1,721,105 research outputs found
Antiviral therapy: old and current issues.
No full textMany antiviral drugs are currently approved and formally licensed for clinical use in the treatment of viral infections caused by human immunodeficiency virus, herpes simplex viruses, varicella-zoster virus, respiratory syncytial virus, cytomegalovirus, hepatitis B virus, hepatitis C virus or influenza virus. Recent decades have seen major advances in our knowledge of the natural history and pathogenesis of viral diseases as well as ongoing developments and improvements in antiviral therapy. However, research is far from complete and indeed previously unknown and unexpected issues are currently arising. This review aims to discuss some of these issues in the belief that they should be carefully addressed to enhance the management of patients with viral infections. © 2012 Elsevier B.V. and the International Society of Chemotherapy. All rights reserved
Cellular factors involved in the induction of resistance of HIV to antiretroviral agents.
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Prostaglandin A inhibits replication of human immunodeficiency virus during acute infection.
No full textAn antiviral effect of prostaglandins (PGs) of the A series on the replication of human immunodeficiency virus (HIV) has been determined. In the T cell line C8166 under single growth cycle conditions, PGA1 reduced the number of infectious progeny 1000-fold in the absence of cytotoxicity. Thus, inhibition of HIV replication by PGA1 represents a true antiviral phenomenon. The number and size of virus-induced syncytia, and the amount of viral antigen were also drastically reduced. The effect was specific for PGAs because PGA2 was also inhibitory, whereas PGB1, PGE1 and PGE2 were inactive. Virus adsorption and penetration do not appear to be targets of antiviral action because PGA1 substantially reduced virus replication, even when added 5 h post-infection. PGA1 did not inhibit viral reverse transcriptase, as determined by in vitro assays, suggesting that its antiviral action is not the consequence of a direct inhibitory effect on this enzyme. PGA1 also inhibited the replication of HIV-1 in CEM x 174 cells, but with less potency. Previously, intravenous infusion of PGA1 into human volunteers has shown no significant deleterious side-effects and thus these observations suggest that PGAs might have potential as antiviral agents in humans
[Acquired immunodeficiency virus (HIV-1). Biological aspects and virological diagnosis].
No full textThe etiologic agent of the acquired immunodeficiency syndrome is a retrovirus included in the subclass of lentiviruses in view of certain characteristics common to these viruses. Their similarity is mainly represented by the extreme slowness of disease manifestation and by the fact that HIV, like other lentiviruses, spreads within the organism in spite of an immune reaction. The mechanism of replication is not dissimilar to that of other retroviruses except for the expression of a particularly large number of regulating genes the most important of which are called tat, rev, and nef. Further genes with a probable regulating function are nef, vpr, and vpx. In the field of diagnostic virology, together with normal isolation tests, a technique that has become particularly important is PCR (polymerase chain reaction) which allows to obtain a relevant amount of specific viral DNA sequences by the use of a DNA polymerase and specific primers
Consolidation of molecular testing in clinical virology
No full textThe development of quantitative methods for the detection of viral nucleic acids have significantly improved our ability to manage disease progression and to assess the efficacy of antiviral treatment. Moreover, major advances in molecular technologies during the last decade have allowed the identification of new host genetic markers associated with antiviral drug response but have also strongly revolutionized the way we see and perform virus diagnostics in the coming years. Areas covered: In this review, we describe the history and development of virology diagnostic methods, dedicating particular emphasis on the gradual evolution and recent advances toward the introduction of multiparametric platforms for the syndromic diagnosis. In parallel, we outline the consolidation of viral genome quantification practice in different clinical settings. Expert commentary: More rapid, accurate and affordable molecular technology can be predictable with particular emphasis on emerging techniques (next generation sequencing, digital PCR, point of care testing and syndromic diagnosis) to simplify viral diagnosis in the next future
Infectious burden and atherosclerosis. A clinical issue
Full text linkAtherosclerotic cardiovascular diseases, chronic inflammatory diseases of multifactorial etiology, are the leading cause of death worldwide. In the last decade, more infectious agents, labeled as "infectious burden", rather than any single pathogen, have been showed to contribute to the development of atherosclerosis through different mechanisms. Some microorganisms, such as Chlamydia pneumoniae (C. pneumoniae), human cytomegalovirus, etc. may act directly on the arterial wall contributing to endothelial dysfunction, foam cell formation, smooth muscle cell proliferation, platelet aggregation as well as cytokine, reactive oxygen specie, growth factor, and cellular adhesion molecule production. Others, such as Helicobacter pylori (H. pylori), influenza virus, etc. may induce a systemic inflammation which in turn may damage the vascular wall (e.g., by cytokines and proteases). Moreover, another indirect mechanism by which some infectious agents (such as H. pylori, C. pneumoniae, periodontal pathogens, etc.) may play a role in the pathogenesis of atherosclerosis is molecular mimicry. Given the complexity of the mechanisms by which each microorganism may contribute to atherosclerosis, defining the interplay of more infectious agents is far more difficult because the pro-atherogenic effect of each pathogen might be amplified. Clearly, continued research and a greater awareness will be helpful to improve our knowledge on the complex interaction between the infectious burden and atherosclerosis
May the drug transporter P glycoprotein affect the antiviral activity of human immunodeficiency virus type 1 proteinase inhibitors?
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