Assisted by surface receptors of susceptible cells, HIV can successfully get access to cells, including the first receptors and the second receptors. Firstly, envelope glycoprotein gp120 of HIV-1 binds to the first receptors, followed by its binding to the second receptors. Its structural changes cause its detachment from gp41, resulting in fusion of HIV and host cellular membrane and its successful access to host cells. Within 24–48 h after its access, HIV reaches the local lymph nodes. At d 5, HIV components can be detected in the peripheral blood. The attack of HIV causes viremia, leading to acute infection.

Because the human immune system cannot eliminate all the virus, chronic infection occurs. Clinically, the infection has three types of clinical manifestations, typical progression, rapid progression and long term no progression. The factors influencing the progression of HIV infection include virus itself, host immunity and genetic background.

Within 2–12 weeks after access of HIV to human body, the human immune system produces various specific antibodies targeting HIV proteins. Only neutralizing antibody has antiviral effects.

The specific cellular immunity includes specific CD4 T lymphocytes responses and specific cytotoxic T lymphocytes responses. CD4 T lymphocytes, as the central cells in human immune system, play critical roles in specific immune responses. By secreting various cytokines, it induces B cell to produce anti-HIV antibody. By promoting the production and maturation of specific anti-HIV CD4 T lymphocytes, it activates macrophage and NK cells. CD8+ T lymphocytes, the effector cells of specific cellular immunity, inhibit the replication of HIV directly or indirectly via secretion of various cytokines, such as tumor necrosis factor and interferon.