Lactoferrin and lactoferricin inhibit Herpes simplex 1 and 2 infection and exhibit synergy when combined with acyclovir

Andersen, Jeanette Hammer; Jenssen, Håvard; Gutteberg, Tore Jarl

doi:10.1016/s0166-3542(02)00214-0

Cited by 111 publications

(83 citation statements)

References 30 publications

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“…8). Combination treatment of acyclovir with a drug that has the ability to inhibit HSV replication could increase the anti-HSV activity in vitro and in vivo (42)(43)(44)(45). In the present study, we found that berberine not only attenuated HSV replication but also depressed the inflammatory response and associated pathway activation.…”

Section: Discussionsupporting

confidence: 56%

Downregulation of Cellular c-Jun N-Terminal Protein Kinase and NF-κB Activation by Berberine May Result in Inhibition of Herpes Simplex Virus Replication

Song

Qiu

Chu

et al. 2014

Antimicrob Agents Chemother

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bBerberine is a quaternary ammonium salt from the protoberberine group of isoquinoline alkaloids. Some reports show that berberine exhibits anti-inflammatory, antitumor, and antiviral properties by modulating multiple cellular signaling pathways, including p53, nuclear factor B (NF-B), and mitogen-activated protein kinase. In the present study, we investigated the antiviral effect of berberine against herpes simplex virus (HSV) infection. Current antiherpes medicines such as acyclovir can lessen the recurring activation when used early at infection but are unable to prevent or cure infections where treatment has selected for resistant mutants. In searching for new antiviral agents against herpesvirus infection, we found that berberine reduced viral RNA transcription, protein synthesis, and virus titers in a dose-dependent manner. To elucidate the mechanism of its antiviral activity, the effect of berberine on the individual steps of viral replication cycle of HSV was investigated via time-of-drug addition assay. We found that berberine acted at the early stage of HSV replication cycle, between viral attachment/entry and genomic DNA replication, probably at the immediate-early gene expression stage. We further demonstrated that berberine significantly reduced HSV-induced NF-B activation, as well as IB-␣ degradation and p65 nuclear translocation. Moreover, we found that berberine also depressed HSV-induced c-Jun N-terminal kinase (JNK) phosphorylation but had little effect on p38 phosphorylation. Our results suggest that the berberine inhibition of HSV infection may be mediated through modulating cellular JNK and NF-B pathways.

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Section: Discussionsupporting

confidence: 56%

Downregulation of Cellular c-Jun N-Terminal Protein Kinase and NF-κB Activation by Berberine May Result in Inhibition of Herpes Simplex Virus Replication

Song

Qiu

Chu

et al. 2014

Antimicrob Agents Chemother

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“…This is supported by the fact that mixing the peptides with HSV prior to interaction did not increase antiviral activity (5). The peptides exhibited different antiviral effects for HSV type 1 (HSV-1) and HSV-2, an observation attributed to the combined effects of the amino acid content and the structures of the peptides (4,119,120,122). Interestingly, differences in antiviral effects against HSV-1 and HSV-2 have also been reported for other polycationic and even polyanionic compounds (109,138).…”

Section: Mode Of Action Of Antiviral Peptidesmentioning

confidence: 83%

“…1), dermaseptin, and melittin have shown quite potent anti-HSV activity (Table 2) (1,3,16,269). Conversely, ␤-sheet peptides such as defensins, tachyplesin, and protegrins as well as the ␤-turn peptide lactoferricin have all shown high activity towards HSV (Table 2) (4,45,120,148,225,269,270). It should be noted that within the different peptide subclasses, activity may vary considerably.…”

Section: Antiviral Activitymentioning

confidence: 99%

Peptide Antimicrobial Agents

2006

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SUMMARY Antimicrobial host defense peptides are produced by all complex organisms as well as some microbes and have diverse and complex antimicrobial activities. Collectively these peptides demonstrate a broad range of antiviral and antibacterial activities and modes of action, and it is important to distinguish between direct microbicidal and indirect activities against such pathogens. The structural requirements of peptides for antiviral and antibacterial activities are evaluated in light of the diverse set of primary and secondary structures described for host defense peptides. Peptides with antifungal and antiparasitic activities are discussed in less detail, although the broad-spectrum activities of such peptides indicate that they are important host defense molecules. Knowledge regarding the relationship between peptide structure and function as well as their mechanism of action is being applied in the design of antimicrobial peptide variants as potential novel therapeutic agents.

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“…Some recently identified peptides include human apolipoprotein E-derived peptide (apoEdp), rabbit neutrophil peptide-1 (NP-1), lactoferrin (LF), indolicidin (a tryptophan-rich peptide from bovine neutrophils), and brevinin-1 (a peptide found in frog skin) (2,3,4,8,39,51). We recently used a phage display random peptide library screening to isolate a 12-mer cationic peptide (G2 peptide) that binds 3-OS HS and blocks HSV-1 infection (43).…”

mentioning

confidence: 99%

A 3- O -Sulfated Heparan Sulfate Binding Peptide Preferentially Targets Herpes Simplex Virus 2-Infected Cells

Ali

Karasneh

Jarding

et al. 2012

J Virol

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Herpes simplex virus 2 (HSV-2) is the primary cause of genital herpes, which is one of the most common sexually transmitted viral infections worldwide and a major cofactor for human immunodeficiency virus infection. The lack of an effective vaccine or treatment and the emergence of drug-resistant strains highlight the need for developing new antivirals for HSV-2. Here, we demonstrate that a low-molecular-weight peptide isolated against 3- O -sulfated heparan sulfate (3-OS HS) can efficiently block HSV-2 infection. Treatment with the peptide inhibited viral entry and cell-to-cell spread both in vitro and in vivo using a mouse model of genital HSV-2 infection. Quite interestingly, the peptide showed a preferential binding to HSV-2-infected cells, with more than 200% increased binding compared to uninfected cells. Our additional results show that heparan sulfate expression is upregulated by 25% upon HSV-2 infection, which is a significant new finding that could be exploited for designing new diagnostic tests and treatment strategies against HSV-2-infected cells. In addition, our results also raise the possibility that 3-OS HS modifications within HS may be upregulated even more to accommodate for a significantly higher increase in the peptide binding to the infected cells.

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Lactoferrin and lactoferricin inhibit Herpes simplex 1 and 2 infection and exhibit synergy when combined with acyclovir

Cited by 111 publications

References 30 publications

Downregulation of Cellular c-Jun N-Terminal Protein Kinase and NF-κB Activation by Berberine May Result in Inhibition of Herpes Simplex Virus Replication

Downregulation of Cellular c-Jun N-Terminal Protein Kinase and NF-κB Activation by Berberine May Result in Inhibition of Herpes Simplex Virus Replication

Peptide Antimicrobial Agents

A 3- O -Sulfated Heparan Sulfate Binding Peptide Preferentially Targets Herpes Simplex Virus 2-Infected Cells

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