Commercially known as Ginleya, fingolimod is an oral medicine used in the treatment of multiple sclerosis, a disease where the body's own immune system attacks the central nervous system. Fingolimod is an immunomodulatory drug that specifically targets Sphingosine-1-phosphate, or S1P, a part of the immune system. In the cell-signalling system, S1P has many functions, including cell proliferation and migration, survival, apoptosis and inflammation (programmed self-destruction). Without S1P binding to its unique receptors (proteins found on the cell surface), which are numbered S1PR1 to S1PR5, none of these processes could occur. On several subsets of CD4 T cells, S1PR1 and S1PR4 are present. They can be modulated by drugs that bind to receptors and create an effect inside cells (called agonists) and also by drugs (antagonists) that block agonists from those receptors. However, the full spectrum of S1P signalling in CD4 T cells is not completely known, as is the influence of HIV-1 on S1P receptors. The researchers looked at the role of S1P signalling in the production of productive HIV infection. For this, they used HIV-negative people's CD4 T cells that they expanded in culture, then triggered. Cells were then treated with multiple doses of fingolimod before being infected with either X4 or R5 tropical HIV-1 infections. This was essential because HIV binds to the cell's CD4 receptor, but also to either the CCR5 coreceptor (R5-tropic) or the CXCR4 coreceptor (R4-tropic) or both (dual-tropic) selectively. This provided evidence that fingolimod does have an impact on the establishment of productive HIV-1 infection through interfering with the S1P signalling. This review tells about the future scope of the new invention towards the field of HIV /AIDS and their medicinal treatment. People who are interested can send their article towards our journal for publication through this https://www.scholarscentral.org/submissions/hiv-aids-research.html