Introduction: Human herpesvirus type 8 (HHV-8) is the main etiological agent of Kaposi's sarcoma. This virus is frequently associated with immunocompromision. This study aimed to detect HHV-8 in people with compromised immune system.
Patients And Methods: This is a cross-sectional study that included 180 subjects: 179 HIV-infected patients and 1 patient with bullous pemphigoid. Blood samples were taken from all subjects, and swabs of lesions were then taken from individuals with symptoms of Kaposi's sarcoma. Viral load and CD4 T lymphocytes count were performed for persons living with HIV and real-time PCR detection of HHV-8 DNA was performed in all subjects in the study.
Results: Among HIV-infected persons, 13.41% had a viral load of more than 10,000 copies/mL, and 22.91% had a CD4 T lymphocytes count of fewer than 350 cells/µL. A total of four (three HIV-1 infected patients and one patient with bullous pemphigoid) patients (2.22%) had apparent lesions of Kaposi's sarcoma. In the plasmas and swabs from associated lesions, HHV-8 DNA was found in only two individuals, with an HHV-8 prevalence of 1.11% (2/180) with 0.55% (1/179) in an HIV-infected patient on antiretroviral therapy.
Conclusion: These results exposing low prevalence levels of HHV-8 in HIV-infected patients could be due to the beneficial effect of antiretroviral drugs.
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http://dx.doi.org/10.2147/HIV.S353166 | DOI Listing |
Oral Surg Oral Med Oral Pathol Oral Radiol
December 2024
Oral Diagnosis Department, Piracicaba Dental School, University of Campinas, Piracicaba, Brazil; Service of Oral Pathology, João de Barros Barreto University Hospital, Federal University of Pará, Pará, Brazil. Electronic address:
Objective: The aim of this study was to provide a comprehensive clinicopathological analysis of oral Kaposi sarcoma (KS) cases and examine its relationship with HIV-related immunosuppression.
Study Design: Paraffin-embedded tissue blocks of patients microscopically diagnosed with oral KS were retrieved from three oral and maxillofacial pathology files. Data including clinical, laboratory, microscopic and immunohistochemical findings and treatment employed were retrieved.
Viruses
December 2024
HIV and AIDS Malignancy Branch, National Cancer Institute, Bethesda, MD 20892, USA.
Gammaherpesviruses are oncogenic pathogens that establish lifelong infections. There are no FDA-approved vaccines against Epstein-Barr virus or Kaposi sarcoma herpesvirus. Murine gammaherpesvirus-68 (MHV68) infection of mice provides a system for investigating gammaherpesvirus pathogenesis and testing vaccine strategies.
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December 2024
Division of Virology, ICMR-National Institute of Translational Virology and AIDS Research, Pune 411026, MH, India.
Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV), which are the only members of the gamma(γ) herpesviruses, are oncogenic viruses that significantly contribute to the development of various human cancers, such as Burkitt's lymphoma, nasopharyngeal carcinoma, Hodgkin's lymphoma, Kaposi's sarcoma, and primary effusion lymphoma. Oncogenesis triggered by γ-herpesviruses involves complex interactions between viral genetics, host cellular mechanisms, and immune evasion strategies. At the genetic level, crucial viral oncogenes participate in the disruption of cell signaling, leading to uncontrolled proliferation and inhibition of apoptosis.
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December 2024
Department of Dermatology, School of Medicine, University of California Davis, Sacramento, CA 95817, USA.
Kaposi's sarcoma-associated herpesvirus (KSHV) is a double-stranded DNA gamma herpesvirus. Like other herpesviruses, KSHV establishes a latent infection with limited gene expression, while KSHV occasionally undergoes the lytic replication phase, which produces KSHV progenies and infects neighboring cells. KSHV genome encodes 80+ open reading frames.
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November 2024
State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan 430072, China.
Kaposi's sarcoma-associated herpesvirus (KSHV), a γ-herpesvirus, is predominantly associated with Kaposi's sarcoma (KS) as well as two lymphoproliferative disorders: primary effusion lymphoma (PEL) and multicentric Castleman disease (MCD). Like other herpesviruses, KSHV employs two distinct life cycles: latency and lytic replication. To establish a lifelong persistent infection, KSHV has evolved various strategies to manipulate the epigenetic machinery of the host.
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