ArticleBMC microbiology2011
Activation of PI3K/AKT and ERK MAPK signal pathways is required for the induction of lytic cycle replication of Kaposi's sarcoma-associated herpesvirus by herpes simplex virus type 1.
Article in BMC microbiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 59 citations in OpenAlex.
- The inflammatory kinase MAP4K4 promotes reactivation of Kaposi's sarcoma herpesvirus and enhances the invasiveness of infected endothelial cells.PLoS pathogens · 2013Trial
- Novel Hsp90 inhibitor JD‑02 inhibits HSV‑1 infection via the Raf/MEK/ERK signaling pathway.International journal of molecular medicine · 2026Article
- Mitogen-Activated Protein Kinases: Therapeutic Signaling Catalysts in Viral Immune Evasion.Pathogens (Basel, Switzerland) · 2026Review
- CMGC Kinases in Viral Infection and Human Disease.Pathogens (Basel, Switzerland) · 2026Review
- "Cytokine-Mediated tumor sensitization: mechanistic frameworks and therapeutic opportunities in cancer Immunotherapy".Clinical and experimental medicine · 2026Review
- Inhibition of MAPK signaling suppresses cytomegalovirus reactivation in CD34Antiviral research · 2025Article
- PINLYP-mediated phospholipid metabolism reprogramming contributes to chronic herpesvirus infection.PLoS pathogens · 2025Article
- Review
- KSHV hijacks the antiviral kinase IKKε to initiate lytic replication.PLoS pathogens · 2025Article
- Article
- The Impact of Co-Infections for Human Gammaherpesvirus Infection and Associated Pathologies.International journal of molecular sciences · 2023Review
- PI3K-Akt pathway-independent PIK3AP1 identified as a replication inhibitor of the African swine fever virus based on iTRAQ proteomic analysis.Virus research · 2023Article
- Suppression of KSHV lytic replication and primary effusion lymphoma by selective RNF5 inhibition.PLoS pathogens · 2023Article
- Modifications of the PI3K/Akt/mTOR axis during FeHV-1 infection in permissive cells.Frontiers in veterinary science · 2023Article
- Upregulation of ATF4-LAMP3 Axis by ORF45 Facilitates Lytic Replication of Kaposi's Sarcoma-Associated Herpesvirus.Journal of virology · 2022Article
- Chlorpromazine, a Clinically Approved Drug, Inhibits SARS-CoV-2 Nucleocapsid-Mediated Induction of IL-6 in Human Monocytes.Molecules (Basel, Switzerland) · 2022Article
- Duck Plague Virus Negatively Regulates IFN Signaling to Promote Virus ProliferationFrontiers in immunology · 2022Article
- 3D culture conditions support Kaposi's sarcoma herpesvirus (KSHV) maintenance and viral spread in endothelial cells.Journal of molecular medicine (Berlin, Germany) · 2021Article
- Potential Drug Strategies to Target Coronaviruses.Advances in experimental medicine and biology · 2021Article
- Antiviral Effectivity of Favipiravir Against Peste Des Petits Ruminants Virus Is Mediated by the JAK/STAT and PI3K/AKT Pathways.Frontiers in veterinary science · 2021Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundKaposi's sarcoma-associated herpesvirus (KSHV) is causally linked to several acquired immunodeficiency syndrome-related malignancies, including Kaposi's sarcoma (KS), primary effusion lymphoma (PEL) and a subset of multicentric Castleman's disease. Regulation of viral lytic replication is critical to the initiation and progression of KS. Recently, we reported that herpes simplex virus type 1 (HSV-1) was an important cofactor that activated lytic cycle replication of KSHV. Here, we further investigated the possible signal pathways involved in HSV-1-induced reactivation of KSHV.
resultsBy transfecting a series of dominant negative mutants and protein expressing constructs and using pharmacologic inhibitors, we found that either Janus kinase 1 (JAK1)/signal transducer and activator of transcription 3 (STAT3) or JAK1/STAT6 signaling failed to regulate HSV-1-induced KSHV replication. However, HSV-1 infection of BCBL-1 cells activated phosphatidylinositol 3-kinase (PI3K)/protein kinase B (PKB, also called AKT) pathway and inactivated phosphatase and tensin homologue deleted on chromosome ten (PTEN) and glycogen synthase kinase-3β (GSK-3β). PTEN/PI3K/AKT/GSK-3β pathway was found to be involved in HSV-1-induced KSHV reactivation. Additionally, extracellular signal-regulated protein kinase (ERK) mitogen-activated protein kinase (MAPK) pathway also partially contributed to HSV-1-induced KSHV replication.
conclusionsHSV-1 infection stimulated PI3K/AKT and ERK MAPK signaling pathways that in turn contributed to KSHV reactivation, which provided further insights into the molecular mechanism controlling KSHV lytic replication, particularly in the context of HSV-1 and KSHV co-infection.
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