Abstract
Recently, leading medical journals emphasized the importance of further studies on the potential application of bacterial viruses (phages) for the treatment of antibiotics-resistant infections outlining the present status of the therapy and perspectives for the future. Furthermore, a leading scientific journal pointed to the recent progress in research on phage interactions with eukaryotic cells (especially cells of the immune system) and potential implications of their results for our broader understanding of the role of phages – not only as “bacteria eaters” – but also as an important part of our body defense protecting against external and internal pathogenic invaders (as suggested previously). This illustrates how our understanding of the actual role and potential of phages is expanding and how worldwide interest in their use in medicine is growing. In this article we envision how this advancement of our knowledge about phages could be translated into the progress in combating herpesvirus infections especially those caused by Epstein–Barr virus (EBV).
Highlights
As assessed by serology, Epstein–Barr virus (EBV) infects >90% of the human population; its predominant host cells are B cells and epithelial cells with life-long latency established in the latter cells (Connolly et al, 2011)
Glycoprotein gHgL binds with high affinity to epithelial cell integrin via prominent KGD motif located on its surface; this was confirmed by ability of KGD-containing peptides to block gHgL binding and EBV infection
The potential of phages to interfere with some viral infections is highlighted by the data on hantavirus interactions with platelets which are facilitated by αIIbβ3 integrin; the role of that integrin is further supported by data indicating that its polymorphism may be a risk factor for hantavirus – induced disease while the intensity of levels of its expression on platelets correlate with disease severity
Summary
EBV infects >90% of the human population; its predominant host cells are B cells and epithelial cells with life-long latency established in the latter cells (Connolly et al, 2011). Its potential interactions are markedly enhanced by this exposure while the functional significance of this motif is confirmed by demonstrated KGD-dependent phage interactions with platelets and blockade of those interactions with a peptide containing the KGD sequence (Integrilin) as well as anti-β3 antibody; what is more, αIIb-β3 integrin-deficient platelets do not interact with phages (Dabrowska et al, 2004a).
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