Abstract
Interactions between viruses and cellular factors are essential for viral replication or host defense. The DNA damage response (DDR) orchestrates a molecular network of cellular mechanisms that integrates cell cycle regulation and DNA repair or apoptosis. Numerous studies have revealed that the DDR is activated by virus infection, aberrant DNA structures generated by viral DNA replication, or the integration of retroviruses. Although the DDR is an essential function for maintaining the genomic integrity of cells, viruses may utilize this mechanism to build a convenient environment for themselves, and the resulting perturbation of the DDR has been shown to increase the risk of tumorigenesis. There have been many studies investigating the roles of the DDR in oncogenic viruses such as Epstein-Barr virus (EBV), human papillomavirus (HPV), hepatitis B virus (HBV), human T-cell leukemia virus type 1 (HTLV-1), and Kaposi’s sarcoma-associated herpesvirus (KSHV). This review summarizes current knowledge on the roles of DDR in the KSHV lifecycle.
Highlights
For the survival of organisms, the faithful transmission of genetic information from a parent cell to its daughter cells is essential
PIKKs: Transducers of DNA Damage Response The cellular responses to DNA damage are mainly controlled by three phosphatidylinositol 3-kinase-like kinases (PIKKs): ATM (Ataxia telangiectasia mutated), ATR (ATM and Rad3-related), and DNA-PK (Cimprich and Cortez, 2008; Davis et al, 2014; Blackford and Jackson, 2017; Menolfi and Zha, 2020), which act as DNA damage transducers
poly (ADPribose) polymerase 1 (PARP1) has a pivotal role in DNA repair and is involved in various repair pathways, such as single-strand break repair (SSBR) (Leppard et al, 2003; Fisher et al, 2007), base excision repair (BER) (Masson et al, 1998; Dantzer et al, 2000; Lavrik et al, 2001; El-Khamisy, 2003; Ronson et al, 2018), nucleotide excision repair (NER) (Pines et al, 2012; Robu et al, 2017), nonhomologous end joining (NHEJ) (Wang et al, 2006; Mansour et al, 2010; Cheng et al, 2011; Spagnolo et al, 2012; Luijsterburg et al, 2016), and homologous recombination (HR) (Hochegger et al, 2006; Hu et al, 2014)
Summary
Between KSHV and the Host DNA Damage Response. Interactions between viruses and cellular factors are essential for viral replication or host defense. The DNA damage response (DDR) orchestrates a molecular network of cellular mechanisms that integrates cell cycle regulation and DNA repair or apoptosis. Numerous studies have revealed that the DDR is activated by virus infection, aberrant DNA structures generated by viral DNA replication, or the integration of retroviruses. The DDR is an essential function for maintaining the genomic integrity of cells, viruses may utilize this mechanism to build a convenient environment for themselves, and the resulting perturbation of the DDR has been shown to increase the risk of tumorigenesis. There have been many studies investigating the roles of the DDR in oncogenic viruses such as Epstein-Barr virus (EBV), human papillomavirus (HPV), hepatitis B virus (HBV), human Tcell leukemia virus type 1 (HTLV-1), and Kaposi’s sarcoma-associated herpesvirus (KSHV).
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