Kaposi sarcoma herpesvirus (KSHV), also known as human herpesvirus 8, is the causative agent of Kaposi sarcoma; this malignant angiosarcoma is usually treated with conventional antitumor agents that can control disease evolution, but do not clear the latent KSHV episome that binds to cellular DNA. Some commercial antibacterial sulfonamides were tested for the ability to suppress latent KSHV. Quantitative PCR (qPCR) and cytofluorometry assays were used for detecting both viral DNA and the latency factor LANA (latency-associated nuclear antigen) in BC3 cells, respectively. The capacity of sulfonamides to impair MDM2-p53 complex formation was detected by an enzyme-linked immunosorbent assay method. The analysis of variance was performed according to one-way analysis of variance with Fisher as a post hoc test. Here we show that sulfonamide antibiotics are able to suppress the KSHV latent state in permanently infected BC3 lymphoma cells and interfere with the formation of the MDM2-p53 complex that KSHV seemingly needs to support latency and to trigger tumor cell transformation. These findings detected a new molecular target for the activity of sulfonamides and offer a new potential perspective for treating KSHV-induced lymphoproliferative diseases.

中文翻译：

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抗菌磺酰胺可清除潜在的卡波西肉瘤疱疹病毒感染并损害MDM2-p53复合物的形成。

卡波西氏肉瘤疱疹病毒（KSHV），又称人疱疹病毒8，是卡波西氏肉瘤的病原体。这种恶性血管肉瘤通常用常规的抗肿瘤药物治疗，这些药物可以控制疾病的进展，但不能清除与细胞DNA结合的潜在KSHV附加体。测试了一些商业抗菌磺酰胺抑制潜在KSHV的能力。定量PCR（qPCR）和细胞荧光分析法分别用于检测BC3细胞中的病毒DNA和潜伏期因子LANA（潜伏期相关核抗原）。通过酶联免疫吸附测定法检测磺酰胺损害MDM2-p53复合物形成的能力。方差分析是根据以Fisher进行事后检验的方差单向分析进行的。在这里，我们表明磺胺类抗生素能够抑制永久感染的BC3淋巴瘤细胞中的KSHV潜伏状态，并干扰KSHV似乎需要支持潜伏期并触发肿瘤细胞转化的MDM2-p53复合物的形成。这些发现为磺酰胺活性检测了新的分子靶标，并为治疗KSHV引起的淋巴增生性疾病提供了新的潜在前景。