Peptide-guided JC polyomavirus-like particles specifically target bladder cancer cells for gene therapy.

The ultimate goal of gene delivery vectors is to establish specific and effective treatments for human diseases. We previously demonstrated that human JC polyomavirus (JCPyV) virus-like particles (VLPs) can package and deliver exogenous DNA into susceptible cells for gene expression. For tissue-specific targeting in this study, JCPyV VLPs were conjugated with a specific peptide for bladder cancer (SPB) that specifically binds to bladder cancer cells.

Inhibition of human lung adenocarcinoma growth and metastasis by JC polyomavirus-like particles packaged with an SP-B promoter-driven CD59-specific shRNA.

Lung cancer ranks first in both incidence and mortality and is a major health concern worldwide. Upon recognition of specific antigens on tumor cells, complement-dependent cytotoxicity (CDC) is activated, arresting cell growth or inducing apoptosis. However, by overexpressing CD59, a membrane complement regulatory protein (mCRP), lung cancer cells develop resistance to CDC.

Gene therapy for human glioblastoma using neurotropic JC virus-like particles as a gene delivery vector.

Glioblastoma multiforme (GBM), the most common malignant brain tumor, has a short period of survival even with recent multimodality treatment. The neurotropic JC polyomavirus (JCPyV) infects glial cells and oligodendrocytes and causes fatal progressive multifocal leukoencephalopathy in patients with AIDS. In this study, a possible gene therapy strategy for GBM using JCPyV virus-like particles (VLPs) as a gene delivery vector was investigated.

and Extracts Effectively Inhibit BK Virus and JC Virus Infection of Host Cells.

The human polyomaviruses BK (BKPyV) and JC (JCPyV) are ubiquitous pathogens long associated with severe disease in immunocompromised individuals. BKPyV causes polyomavirus-associated nephropathy and hemorrhagic cystitis, whereas JCPyV is the causative agent of the fatal demyelinating disease progressive multifocal leukoencephalopathy. No effective therapies targeting these viruses are currently available.

Inhibition of BK virus replication in human kidney cells by BK virus large tumor antigen-specific shRNA delivered by JC virus-like particles.

Polyomavirus-associated nephropathy (PVAN) due to lytic infection by the BK polyomavirus (BKPyV) remains an important cause of allograft dysfunction and graft loss in renal transplant recipients. PVAN is commonly treated by reducing the dosage of immunosuppressive drugs and adding adjuvant antiviral agents, but the outcomes have been less than satisfactory. The BKPyV early protein large tumor antigen (LT) is indispensable for viral genome replication and viral late protein expression.

Recombined sequences between the non-coding control regions of JC and BK viruses found in the urine of a renal transplantation patient.

Kidney cells are the common host for JC virus (JCV) and BK virus (BKV). Reactivation of JCV and/or BKV in patients after organ transplantation, such as renal transplantation, may cause hemorrhagic cystitis and polyomavirus-associated nephropathy. Furthermore, JCV and BKV may be shed in the urine after reactivation in the kidney.