Overview
Although HIV-2 is predominantly a disease of West Africa, it has spread to other parts of the world, including Europe, India, and the United States. As such, it is important for practicing clinicians to be familiar with the clinical features, diagnosis, and management of HIV-2 disease.
Most of the global AIDS pandemic is attributable to HIV-1 infection, but HIV-2 infection is prevalent in West Africa and occurs in other parts of the world, especially in regions with historical and economic relationships with West Africa. Because cases of HIV-2 infection and HIV-1/2 coinfection have been reported in Europe, India, the United States, South America, and other areas, it is important for clinicians to understand the clinical features of HIV-2 infection, as well as its epidemiology, diagnostic challenges, and therapeutic options.
HIV-2 infection, which was first described in 1986, originated in West Africa.[1] The highest prevalence of HIV-2 infection is in Guinea-Bissau, the Gambia, Senegal, and Cape Verde, although it also occurs in Cote d’Ivoire, Mali, Sierra Leone, and Nigeria.[2] Over time, because of established trade routes, cases of HIV-2 infection have been reported in other countries with historical and economic ties to West Africa, such as France and Portugal and the latter’s former colonies of Angola, Mozambique, Brazil, and Goa, India.[2,3]
Like HIV-1 infection, HIV-2 can lead to AIDS, predisposing infected individuals to opportunistic conditions. HIV-2 infection often progresses at a slower pace than HIV-1 infection, with longer preservation of CD4+ T cells and immune function.[4–6] Further, patients with HIV-2 infection tend to have lower viral loads than those with HIV-1 infection;[7–10] the median viral load is approximately 30-fold lower in HIV-2–infected individuals who have seroconverted than in HIV-1–infected individuals who have seroconverted.[11] Moreover, a substantial proportion (one-quarter to one-third) of HIV-2–infected individuals have viral RNA levels below the limit of detection.[12] It is thought that this lower viral load accounts for the reduced pathogenicity and transmissibility of HIV-2 compared with HIV-1 infection. Lower transmissibility is the likely reason that the number of HIV-2–infected individuals appears to be plateauing at 1 million worldwide and that, in some areas, the prevalence of HIV-2 infection is declining.[13–15] Nevertheless, untreated individuals with HIV-2 infection may develop low CD4+ cell counts and opportunistic conditions similar to those seen in the HIV-1–infected population, including tuberculosis, wasting syndrome, Candida esophagitis, disseminated Mycobacterium avium infection, Pneumocystis pneumonia, cryptococcosis, and cytomegalovirus infection.[3]
Currently, screening immunoassays detect HIV-1 antigen and antibodies and HIV-2 antibodies. However, HIV-1 RNA assays do not reliably detect or quantify HIV-2 RNA, and most laboratories do not routinely perform testing for plasma HIV-2 RNA. Although some commercial laboratories perform qualitative HIV-2 nucleic acid testing, only a few reference labs perform quantitative measurements. Assays to detect resistance of HIV-2 to antiretroviral drugs are not validated for clinical use. This dearth of HIV-2 nucleic acid assays leads to challenges in monitoring the infection before and after initiation of antiretroviral therapy.
Therapy itself brings unique challenges, as antiretroviral medications are developed to target HIV-1 reverse transcriptase, protease, or integrase, and hence not all antiretroviral drugs are effective against HIV-2 infection. In the following case, diagnostic testing, when to initiate antiretroviral therapy, and which initial antiretroviral regimen to choose for an HIV-2–infected patient are discussed in light of these considerations.