N of monocytesmacrophages, is released by HIV infected macrophages and dampens the synthesis of AG, overriding the IFNinduced upregulation of AG (Souza et al).All round, the transcriptional regulation of A genes appears to play a major role in Adependent defenses against viruses.Remarkably, following mucosal immunization of nonhuman primates, two research reported the upregulation of AG in CCR CD memory T cells (Wang et al) as well as in mucosal DC and CD cells (Sui et al), all possible cellular targets of HIV replication.AG mRNA upregulation was maintained over a number of weeks right after immunization and upon challenge with SIV, and correlated inversely with viral loads and positively using a better preservation of CD T cells within the gut (Sui et al).These studies strongly suggest that AG delivers an antiviral impact in vivo.Additionally they demonstrate that mucosal immunization triggers an innate signature that promotes adaptive immune responses.The exact mechanism underlying vaccineinduced AG expresssion with protection from SIV infection is not clear.As observed within the murine model of Buddy retrovirus (FV) infection (Santiago et al), by limiting early viral replication, AG could delay virusinduced immune dysfunction and therefore might favor the establishment of humoral [e.g generation of FVneutralizing antibodies (Santiago et al)] and cellular immunity.A Role OF AG In the ACTIVATION OF CELLULAR AND ADAPTIVE IMMUNITY There is expanding proof that AG bridges intrinsic and cellular immunity as is definitely the case with Aid, that shapes the Ab repertoire, blocks virusinduced cancer by inducing cell cycle arrest and activates NK cells (Gourzi et al).AG has been implicated in enhancing NKcell killing of HIVinfected T cells (Norman et al).This approach calls for AGediting of HIV DNA (Norman et al).Within this study, the authors propose that the cellular DNArepair machinery activates DNAdamage and stress esponse pathways in response to uraciledited HIV DNA, leading to the upregulation of activating NK cell ligands (NKGD ligands) and killing of HIV infected cells.The authors also implicate the HIV Vpr protein and itscapacity to recruit the DNArepair machinery as a key element in NKGD ligand expression.In contrast, HIV PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/21509752 Vif counteracts the action of AG plus the NK cellmediated elimination of HIVinfected cells (Norman et al).Interestingly, inside the function of Norman et al cytoplasmic AG (expressed by the target cell) seems responsible for HIV editing and hence NK cell recognition.Cytoplasmic AG has been shown to impact HIV genome integration but has not been assigned a role in HIV genome editing, to our Macropa-NH2 Biological Activity information (Vetter and D’Aquila,).Regardless of whether the accumulation of unintegrated HIV genomes or the editing of HIV genomes per se might be responsible for the induction of strain responses and as a result NK cell recognition remains to be clarified (Norman et al).Nonetheless, this study suggests that AG antiviral functions enable triggering of danger signals that, in turn, activate effectors of cellular immunity.AGmediated editing also contributes for the activation of effectors of adaptive immunity (Casartelli et al ), namely, CD cytotoxic T cells (CTLs).CTLs, whose function is crucial within the control of HIV infection, are triggered by viral peptides presented by MHC classI molecules around the surface of infected cells.These antigenic peptides originate from proteasomal degradation of native viral proteins and of defectiveabortive proteins generated in the course of translation (Yewdell and Nicchitta,).We ma.