We evaluated three non-invasive method, thermography, laser Doppler imaging and near infrared multi-spectral imaging to quantitatively assess parameters of vascularity in Kaposi's sarcoma. The KS lesion generally has increased temperature, blood velocity and blood deoxy-hemoglobin. There is a strong correlation between temperature and blood velocity (R= 81, p <0.001). After treatment with experimental drug (liposomal doxorubicin and interleukin-12), temperature, blood velocity, blood volume and deoxy-hemoglobin of the lesions are reduced from the baseline at week 18. The techniques are objective, easy to perform, and appear to be very sensitive in assessing improvement in the lesions upon administration of therapy.
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http://dx.doi.org/10.1109/IEMBS.2005.1616508 | DOI Listing |
Kidney Int
February 2025
Division of Nephrology, Department of Internal Medicine, School of Medicine, Marmara University, Istanbul, Türkiye. Electronic address:
Front Microbiol
January 2025
Departments of Otorhinolaryngology-Head and Neck Surgery and Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States.
Oncogenic gamma herpesviruses, including Epstein-Barr Virus (EBV) and Kaposi's Sarcoma-associated Herpesvirus (KSHV), are opportunistic cancer-causing viruses and induces oncogenesis through complex mechanisms, which involves manipulation of cellular physiology as well as epigenetic and epitranscriptomic reprogramming. In this review, we describe the intricate processes by which these viruses interact with the epigenetic machinery, leading to alterations in DNA methylation, histone modifications, and the involvement of non-coding RNAs. The key viral proteins such as EBNA1 and LMP1 encoded by EBV; LANA and vGPCR encoded by KSHV; play pivotal roles in these modifications by interacting with host factors, and dysregulating signaling pathways.
View Article and Find Full Text PDFVirology
December 2024
Lineberger Comprehensive Cancer Center and Department of Microbiology and Immunology, The University of North Carolina at Chapel Hill, USA. Electronic address:
Infection with Kaposi sarcoma-associated herpesvirus (KSHV) is a prerequisite for the development of several human cancers, including Kaposi sarcoma and primary effusion lymphoma. Efficient long-term infection with KSHV and subsequent virally induced cell transformation is limited to humans, resulting in a lack of small animal models for KSHV-driven malignancies. Various attempts to create a mouse model for KSHV include infection of humanized mice, generating transgenic mice that ectopically express viral proteins, and grafting KSHV-infected tumor, primary, or immortalized cells onto immunodeficient mice.
View Article and Find Full Text PDFJ Virol
January 2025
Vaccine and Gene Therapy Institute, Oregon Health & Science University, Beaverton, Oregon, USA.
Kaposi's sarcoma-associated herpesvirus (KSHV) is a human gammaherpesvirus associated with Kaposi's sarcoma and B cell malignancies. Like all herpesviruses, KSHV contains conserved envelope glycoproteins (gps) involved in virus binding, entry, assembly, and release from infected cells, which are also targets of the immune response. Due to the lack of a reproducible animal model of KSHV infection, the precise functions of the KSHV gps during infection are not completely known.
View Article and Find Full Text PDFJ Med Virol
January 2025
Department of Infection Biology, Global Center for Pathogen and Human Health Research, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, USA.
Kaposi's sarcoma-associated herpesvirus (KSHV) employs diverse mechanisms to subvert host immune responses, contributing to its infection and pathogenicity. As an immune evasion strategy, KSHV encodes the Membrane-Associated RING-CH (MARCH)-family E3 ligases, K3, and K5, which target and remove several immune regulators from the cell surface. In this study, we investigate the impact of K3 and K5 on lymphotoxin receptor (LTβR) ligands, LTβ and LIGHT, which are type II transmembrane proteins and function as pivotal immune mediators during virus infection.
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