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Virus Details


VHFID3838

Host Factor Information

Pathogen Information

Publication Information

Host Factor Information

Gene Name CSNK2A1
HF Protein Name Casein kinase II subunit alpha
HF Function Essential for virus replication
Uniprot ID P68400
Protein Sequence View Fasta Sequence
NCBI Gene ID 1457
Host Factor (HF) Name in Paper CK2
Gene synonyms CK2A1
Ensemble Gene ID ENSG00000101266
Ensemble Transcript ENST00000217244 [P68400-1];ENST00000349736 [P68400-1];ENST00000400217 [P68400-2]
KEGG ID Go to KEGG Database
Gene Ontology ID(s) GO:0004674, GO:0005524, GO:0005634, GO:0005654, GO:0005829, GO:0005886, GO:0005956, GO:0006351, GO:0006355, GO:0006457, GO:0006468, GO:0006656, GO:0006915, GO:0007049, GO:0007165, GO:0008284, GO:0016055, GO:0016236, GO:0016301, GO:0018107, GO:0030177, GO:0030307, GO:0042802, GO:0043154, GO:0045732, GO:0047485, GO:0048511, GO:0051879, GO:0061077, GO:1901796, GO:1905818,
MINT ID P68400
STRING Click to see interaction map
GWAS Analysis Click to see gwas analysis
OMIM ID 115440
PANTHER ID N.A.
PDB ID(s) 1JWH, 1NA7, 1PJK, 2PVR, 2ZJW, 3AMY, 3AT2, 3AT3, 3AT4, 3AXW, 3BQC, 3C13, 3FWQ, 3H30, 3JUH, 3MB6, 3MB7, 3NGA, 3NSZ, 3OWJ, 3OWK, 3OWL, 3PE1, 3PE2, 3PE4, 3Q04, 3Q9W, 3Q9X, 3Q9Y, 3Q9Z, 3QA0, 3R0T, 3RPS, 3TAX, 3U4U, 3U87, 3U9C, 3W8L, 3WAR, 3WIK, 3WIL, 3WOW, 4DGL, 4FBX, 4GRB, 4GUB, 4GYW, 4GYY, 4GZ3, 4IB5, 4KWP, 4MD7, 4MD8, 4MD9, 4NH1, 4RLL, 4UB7, 4UBA, 5B0X, 5CLP, 5CQU, 5CQW, 5CS6, 5CSH, 5CSP, 5CSV, 5CT0, 5CTP, 5CU0, 5CU2, 5CU3, 5CU4, 5CU6, 5CVF, 5CVG, 5CVH, 5CX9, 5H8B, 5H8E, 5H8G, 5HGV, 5KU8, 5KWH, 5M44, 5M4C, 5M4F, 5M4I, 5MMF, 5MMR, 5MO5, 5MO6, 5MO7, 5MO8, 5MOD, 5MOE, 5MOH, 5MOT, 5MOV, 5MOW, 5MP8, 5MPJ, 5N1V, 5N9K, 5N9L, 5N9N, 5NQC, 5OMY, 5ONI, 5OQU, 5ORH, 5ORJ, 5ORK, 5OS7, 5OS8, 5OSL, 5OSZ, 5OT5, 5OT6, 5OTD, 5OTH, 5OTI, 5OTL, 5OTO, 5OTQ, 5OTR, 5OTY, 5OTZ, 5OUE, 5OUL, 5OUM, 5OUU, 5OYF, 5T1H, 5VIE, 5VIF, 6EHK, 6EHU, 6EII,
pfam ID PF00069,
Drug Bank ID DB03127, DB08846, DB04395, DB02709, DB04462,
ChEMBL ID CHEMBL3629
Organism Homo sapiens (Human)

Pathogen Information

Virus Name Human herpesvirus 1
Virus Short Name HSV1
Order Herpesvirales
Virus Family Herpesviridae
Virus Subfamily Alphaherpesvirinae
Genus Simplexvirus
Species Herpes simplex virus 1
Host Human, mammals
Cell Tropism Primary site of infection: epithelial mucosal cells , latency: remains latent in sensory neurons (ganglions)
Associated Disease Skin vesicles or mucosal ulcers, rarely encephalitis and meningitis
Mode of Transmission Contact, saliva
VIPR DB link http://www.viprbrc.org/brc/vipr_allSpecies_search.do?method=SubmitForm&decorator=herpes
ICTV DB link https://talk.ictvonline.org/ictv-reports/ictv_9th_report/dsdna-viruses-2011/w/dsdna_viruses/91/herpesviridae
Virus Host DB link http://www.genome.jp/virushostdb/view/?virus_lineage=Herpesviridae

Publication Information

Paper Title CK2 Inhibitors Increase the Sensitivity of HSV-1 to Interferon-beta
Author's Name Miles C. Smith, Adam M. Bayless, Erica T. Goddard, and David J. Davido
Journal Name Antiviral Research
Pubmed ID 21722672
Abstract Herpes simplex virus type 1 (HSV-1) requires the activities of cellular kinases for efficient replication. The host kinase, CK2, has been shown or is predicted to modify several HSV-1 proteins and has been proposed to affect one or more steps in the viral life cycle. Furthermore, potential cellular and viral substrates of CK2 are involved in antiviral pathways and viral counter-defenses, respectively, suggesting that CK2 regulates these processes. Consequently, we tested whether pharmacological inhibitors of CK2 impaired HSV-1 replication, either alone or in combination with the cellular antiviral factor, interferon-beta (IFN-beta). Our results indicate that the use of CK2 inhibitors results in a minor reduction in HSV-1 replication but enhanced the inhibitory effect of IFN-beta on replication. This effect was dependent on the HSV-1 E3 ubiquitin ligase, infected cell protein 0 (ICP0), which impairs several host antiviral responses, including that produced by IFN-beta. Inhibitors of CK2 did not, however, impede the ability of ICP0 to induce the degradation of two cellular targets: the promyelocytic leukemia protein (PML) and the DNA-dependent protein kinase catalytic subunit (DNA-PKcs). Notably, this effect was only apparent for HSV-1, as the CK2 inhibitors did not enhance the antiviral effect of IFN-beta on either vesicular stomatitis virus or adenovirus type 5. Thus, our data suggest that the activity of CK2 is required for an early function during viral infection that assists the growth of HSV-1 in IFN-beta-treated cells.
Used Model HEL,Vero,and L7 cells
DOI 10.1016/j.antiviral.2011.06.009