Gene-gene interactions, and developmental and individual differences in gene expression, for regional brain development and normal visuo-spatial function and social behavior. Several decades have passed since the identification of the human immunodeficiency virus as the causative agent of acquired immune deficiency syndrome. However, we are still unable to eradicate the virus from infected patients. Because of the difficulties that are encountered in developing traditional vaccines, investigating the potentials of antiviral factors as prophylactics or therapies will be very valuable. The replication of HIV-1 in infected cells encompasses fusion, viral core release and uncoating, reverse transcription, the translocation of the preCT99021 integration complex to the nucleus, viral DNA integration, proviral transcription and translation and viral assembly and budding. Most of these steps were reported to be widely challenged by host antiviral factors, especially TRIM family members, which share an N-terminal RING domain, one or two B-boxes, a putative coiled-coil domain and a variable Cterminus. For example, the well-known restriction factor TRIM5a limits retroviral replication at multiple-steps in a speciesspecific manner. TRIM37 reduces HIV-1 DNA synthesis by being incorporated into virus particles, whereas TRIM28 functions via a different mechanism by inducing the deacetylation of integrase, resulting in the reduction of HIV-1 DNA integration. A screening of 36 human TRIM proteins for potential antiHIV-1 activity identified several TRIM proteins that could affect both the early and/or late stages of the virus life cycle. Among those proteins, TRIM11 inhibited both the entry and release of HIV-1. However, the precise mechanisms of underlying these inhibitory functions have not yet been analyzed. Oncolytic virotherapy has existed for over 100 years and is a promising method for the treatment of cancer patients because of the strong cytolytic response of virus-infected tumor cells; however, complications may result from the use of oncolytic viruses including toxicity against normal cells. Thus, artificially modified oncolytic viruses have been engineered to achieve low toxicity against normal tissues together with sufficient antitumor activity. Oncolytic viruses that have been modified to express human cytokines, such as granulocyte macrophage colonystimulating factor have the potential for future therapeutic use in the treatment of solid tumors. JX-594 is a GM-CSF-armed oncolytic poxvirus that has shown promising outcomes.