Publications by authors named "W K Songock"

Multidrug-resistant tuberculosis (TB) (MDR-TB), or TB that is simultaneously resistant to both isoniazid (INH) and rifampicin (RIF), is a barrier to successful TB control and treatment. Stratified data on MDR-TB, particularly in the high-burden western Kenya region, remain unknown. This data is important to monitor the efficacy of TB control and treatment efforts.

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Persistent infection by human papillomaviruses (HPVs), small, double-stranded DNA viruses that infect keratinocytes of the squamous epithelia, can lead to the development of cervical and other cancers. The viral oncoprotein E7 contributes to viral persistence in part by regulating host gene expression through binding host transcriptional regulators, although mechanisms responsible for E7-mediated transcriptional regulation are incompletely understood. Type I IFN signaling promotes the expression of anti-viral genes, called interferon-stimulated genes (ISGs), through the phosphorylation and activation of STAT1.

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Human papillomaviruses (HPVs) infect keratinocytes of stratified epithelia. Long-term persistence of infection is a critical risk factor for the development of HPV-induced malignancies. Through the actions of its oncogenes, HPV evades host immune responses to facilitate its productive life cycle.

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Article Synopsis
  • The Epstein-Barr virus (EBV) is linked to the development of oropharyngeal squamous cell carcinoma (OSCC) associated with human papillomavirus (HPV), particularly highlighting the role of latent EBV infection and viral oncogenes.
  • In a study with HPV16-immortalized cells, EBV replication was significantly lower in these cells than in HPV-negative cells, suggesting that HPV may interfere with EBV's life cycle.
  • The HPV E7 oncogene appears to inhibit EBV replication, potentially allowing EBV to persist in a latent state within tumors by affecting the epithelial differentiation markers essential for EBV expression.
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Human papillomaviruses (HPVs) cause benign lesions that can lead to malignancy. How cellular changes induced by viral oncogenes contribute to the progeny virion production is not always clear. Stromally-derived growth factors and their receptors are critical for development of malignancy, but their impact on the pre-malignant HPV life cycle is unknown.

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