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Influenza virus multiplication

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. [Pg.117]

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]. [Pg.209]

The initial step in the sequence of events leading to influenza virus infections in mammalian hosts is mediated by the multiple attachment of virus particles to host sialoside receptors in the nasopharynx [41]. These receptors consist largely of cell surface sialylated glycoproteins and gangliosides. The subsequent steps involve receptor-mediated endocytosis with ensuing release of the viral nucleo-plasmid. The first event responsible for the receptor-virus interaction is therefore an attractive target for both antiviral and related microbial intervention. [Pg.363]

Both GW, Sleigh MJ, Cox NJ, Kendal AP. Antigenic drift in influenza virus H3 haemagglutinin from 1968 to 1980 multiple evolutionary pathways and sequential amino acid changes at key antigenic sites. J Virol 1983 48 52-60. [Pg.481]

LF has been demonstrated to inhibit in vitro the multiplication of different viruses, such as human cytomegalovirus, HIV, herpes simplex viruses 1 and 2, influenza virus, human hepatitis C virus and human poliovirus type 1 (Vorland, 1999). Also, LF has been shown to prevent rotavirus infection in the human enterocyte-like cell-line HT-29 (Superti et al., 1997). It is speculated that LF prevents the binding of viruses to the host cells by... [Pg.186]

Ribavirin monophosphate competitively inhibits cellular inosine-5 -phosphate dehydrogenase and interferes with the synthesis of guanosine triphosphate (GTP) and, thus, nucleic acid synthesis in general. Ribavirin triphosphate also competitively inhibits the GTP-dependent 5 -capping of viral messenger RNA and, specifically, influenza virus transcriptase activity. Ribavirin appears to have multiple sites of action, and some of these (e.g., inhibition of GTP synthesis) may potentiate others (e.g., inhibition of GTP-dependent enzymes). [Pg.619]

The first instance of a vaccine being made in plants was in 1990 when a patent was filed for a Streptococcus mutans protein (SpaA) expressed in tobacco. Since then, many other vaccines (e.g., cholera toxin B, Hepatitis virus surface antigen, Plasmodium surface protein) have been produced, and multiple different plant species (e.g., tomato, potato, banana, and rice) have been used, particularly as an edible host is needed for oral administration. An important sdentific milestone was when the E. coU heat labile enterotoxin (LT-B) was expressed in potatoes and was shown to be orally immunogenic when 5 g of transformed tuber was fed to mice over 18 days [70]. However how this might translate to an effective dose in humans is not yet established. Numerous other workers have since demonstrated for animal models that oral or injected immunization with plant-produced antigen would provide protection against diseases such as Yersinia pestis [71], or Avian Influenza Virus [72]. [Pg.24]

Sieben, C., Kappel, C., Zhu, R., Wozniak, A., Rankl, C., Hinterdorfer, P., Grubmller, H., Herrmann, A. Influenza virus binds its host cell using multiple dynamic interactions. Proc. Natl. Acad. Sci. U.S.A. (2012). doi 10.1073/pnas.l 120265109... [Pg.67]

The progression of viral mRNA production during the infection cycle was characterized by means of qPCR measurements. MDCK cells infected with influenza A/PR/8 virus (multiplicity of infection = 100 one cell is virtually infected by 100 virus particles) were harvested at various points post infection. Noninfected cells were collected for control experiments. The total RNA was isolated and purified by using commercially available kits. The optical density (OD) of isolated RNA was measured and aliquots were subjected to in vitro transcription. After quantification (by OD measurements), the resulting complementary deoxyribonucleic acid (cDNA) was analyzed in qPCR experiments. [Pg.356]

The animal toxicological and pharmacological properties of adamantanamine have been described in detail. Both oyclo-octylamine and adamantanamine inhibited the growth of a 19 9 clinical isolate of influenza A2 in tissue culture when the drug was present before infection. Rous and Esh sarcoma virus multiplication in tissue culture is inhibited by (X-methyl-l-adamantanemethylamineAdamantanamine and Rec.l5/ 0209 in combination had synergistic anti-influenza activity in eggs but not in mice. ... [Pg.102]

The ubiquitous chelates of 1,10-phenanthroline were studied some time ago for their antiviral activity [17]. The inhibitory effect of various chelates on the multiplication of influenza virus (Melbourne strain) in chick chorioallantoic membrane in vitro was studied, and the most effective complex was shown to be the [Ru(acac) (3,5,6,8-Me4-l,10-phen)2] cation, which inhibited multiplication at concentrations of 6 X 10 M(—log M = 6.2). Other chelate complexes were active at concentrations of 10 to 10 M. A structure—activity study of metal chelates showed, however, that for a given chelate ligand, more labile complexes such as those of Cd or Cu were more active than their inert counterparts, the order for doubly-charged (2+) chelates being Cd(II) > Cu(II) > Zn(II) > Mn(II) > Fe(II) > Co(II) > Ni(II) > Ru(II) [18]. This correlation coincided with that found for some antibacterial effects (Chapter 9). Further studies showed that the virostatic activity may be manifested by either direct inactivation of the virus (possibly through dissociation of the more labile chelates) or by direct action on the host cell (for inert complexes). The latter effect is indicated by the fact that the trend in virostatic activity is similar to that in antitumour activity [19] (see also Chapter 6) and the fact that, of the various 1,10-phenanthrolines studied, the tetramethyl derivatives most easily penetrate cells [20]. [Pg.226]


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See also in sourсe #XX -- [ Pg.72 , Pg.75 ]




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