The interplay between human herpes simplex virus infection and the apoptosis and necroptosis cell death pathways
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REVIEW
Open Access
The interplay between human herpes simplex virus infection and the apoptosis and necroptosis cell death pathways Xiaoliang Yu1,2 and Sudan He1,2*
Abstract Human herpes simplex virus (HSV) is a ubiquitous human pathogen that establishes a lifelong latent infection and is associated with mucocutaneous lesions. In multicellular organisms, cell death is a crucial host defense mechanism that eliminates pathogen-infected cells. Apoptosis is a well-defined form of programmed cell death executed by a group of cysteine proteases, called caspases. Studies have shown that HSV has evolved strategies to counteract caspase activation and apoptosis by encoding anti-apoptotic viral proteins such as gD, gJ, Us3, LAT, and the ribonucleotide reductase large subunit (R1). Recently, necroptosis has been identified as a regulated form of necrosis that can be invoked in the absence of caspase activity. Receptor-interacting kinase 3 (RIP3 or RIPK3) has emerged as a central signaling molecule in necroptosis; it is activated via interaction with other RIP homotypic interaction motif (RHIM)-containing proteins such as RIP1 (or RIPK1). There is increasing evidence that HSV R1 manipulates necroptosis via the RHIM-dependent inactivation or activation ofRIP3 in a species-specific manner. This review summarizes the current understanding of the interplay between HSV infection and cell death pathways, with an emphasis on apoptosis and necroptosis. Keywords: Herpes simplex virus, Host defense, Cell death, Apoptosis, Necroptosis
Background Herpes simplex virus(HSV) is a ubiquitous human pathogen from the alpha-herpesvirinae subfamily [1]. There are two serotypes of HSV: HSV type 1 (HSV-1) and HSV type 2(HSV-2). It is a well-documented fact that the seropositivity rates for HSV-1 and HSV-2 in the general adult population are around 90 % and 25 %, respectively. HSV-1 is primarily associated with oral-labial lesions, whereas HSV-2 is the main cause of genital herpes [1, 2]. Rarely, severe infection of HSV-1 leads to fatal sporadic encephalitis [3]. HSV contains a large doublestranded DNA genome of around 150 K base pairs. There is around 83 % sequence homology of the protein-coding regions between HSV-1 and HSV-2 [4]. Therefore, HSV-1 and HSV-2 exhibit numerous biological similarities.
* Correspondence: [email protected] 1 Cyrus Tang Hematology Center and Collaborative Innovation Center of Hematology, Jiangsu Institute of Hematology, the First Affiliated Hospital, Soochow UniversitY, Suzhou, China 2 Jiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric Diseases, Soochow University, Suzhou, China
Cells have an innate capacity to activate effective antiviral countermeasures that can limit viral replication and viral dissemination. Among these antiviral responses, cell death is a common host defense mechanism against viral infection that eliminates virus-infected cells before the production of progeny virions. As would be expected, viruses tend to develop an ability to evade cell-death-based defenses; this
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