Induction of lytic cycle replication of Kaposi's sarcoma-associated herpesvirus by herpes simplex virus type 1: involvement of IL-10 and IL-4

Qin, Di; Zeng, Yi; Qian, Chao Nan; Huang, Zan; Lv, Zhigang; Cheng, Lin; Yao, Shuang; Qiao, Tiankui; Chen, Xiuying; Liu, Chun

doi:10.1111/j.1462-5822.2007.01079.x

Cited by 33 publications

(39 citation statements)

References 57 publications

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“…The sequences of specific primers and probes of real-time quantitative reverse transcription-PCR (RT-qPCR) for KSHV RTA, ORF26, and LANA genes were described previously (54) and are listed in Table 1. Real-time quantification of miRNAs was performed by stem-loop RT-qPCR (52).…”

Section: Methodsmentioning

confidence: 99%

“…RT-PCR was performed as previously described (54). Primers for amplifying KSHV T1.1, vIL-6, ORF57, ORF26 (also known as KS330), and ␤-actin were described previously (54).…”

Section: Methodsmentioning

confidence: 99%

“…Western blotting was performed as previously described (54). To detect KSHV latent nuclear antigen ORF73, nuclear extracts of cells were prepared with an extraction kit (Active Motif, Tokyo, Japan).…”

Section: Western Blot Analysismentioning

confidence: 99%

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Inhibition of Kaposi's Sarcoma-Associated Herpesvirus Lytic Replication by HIV-1 Nef and Cellular MicroRNA hsa-miR-1258

Yan

Shen

et al. 2014

J Virol

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Kaposi's sarcoma-associated herpesvirus (KSHV) is causally linked to several AIDS-related malignancies, including IMPORTANCEThis study found that Nef, a secreted HIV-1 protein, suppressed KSHV lytic replication to promote KSHV latency. Mechanistic studies indicated that a Nef-upregulated cellular miRNA, hsa-miR-1258, inhibits KSHV replication by directly targeting a seed sequence in the KSHV RTA 3=UTR. These results illustrate that, in addition to viral miRNAs, cellular miRNAs also play an important role in regulating the life cycle of KSHV. Overall, this is the first study to report the involvement of Nef in KSHV latency, implying its likely important role in the pathogenesis of AIDS-related malignancies.

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Section: Methodsmentioning

confidence: 99%

“…RT-PCR was performed as previously described (54). Primers for amplifying KSHV T1.1, vIL-6, ORF57, ORF26 (also known as KS330), and ␤-actin were described previously (54).…”

Section: Methodsmentioning

confidence: 99%

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Inhibition of Kaposi's Sarcoma-Associated Herpesvirus Lytic Replication by HIV-1 Nef and Cellular MicroRNA hsa-miR-1258

Yan

Shen

et al. 2014

J Virol

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“…The procedure for Western blotting was previously described (14). Densitometry analysis of protein expression levels was performed with Scion Image software (Scion Corporation, Frederick, MD).…”

Section: Preparation Of Soluble Vpr Protein (Svpr)mentioning

confidence: 99%

“…(HIV-1), and human cytomegalovirus (HCMV) infections, regulate the life cycle of KSHV and cell proliferation and survival and thus might contribute to the development of these malignancies (13)(14)(15)(16)(17). Among these cofactors, HIV-1 infection increases KS incidence in HIV-infected individuals (3).…”

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confidence: 99%

HIV-1 Vpr Inhibits Kaposi's Sarcoma-Associated Herpesvirus Lytic Replication by Inducing MicroRNA miR-942-5p and Activating NF-κB Signaling

