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Download LACTOFERRIN MODULATES HSV-1 INFECTION AT EARLY
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LACTOFERRIN MODULATES HSV-1 INFECTION AT EARLY STAGES OF THE VIRAL LIFE CYCLE AND THIS IS A TEST ABSTRACT Välimaa H1,2, Hukkanen V1, Waris M1, Tenovuo J2 1 Department of Virology, 2Department of Cariology, University of Turku, Turku, Finland The abstract should describe the purpose of the study and the major results and conclusions. If you prefer breaking the text into paragraphs, please do not leave space between them. Oral mucosa is a frequent site of primary herpes simplex virus (HSV) type 1 infection. However, although intraoral shedding of HSV is common, clinical signs of reactivation are far more frequently observed at extraoral compared to intraoral sites, suggesting that reactivation may be inhibited by the intraoral environment. We have previously shown that salivary neutralization activity of HSV correlates with concentration of lactoferrin (an iron-binding glycoprotein) in asymptomatic HSV seropositive subjects. In the current study, we investigated further the mechanism of lactoferrin-mediated inhibition of HSV-1 infection. These studies show that lactoferrin is effective in blocking HSV infection at physiological concentrations. Preincubation of HSV virions with lactoferrin significantly decreased HSV infectivity at higher concentrations. Presence of lactoferrin during either the viral absorption period or the entire HSV infection cycle inhibited HSV in a dose-dependent manner. Wild type HSV was more sensitive to inhibition compared to HSV gC-39, a gC-negative strain of HSV-1, suggesting a mechanism of lactoferrin interference with gC-heparan sulfate binding at the initial attachment of HSV virion to the cell surface. Interestingly, an incomplete monolayer of keratinocytes on rafts at the time of viral inoculation enabled a more efficient production of infectious virus as assessed by the amount of progeny virus in raft homogenates. Our results suggest that lactoferrin is a critical component of the innate immune response that can efficiently modulate the infectivity of HSV in the oral environment, possibly by interference with early stages of infection.