Video S1 Release of filamentous Marburg virus particles at one day post infection. Animation through a z-series of 2 nm digital slices of a double axis tomogram, reconstructed from a tilt series taken of a ,300 nm thick section of a MARV-infected HUH-7 cell at one day post infection. Coloured overlay shows a 3D surface model of membranes and cytoplasm (yellow) and representations of the viral NCs (blue). A filamentous viral budding structure with the NC completely inserted into the budding site as well as several released filamentous viruses are seen.  Peptide-Mediated Liposomal Drug Delivery System Targeting Tumor Blood Vessels in Anticancer Therapy Solid tumors are known to recruit new blood vessels to support their growth. Therefore, unique molecules expressed on tumor endothelial cells can function as targets for the antiangiogenic therapy of cancer. Current efforts are focusing on developing therapeutic agents capable of specifically targeting cancer cells and tumor-associated microenvironments including tumor blood vessels. These therapies hold the promise of high efficacy and low toxicity. One recognized strategy for improving the therapeutic effectiveness of conventional chemotherapeutics is to encapsulate anticancer drugs into targeting liposomes that bind to the cell surface receptors expressed on tumor-associated endothelial cells. These anti-angiogenic drug delivery systems could be used to target both tumor blood vessels as well as the tumor cells, themselves. This article reviews the mechanisms and advantages of various present and potential methods using peptide-conjugated liposomes to specifically destroy tumor blood vessels in anticancer therapy. One of the primary goals of a successful cancer treatment regimen is to deliver sufficient amounts of drug to tumors while minimizing damage to normal tissues. Most chemotherapeutic agents enter normal tissues in the body with indiscriminate cytotoxicity and do not preferentially accumulate at tumor sites. At times the dose reaching the tumor may be as little as 5% to 10% of the doses accumulating in normal organs [1, 2] . One reason for the inability for drugs to accumulate at target sites is that the interstitial fluid pressure (IFP) in solid tumors is higher than in normal tissues, that blocking transcapillary transport of chemotherapeutic drugs or antibodies [3] [4] [5] . In this way, the anticancer effect is decreased and toxic effect to normal cells is increased. Fear of severely harming the patients often limits the dose of anticancer drugs that can be given to a patient. These lower than optimal doses elicit incomplete tumor responses which leads to disease relapse and drug resistance. Therefore, most cancer drugs fail in clinical studies not because they are ineffective in killing cancer cells but because they cannot be administered in doses high enough to eradicate the tumor without severely harming the patient.