Human Immunodeficiency Virus 2 (HIV‑2) is an enveloped retrovirus that causes a form of human immunodeficiency similar to, but generally less severe than, infection with HIV‑1. It belongs to the genus Lentivirus in the family Retroviridae. The virion is roughly 80–100 nm in diameter and contains two copies of a positive‑sense single‑stranded RNA genome of about 9 kb enclosed in a conical capsid. HIV‑2 was first identified in 1986 in West Africa and remains largely endemic to that region, though cases have been reported worldwide due to travel and migration.
Genomic organization and biology
The HIV‑2 genome encodes structural polyproteins (Gag, Pol and Env) and accessory proteins (Tat, Rev, Nef, Vif, Vpr and Vpx). Long terminal repeat sequences flank the genome and act as promoters for transcription. Entry into host cells requires binding of the surface glycoprotein gp125 to the CD4 receptor, followed by interaction with CCR5 co‑receptor; usage of CXCR4 is rare. Fusion mediated by gp36 releases the viral core, and reverse transcriptase synthesizes complementary DNA that is integrated into the host genome. Compared with HIV‑1, HIV‑2 replicates less efficiently and produces lower plasma viral loads, contributing to a slower decline of CD4 T‑cell counts. Genetic diversity of HIV‑2 is lower; nine groups (A–I) have been described, with groups A and B causing most human infections. Phylogenetic analyses indicate that HIV‑2 originated from simian immunodeficiency viruses of sooty mangabeys in West Africa. Non‑nucleoside reverse transcriptase inhibitors are largely inactive against HIV‑2 due to differences in the reverse transcriptase enzyme, but protease inhibitors and integrase inhibitors retain activity.
Epidemiology and clinical significance
HIV‑2 remains concentrated in countries such as Guinea‑Bissau, Senegal, Gambia and Cape Verde, with sporadic cases elsewhere. An estimated 1–2 million people worldwide are infected. Transmission occurs via sexual contact, blood exposure and vertical routes but is less efficient than for HIV‑1. Many individuals remain asymptomatic for extended periods, and progression to AIDS is slower, often taking decades. Nonetheless, without treatment HIV‑2 can cause profound immunodeficiency and opportunistic infections. Diagnosis requires specific serologic and nucleic‑acid tests because some screening assays have reduced sensitivity. Combination antiretroviral therapy is recommended for symptomatic patients or those with declining CD4 counts. Treatment regimens usually include nucleoside reverse transcriptase inhibitors, integrase inhibitors and protease inhibitors; non‑nucleoside reverse transcriptase inhibitors should be avoided due to intrinsic resistance. Prevention strategies mirror those for HIV‑1, including safe sex practices, harm‑reduction programs and screening of blood products. HIV‑2 illustrates the diversity of lentiviral infections in humans. Its limited geographic range and lower transmissibility have constrained its spread, but ongoing surveillance and tailored treatment are essential to manage infections and prevent further dissemination. Related Terms: Human Immunodeficiency Virus 1, Human T‑Cell Leukemia Virus 1, Human T‑Cell Leukemia Virus 2, Human T‑Cell Leukemia Virus 3, Hepatitis D Virus