title: Functional interaction of nuclear domain 10 and its components with cytomegalovirus after infections: cross-species host cells versus native cells.
abstract: Species-specificity is one of the major characteristics of cytomegaloviruses (CMVs) and is the primary reason for the lack of a mouse model for the direct infection of human CMV (HCMV). It has been determined that CMV cross-species infections are blocked at the post-entry level by intrinsic cellular defense mechanisms, but few details are known. It is important to explore how CMVs interact with the subnuclear structure of the cross-species host cell. In our present study, we discovered that nuclear domain 10 (ND10) of human cells was not disrupted by murine CMV (MCMV) and that the ND10 of mouse cells was not disrupted by HCMV, although the ND10-disrupting protein, immediate-early protein 1 (IE1), also colocalized with ND10 in cross-species infections. In addition, we found that the UL131-repaired HCMV strain AD169 (vDW215-BADrUL131) can infect mouse cells to produce immediate-early (IE) and early (E) proteins but that neither DNA replication nor viral particles were detectable in mouse cells. Unrepaired AD169 can express IE1 only in mouse cells. In both HCMV-infected mouse cells and MCMV-infected human cells, the knocking-down of ND10 components (PML, Daxx, and SP100) resulted in significantly increased viral-protein production. Our observations provide evidence to support our hypothesis that ND10 and ND10 components might be important defensive factors against the CMV cross-species infection.
authors.affiliation: Department of Microbiology/AIDS Research Program, Ponce School of Medicine and Health Sciences, Ponce, Puerto Rico, United States of America.
authors.forename: Ruth Cruz
authors.initials: RC
authors.lastname: Cosme
authors.forename: Francisco Puerta
authors.initials: FP
authors.lastname: Martínez
authors.forename: Qiyi
authors.initials: Q
authors.lastname: Tang
mesh_terms: D000818:Animals; D003587:Cytomegalovirus / Q000235:genetics / Q000378:metabolism* / Q000502:physiology; D015967:Gene Expression Regulation, Viral; D055785:Gene Knockdown Techniques; D057809:HEK293 Cells; D006801:Humans; D017874:Immediate-Early Proteins / Q000096:biosynthesis / Q000378:metabolism; D051379:Mice; D018146:Muromegalovirus / Q000235:genetics / Q000378:metabolism* / Q000502:physiology; D041681:NIH 3T3 Cells; D009687:Nuclear Proteins / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D011485:Protein Binding; D021381:Protein Transport; D013045:Species Specificity; D014764:Viral Proteins / Q000096:biosynthesis / Q000378:metabolism
chemical_list: C094297:CALCOCO2 protein, human; C088645:IE1 protein, cytomegalovirus; D017874:Immediate-Early Proteins; D009687:Nuclear Proteins; D014764:Viral Proteins