Acquired immune deficiency syndrome (AIDS) is caused by infection of human immunodeficiency virus type 1 (HIV-1) and is one of the most destructive pandemics . The virus is presented in the form of both free viruses and virus-infected immune cells. HIV is a Lentivirus and mainly infects dendritic cells, CD4+ T lymphocytes, and monocytes/macrophages in the human immune system . HIV-1 enters its target cells through interaction of viral glycoprotein spikes with CD4 and chemokine receptor CCR5 or CXCR4 on the cell surface. CCR5 is used by macrophage-tropic HIV-1 isolates at the early stage of HIV-1 infection, while CXCR4 is used by T cell-tropic HIV-1 isolates at later stages of HIV-1 infection. Then, the viral envelope is fused with the cell membrane; the virion core including RNA genome, capsid, and viral enzymes is released into the cell. After the virion core enters the cell, reverse transcriptase converts singlestranded viral RNA into proviral DNA. This process often gives rise to mutations that offer drug-resistance or allow the virus to evade the body's immune response because of the highly error-prone nature of reverse transcriptase. Proviral DNA is then imported into the nucleus and becomes integrated into host genome by viral integrase . Viral RNA are transcribed from the integrated proviral DNA and exported into cytoplasm for viral protein synthesis. The final step of the viral cycle is assembly of new HIV-1 virons, which occurs at the plasma membrane of the host cells. During the maturation of virons, HIV protease cleaves the polyproteins into individual functional HIV structural proteins and enzymes and the virus becomes mature and ready for the new round of infection