Viruses multiplication

When a virus multiplies, the genome becomes released from the coat. This process occurs during the infection process. The present chapter is divided into three parts. The first part deals with basic concepts of virus structure and function. The second part deals with the nature and manner of multiplication of the bacterial viruses (bacteriophages). In this part we introduce the basic molecular biology of virus multiplication. The third part deals with important groups of animal viruses, with emphasis on molecular aspects of animal virus multiplication. 

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. 

It should already be clear from what has been stated that a great diversity of viruses exist. It should therefore not be surprising that there is also a great diversity in the manner by which virus multiplication occurs. Interestingly, many viruses have special features of their nucleic acid and protein synthesis processes that are not found in cells. In the present chapter, we are only able to present some of the major types of virus replication patterns, and must skip some of the interesting exceptional cases. 

Gupta, P. et al., Lead exposure enhances virus multiplication and pathogenesis in mice, Vet. Hum. Toxicol. 44, 205, 2002. 

A. Virus multiplication and modes of action of antiviral agents... 

Figure 1. Inhibition of Potato-X-virus Multiplication by Sparteine.

Inhibition of glycosylation in virus-infected cells usually has dramatic effects on virus multiplication. This discovery prompted promulgation of a new concept in the experimental therapy of virus-induced diseases. Local treatment of the affected regions with 2-deoxy-D-arabtno-hexose led50n s02 to significant improvements in human-genital herpes infections, or Herpes simplex virus infection of the eye. 

M. J. Carlucci, L. A. Scolaro, M. I. Errea, M. C. Matulewicz, and E. B. Damonte, Antiviral activity of natural sulphated galactans on herpes virus multiplication in cell culture, Planta Med., 63 (1997) 429 132. 

The assessment of antiviral activity is relatively difficult. As a result, only a few investigators have studied the influence of alkaloids on virus multiplication. Nevertheless, at least 45 alkaloids have been reported with antiviral properties (Table VIII). Only sparteine (527) and cinchonidine 142) have been tested for antiviral activities against a plant virus, the potato X virus. All other evidence for antiviral activities (Table VIII) of alkaloids comes from experiments with animal viruses. Because viral life strategies are related in plants and animals, we suggest that a wider number of plant viruses may be controlled by alkaloids in Nature than the limited data imply. 

Hou J, Major EO. The efficacy of nucleoside analogs against JC virus multiplication in a persistently infected human fetal brain cell line. J Neurovirol 1998 4 451-6. 

Fig. 10 shows the viral yields obtained on days 2, 3,4 and 5 after the infection, in control cultures and in cultures treated with distamycin-5. The inhibition of virus production was almost constant on any day tested, suggesting that an early step in virus multiplication is blocked. Similar results were obtained with distamycin-4, but virus inhibition was less than with distamycin-5. 

Compound tested Cytotoxicity1) Inhibition of vaccinia virus multiplication, inhibition (%) )... 

Viral implantation into oropharynx/respiratory tract spreads to regional lymph nodes viremia with virus multiplication in spleen, bone marrow, lymph nodes locates in leukocytes, small dermal blood vessels, and submucosal oral and pharyngeal cells... 

Benzo[a]pyrene has also been shown to affect immune responses to viral infection. Benzo[a]pyrene can reversibly inhibit the induction of viral interferon in 32 different mammalian cell lines but only in the presence of S9 metabolic activation (Hahon and Booth 1988). This inhibition must occur at an early level and not affect viral interferon interactions because the activity of exogenous interferon was unaffected. In addition, influenza virus multiplication was also inhibited by activated benzo[a]pyrene. Benzo[e]pyrene had no effect on interferon induction. The authors suggest that benzo[a]pyrene s inhibition of interferon induction may be an early step in compromising the host s immune function, thereby allowing the induction of carcinogenesis. 

The toxicity of starfishes may be derived from the saponins. The biological activities of these compounds were reported, including haemolytic properties, and antitumour [104] and antibacterial activities [105]. Inhibition activities for influenza virus multiplication, and anti-inflammatory activity towards contraction of the rat phrenic nerve diaphragm preparation, were also reported [106]. Saponins are chemical defence agents in starfishes, and they also induce escape reactions in bivalve molluscs [107]. It is of interest to note that the sperm agglutination substance in the egg jelly of starfish is similar to asterosaponin A [108]. 

Rubin BY (1992) TNF and viruses multiple interrelationships. In Aggarwal BB, Vilcek ) (eds) Tumor necrosis factors. Structure, function and mechanisms of action. Dekker, New York, pp 331-340... 

Nature has found two basic ways of arranging the multiple capsid protein subunits and the viral genome into a nucleocapsid. In some viruses, multiple copies of a single coat protein form a helical structure that encloses and protects the viral RNA or DNA, which runs In a helical groove within the protein tube. Viruses with such a helical nucleocapsid, such as tobacco mosaic virus, have a rodlike shape. The other major structural type is based on the icosahedron, a solid, approximately spherical object built of 20 identical faces, each of which is an equilateral triangle. 

The inhibitory effects of the pyrrolinone derivatives were evaluated using enzyme inhibition and cellular activation assays. Compound 6 (Fig. 4.3-5) showed an IC50 of 10 nM, compared to 0.6 nM for the related peptide inhibitor 5 (L682,679). However, the synthetic agent 6 showed better cell transport capacity. In a cellular antiviral assay, 5 and 6 showed CIC95 values (the concentration that inhibits 95% of virus multiplication in the cellular cultures) of 6.0 and 1.5 pM, respectively. Smith and Hirschmann proposed that the improved cellular uptake properties of polypyrrolinones are due to a reduction in the inhibitor solvation. Solvation is an impediment to transport because extraction of a molecule into a lipid bilayer from an aqueous phase is... 

The viral infectivity in cultured cells is determined during virus multiplication in the presence of a single tested compound or extract or after extracellular incubation. 

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