ArticleJournal of clinical virology : the official publication of the Pan American Society for Clinical Virology2009
Evidence of inability of human cytomegalovirus to reactivate Kaposi's sarcoma-associated herpesvirus from latency in body cavity-based lymphocytes.
Article in Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- The Impact of Co-Infections for Human Gammaherpesvirus Infection and Associated Pathologies.International journal of molecular sciences · 2023Review
- Sirtuin 6 Attenuates Kaposi's Sarcoma-Associated Herpesvirus Reactivation by Suppressing Ori-Lyt Activity and Expression of RTA.Journal of virology · 2019Article
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Corrections and comments
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Authors and funding
4 authors at 3 institutions in 3 countries.
Funding
Abstract
backgroundKaposi's sarcoma-associated herpesvirus (KSHV; also known as human herpesvirus 8 (HHV-8)) has been determined to be the most frequent cause of malignancies in AIDS patients. It is associated primarily with Kaposi's sarcoma (KS) and primary effusion lymphoma (PEL), as well as with multicentric Castleman's disease (MCD).(2) The switch from the latent to the lytic stage is important in the maintenance of malignancy and viral infection. So far, the mechanism of its reactivation has not been fully understood.
objectivesHuman cytomegalovirus (HCMV) and KSHV might infect the same cells, and it was found by other groups that several viruses could reactivate KSHV from latency. We investigate whether HCMV infection could reactivate KSHV from latency in body cavity-based lymphocyte (BCBL-1) cells. STUDY DESIGN AND
resultsLaboratory strains of HCMV cannot infect B cells. In this article, we demonstrate that the UL131-repaired HCMV (vDW215-BADrUL131) derived from AD169 strain is able to infect B lymphocytes. We directly infected KSHV latent cells including BCBL-1 with vDW215-BADrUL131 to evaluate the ability of HCMV to reactivate KSHV. Inconsistent with previous reports in human fibroblast cells, our results provide direct evidence that HCMV is unable to reactivate KSHV from latency-to-lytic infection in BCBL-1 cell lines. As a control, herpes simplex virus type 1 (HSV-1) was shown to be able to reactivate KSHV.
conclusionsOur observations, different from others, suggest that reactivation mechanisms for KSHV might vary in different cells.
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