Many types of cells are permissive for CMV infection, which infection results in the production of infectious particles, but CMV infection and replication are limited to a narrow host range. For example, murine CMV can produce viral particles in both mouse and rat cells, while rat CMV cannot successfully replicate in mouse cells. Similar observations were also reported for human CMV and simian CMV. SCMV productively infected human and monkey cells, but HCMV failed to replicate in monkey cells. CMV replication in native host cells is a well-defined sequential process: entry into cells, immediate-early and early gene expression, DNA replication, late gene expression, and viral production. Blocking any stage will cause the failure of infection. It has been determined that both CMV cross-species infections and low MOI infections in permissive cells are blocked at the post-entry level by intrinsic cellular defense mechanisms, but few details are known. We and others recently discovered that TMN 355 viruses encode gene products that counter cellular defenses in human cells, which preventive action can help MCMV to successfully infect human cells. For instance, we discovered that intrinsic cellular defense mechanisms are involved in blocking MCMV infection in human cells and that these mechanisms can be overcome by HCMV-encoded proteins, resulting in successful cross-species infection. The Brune group discovered that the inhibition of apoptosis by the overexpression of Bcl-2 and other apoptosis inhibitors caused the successful replication of MCMV in human cells. However, very few efforts have attempted to determine how HCMV replication is blocked in mouse cells other than to observe that HCMV infection in mouse cells is blocked at the IE stage. The significance of successfully infecting mouse cells with HCMV is that doing so would enable the development of an HCMV mouse model. We are also curious whether any nuclear structure is involved in blocking cytomegalovirus cross-species infection. A nuclear structure called ND10 has been attracting intense attention from virologists due to the functional interaction of its components with viruses. Several herpes viruses were found to be capable of disrupting ND10, and various viral proteins have been identified as being related to ND10 and ND10 proteins, which identification has been summarized by Dr. Kalejta and colleagues. Recently, accumulated evidence showed that major ND10 components have negative impacts on the herpesviruses. Therefore, it has been assumed that ND10 defends RS 102895 hydrochloride against herpes viral infection, but this assumption is contradicted by the fact that several DNA viruses replicate DNA and transcribe RNA predominately at ND10.