The infection of HIV causes AIDS, which is a prevalent problem today. Retroviral infection happens upon the integration of a copy of the DNA of the viral genome into the host DNA at any location in the genome but is preferred in certain regions of the chromatin as a necessary step in the replication. The challenge in the treatment of retroviral infections is that the integrated viral DNA is sustainably maintained and replicated along with cellular DNA through the cell division. Although wide prospects have been made in antiviral therapy of HIV, the integrated virus persists in long-lived cells and eradication is an elusive goal. Integrase protein is the key enzyme in the virus that integrates retroviral DNA into the host genome. As the rapid development of drug resistance in the existing drug classes, discovery of new targets is the need of the hour. The three major enzymes of HIV-1 integrase IN (HIV-1 IN), protease, and reverse transcriptase have been of special interest. Integration of viral genetic material with the host genome is an important step in the process of viral replication catalyzed by HIV-1 IN. 6 chloro 2 oxo 4 phenyl 1,2 dihydroquinolin-3-yl acetic acid, Quinoline class of inhibitors of HIV-1 integrase, was used in the present study to analyze the drug-protein interaction.