Yan

Shen

Qin

et al. 2016

J Virol

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Kaposi's sarcoma-associated herpesvirus (KSHV) infection is required for the development of several AIDS-related malignancies, including Kaposi's sarcoma (KS) and primary effusion lymphoma (PEL). The high incidence of AIDS-KS has been ascribed to the interaction of KSHV and HIV-1. We have previously shown that HIV-1-secreted proteins Tat and Nef regulate the KSHV life cycle and synergize with KSHV oncogenes to promote angiogenesis and tumorigenesis. Here, we examined the regulation of KSHV latency by HIV-1 viral protein R (Vpr). We found that soluble Vpr inhibits the expression of KSHV lytic transcripts and proteins, as well as viral particle production by activating NF-B signaling following internalization into PEL cells. By analyzing the expression profiles of microRNAs combined with target search by bioinformatics and luciferase reporter analyses, we identi- Kaposi's sarcoma-associated herpesvirus (KSHV), also known as human herpesvirus 8 (HHV-8), is the causative agent of Kaposi's sarcoma (KS). AIDS-associated Kaposi's sarcoma (AIDS-KS) remains a clinical challenge in sub-Saharan Africa and the United States, including a subset of AIDS patients receiving highly active antiretroviral therapy (HAART) (1-4). KSHV infection is also linked to two B-cell lymphoproliferative disorders associated with AIDS, including primary effusion lymphoma (PEL) and a subset of multicentric Castleman's disease (MCD) (5, 6).KSHV displays two distinct replication phases: a latent phase and a productive lytic phase. Following acute infection, KSHV in general establishes lifetime persistence in the infected individuals. During the latent phase, only a limited number of viral genes are expressed, which serve to maintain the persistence of the viral genome, restrict host immune responses, and enhance cell survival. KSHV latently infected cells can be reactivated into lytic replication by several intracellular or extracellular stimuli, such as hypoxia, oxidative stress, and certain cytokines (7-10). Activation of viral lytic replication results in the expression of viral lytic genes and the production of infectious virions (11). Both latent and lytic replication phases are crucial for the long-term persistence of KSHV in the host, and their gene products play critical roles in the pathogenesis of KSHV-associated disease.As is true of infection with other human oncogenic viruses, KSHV infection alone is not sufficient to cause KSHV-associated malignancy (1, 12). Previously, we and others demonstrated that other cofactors, such as human herpesvirus 6 (HHV-6), herpes simplex virus 1 (HSV-1), human immunodeficiency virus type 1

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Nitric oxide is induced and required for efficient Kaposi's sarcoma‐associated herpesvirus lytic replication

Herrera-Ortíz

Meng

Gao

2021

Journal of Medical Virology

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Kaposi's sarcoma-associated herpesvirus (KSHV) is an oncogenic virus associated with several human malignancies. KSHV lytic replication promotes the spread of infection and progression of KSHV-associated malignancies; however, the mechanism regulating KSHV lytic replication remains unclear. In this study, we investigated the role of nitric oxide (NO) in KSHV lytic replication. In the TREx BCBL1-RTA KSHV lytic replication cell system, induction of KSHV lytic replication increased intracellular and extracellular NO. Chemical inhibition of NO production resulted in a lower level of KSHV lytic replication as shown by a reduced level of infectious virions, and decreased levels of viral lytic transcripts and proteins. In a second KSHV lytic replication system of iSLK-RGB-BAC16 cells, we confirmed that KSHV lytic replication increased NO production. Chemical inhibition of NO production resulted in reduced numbers of cells expressing enhanced green fluorescent protein and blue fluorescent protein, two reporters that closely track the expression of KSHV early and late genes, respectively. Consistent with these results, inhibition of NO production resulted in reduced levels of infectious virions, and viral lytic transcripts and proteins. Importantly, exogenous addition of a NO donor was sufficient to enhance the full KSHV lytic replication program. These results demonstrate that NO is required for efficient KSHV lytic replication, and NO plays a crucial role in the KSHV life cycle and KSHV-induced malignancies.

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Induction of lytic cycle replication of Kaposi's sarcoma-associated herpesvirus by herpes simplex virus type 1: involvement of IL-10 and IL-4

Cited by 33 publications

References 57 publications

Inhibition of Kaposi's Sarcoma-Associated Herpesvirus Lytic Replication by HIV-1 Nef and Cellular MicroRNA hsa-miR-1258

Inhibition of Kaposi's Sarcoma-Associated Herpesvirus Lytic Replication by HIV-1 Nef and Cellular MicroRNA hsa-miR-1258

HIV-1 Vpr Inhibits Kaposi's Sarcoma-Associated Herpesvirus Lytic Replication by Inducing MicroRNA miR-942-5p and Activating NF-κB Signaling

Nitric oxide is induced and required for efficient Kaposi's sarcoma‐associated herpesvirus lytic replication

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