complementary monomer for incorporation into the propagating strand (Fig. 9). It was widely accepted that the polymerase enzymes accomplish this by matching the nucleotide to the template on the basis of complementary... 

Chrysophanic acid (l,8-dihydroxy-3-methylanthraquinone), isolated from the Australian Aboriginal medicinal plant Dianella longifolia, has been found to inhibit the replication of poliovirus types 2 and 3 (Picornaviridae) in vitro (Fig. 3.7 Semple et al. 2001). The compound inhibited an early stage in the viral replication cycle, but did not have an irreversible virucidal effect on poliovirus particles. Chrysophanic acid did not have significant antiviral activity against five other viruses which were tested Coxsackievirus types A21 and B4, human rhinovirus type 2 (Picornaviridae), and the enveloped viruses Ross River virus (Jogaviridae) and HS V-1 (Herpesviridae). 

Indeed, the whole question of the variable responses of mammalian cells to different human adenovirus serotypes is poorly understood, despite the fascinating range of interactions displayed. The variable abilities of cells derived from different species, or different tissues, to support adenovirus replication is generally interpreted in terms of the presence, or lack of, cellular factors that the virus needs to complete various steps in the replication cycle. More precisely, putative factors that permit human adenovirus replication in human cells may be present in, say, murine cells, but sufficiently divergent that they fail to interact optimally with the relevant viral components. Thus, an understanding in molecular terms of the steps in the viral replication cycle that are blocked in non- or semipermissive cells should provide important information about the host cell components utilized by the virus and, thus, the molecular interactions among viral and cellular products. 

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