Clinical Significance

Human immunodeficiency virus is the causative agent of acquired immunodeficiency syndrome (AIDS). AIDS was first described in the United States in 1981 and has become one of the leading causes of death worldwide. Despite educational efforts directed toward reducing the transmission of AIDS and increased advancements in treatment, the number of AIDS cases continues to increase.

Human immunodeficiency virus type 1 (HIV‑1) has been identified as the primary cause of acquired immunodeficiency syndrome (AIDS). This retrovirus, a member of the lentivirinae subfamily, is spread by sexual contact, exposure to infected blood or blood products, and perinatal transmission. In 1986, human immunodeficiency virus type 2 (HIV‑2) was isolated from AIDS patients in West Africa. These viruses share epitopes of the core proteins, but exhibit little or no cross-reactivity between the envelope glycoproteins.

Comparison of the nucleic acid sequences for HIV‑1 and HIV‑2 shows approximately 60% homology in the conserved genes, such as gag and pol (encoding core proteins), and 30%–40% homology in less conserved regions (encoding envelope proteins). HIV‑1 has been subdivided into group M (subtypes A–H) and group O.

The routes of transmission of HIV‑1 and HIV‑2 are the same. However, the transmission and the viral replication rate are much lower in HIV‑2 infections. Clinical studies have shown that in HIV‑2 infections there is a slower disease progression than in HIV‑1 infections. In HIV‑2 infections, there is a slower rate in the decline of CD4 T‑cells and reduced viremia. Individuals infected with HIV‑2 generally have a better clinical outcome.