Herpes viruses interactions

Another important application of this interaction is in the formation of self-assembled bilayers on silver or gold surfaces. Ebersole et al. [457] showed that avidin and streptavidin molecules will adsorb onto clean layers of Au or Ag from an aqueous solution. Such layers can then be employed to capture biotinylated compounds. These authors used this technique to attach fragments of nucleic acid derived from the herpes virus to a solid support. A more popular approach to this general problem has, however, been to start by adsorption of a suitable biotin... 

Cidofovir (Figure 24.4) is an antiviral cytidine nucleotide analog with inhibitory activity against HCMV and other herpes viruses. Cidofovir is first converted to an active diphosphate form by cellular enzymes. Antiviral effects of cidofovir are due to inhibition of viral DNA polymerase by the diphosphate metabolite (Neyts and De Clercq, 1994 Plosker and Noble, 1999 Scholar and Pratt, 2000). The diphosphate probably interacts with DNA polymerase either as an alternate substrate (incorporation at the 3 end or within the interior of the DNA chain) or as a competitive inhibitor (with respect to the normal substrate dCTP). Cidofovir inhibits HCMV DNA synthesis at intracellular concentrations 1000-fold lower than are required to inhibit cellular DNA synthesis (Neyts and De Clercq, 1994). For HSV-1 and HSV-2 corresponding concentrations are at least 50-fold lower. 

Caspase-8 is recruited to FADD via interaction between death effector domains. We found that ORF E8 of the equine herpes virus-2 encoded a protein with two predicted death effector domains. This protein, called v-FLIP, is also present in several other viruses including human herpes virus-8. It interferes with the apoptotic pathway of FasL by binding to FADD and potently inhibits TRAIL-mediated cell death (Thome et al., 1997). The sequence information from v-FLIP led to the discovery of a mammalian homo-logue, cellular FLIP (c-FLIP, also called CASPER/I-... 

Previous studies demonstrated the antiviral activity of ascorbate against a broad spectrum of RNA and DNA viruses in vitro (1-4) and in vivo (5, 6). It has been claimed that ascorbate inhibited the activation of a latent human retrovirus (human T-cell leukemia virus 1) induced by 5-iodo-2 -deoxyuridine and JV-methyl-A/ -nitro-A-nitrosoguanidine (7). However, it was not established whether ascorbate exerted a virus-specific effect or interacted directly with the activating substances. In addition, the effects of ascorbate on acute infection by human retroviruses have not been determined. In vivo, oral, and intravenous administration of ascorbate is said to have produced clinical improvements in patients afflicted with influenza, hepatitis, and herpes virus infections, including infectious mononucleosis (5, 6). Clinical improvement was claimed in AIDS patients who voluntarily ingested high doses of ascorbic acid (8). 

Hernandez FP, Sandri-Goldin RM (2010) Herpes simplex virus 1 regulatory protein 1CP27 undergoes a head-to-tail intramolecular interaction. J Virol 84 4124-4135... 

The high density of negative charges in heparan sulfate brings positively charged molecules of lipoprotein lipase into the vicinity and holds them by electrostatic interactions as well as by sequence-specific interactions with S domains. Such interactions are also central in the first step in the entry of certain viruses (such as herpes simplex viruses HSV-1 and HSV-2) into cells. 

Herpes Simplex. There are two types of herpes simplex virus (HSV) that infect humans. Type I causes orofacial lesions and 30% of the U.S population suffers from recurrent episodes. Type II is responsible for genital disease and anywhere from 3 x 104 — 3 107 cases per year (including recurrent infectionsi occur. The primary source of neonatal herpes infections, which are severe and often fatal, is the mother infected with type II. In addition, there is evidence to suggest that cervical carcinoma may be associated with HSV-II infection. Vaccine development is hampered by die fact that recurrent disease is common. Thus, natural infection does not provide immunity and the best method to induce immunity artificially is not clear. A much better understanding of the pathogenesis of die virus and virus-host interactions are required for the efficient development of the vaccine. 

Kurt-Jones EA, Chan M, Zhou S, Wang J, Reed G, Bronson R, Arnold MA, Knipe DM, Finberg RW (2004) Herpes simplex virus 1 interaction with toll-like receptor 2 contributes to lethal encephalitis. Proc Natl Acad Sci USA 101 1315-1320. 

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