Viruses as host assemblies

Stability Constants Definition and Determination, p. 1360 Viruses as Host Assemblies, p. 1563... 

Self-Assembling Catenanes. p. 1240 Self-Assembly in Biochemistry-, p. 1257 Self-Assembly Terminology, p. 1263 Strict Self-Assembly and Self-Assembly with Covalent Modifications, p. 1372 The Template Effect, p. 1493 Viruses as Host Assemblies, p. 1563... 

Dendrimers are being used as host molecules, catalysts, self-assembling nanostructures analogs of proteins, enzymes, and viruses and in analytical applications including in ion-exchange displacement chromatography and electrokinetic chromatography. 

Interferons exert their antiviral effects on the cells that they protect rather than on the virus as such. The interferon binds to the surface of the host cells and initiates the synthesis of a number of proteins whose encoding genes are normally repressed. The proteins include several enzymes that block virus replication, assembly and release. 

Volumes 5 and 6 represent the first in a series that focuses primarily on the structure and assembly of virus particles. Volume 5 is devoted to general structural principles involving the relationship and specificity of interaction of viral capsid proteins and their nucleic acids, or host nucleic acids. It deals primarily with helical and the simpler isometric viruses, as well as with the relationship of nucleic acid to protein shell in the T-even phages. Volume 6 is concerned with the structure of the picornaviruses, and with the reconstitution of plant and bacterial RNA viruses. 

The eclipse is the period during which the stages of virus multiplication occur. This is called the latent period, because no infectious virus particles are evident. Finally, maturation begins as the newly synthesized nucleic acid molecules become assembled inside protein coats. During the maturation phase, the titer of active virus particles inside the cell rises dramatically. At the end of maturation, release of mature virus particles occurs, either as a result of cell lysis or because of some budding or excretion process. The number of virus particles released, called the burst size, will vary with the particular virus and the particular host cell, and can range from a few to a few thousand. The timing of this overall virus replication cycle varies from 20-30 minutes in many bacterial viruses to 8-40 hours in most animal viruses. We now consider each of the steps of the virus multiplication cycle in more detail. 

As seen in the genetic map, the genes after gene 1.1, transcribed by the T7 RNA polymerase, code for proteins that are involved in T7 DNA synthesis, the formation of virus coat proteins, and assembly. Three classes of T7 proteins are formed class I, made 4-8 minutes after infection, which use the cell RNA polymerase class II, made 6-15 minutes after infection, which are made from T7 RNA polymerase and are involved in DNA metabolism class III, made from 6 minutes to lysis, which are transcribed by T7 RNA polymerase and which code for phage assembly and coat protein. This sort of sequential pattern, commonly seen in many large double-stranded DNA phages, results in an efficient channeling of host resources, first toward DNA metabolism and replication, then on to formation of virus particles and release of virus by cell lysis. 

Completely different mechanisms are involved in the self-assembly of the tobacco mosaic virus (TMV). This virus consists of single-strand RNA, which is surrounded by 2,130 identical protein units, each of which consists of 158 amino acid residues. A virus particle, which requires the tobacco plant as a host, has a rodlike structure with helical symmetry ( Stanley needles ). It is 300 nm long, with a diameter of 18nm. The protein and RNA fractions can be separated, and the viral... 

Antibodies against the virus but also amantadine and derivatives, interfere with host cell penetration. There are nucleoside analogues such as aciclovir and ganciclovir, which interfere with DNA synthesis, especially of herpes viruses. Others like zidovudine and didanosine, inhibit reverse transcriptase of retroviruses. Recently a number of non-nucleoside reverse transcriptase inhibitors was developed for the treatment of HIV infections. Foscarnet, a pyrophosphate analogue, inhibits both reverse transcriptase and DNA synthesis. Protease inhibitors, also developed for the treatment of HIV infections, are active during the fifth step of virus replication. They prevent viral replication by inhibiting the activity of HIV-1 protease, an enzyme used by the viruses to cleave nascent proteins for final assembly of new vi-rons. 

Following their production, the viral components are assembled to form a mature virus particle. The viral genome is encapsulated by viral protein in some cases (e.g. adenovirus, poliovirus), it is not encapsulated. In certain viruses, such as the poxviruses, multiple membranes surround the capsid. Release of the virus from the host cell may be rapid and produce cell lysis and death. A slower process resembling budding may allow the host cell to survive. 

---