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. 2017 May 23;8:580. doi: 10.3389/fimmu.2017.00580

Table 1.

Comparison of HIV-1 and HIV-2 infection.

Human immunodeficiency virus (HIV)-1 HIV-2
Epidemiological and clinical significance between HIV-1 and HIV-2 infection

Geographical distribution Global Confined to West Africa with limited spread; also reported in former Portuguese colonies, such as Angola, Mozambique, and Brazil, and in parts of India

Heterosexual transmission Sexual mode of transmission is higher Fivefold lower rate than HIV-1

Vertical transmission Mother to child transmission is higher 20- to 30-fold lower rate than HIV-1

Duration of asymptomatic stage Time to develop acquired immune deficiency syndrome (AIDS) varies, ranging from a few months to many years, with an estimated median time of 9.8 years Longer duration, ranging from 10–25 years

Clinical illness If untreated, around half of people infected with HIV-1 will develop AIDS within 10 years 86–95% of people infected with HIV-2 are long-term non-progressors

Proviral DNA load Similar Similar

Plasma RNA load Higher Significantly lower than HIV-1

Viral replication kinetics Higher replication and 100-fold more fit Transient replication and less fit

Infectivity and transmission fitness Similar and 100-fold more fit Similar and less fit

Co-receptor usage Uses CXCR4 and CCR5 Uses a range of co-receptors, including CCR1, CCR2, CCR3, CXCR6, BOB, CCR5, and CXCR4

CD4+ T-cell responses between HIV-1 and HIV-2 infection

CD4+ T-cell count Lower compared to HIV-2 with undetectable viral load but similar to HIV-2 with higher viral load Higher in HIV-2 with undetectable viral load and similar to HIV-1 with higher viral load

CD4+ T-cell response Lesser proliferative capacity and polyfunctionality, and increased differentiation Better proliferative capacity, more polyfunctionality, and lesser differentiation

Thymic function HIV-1 can replicate efficiently in thymus tissue. No correlation with the rate of CD4+ T-cell loss HIV-2 is able to infect the human thymus, but this is associated with limited viral replication. Correlates with lower rates of CD4+ T-cell

Production of cytokines Interleukin (IL)-2- and IL-4-producing cells decline as disease progresses IL-2- and IL-4-producing cells better preserved. Expressions of both IL-2- and IFN-γ-producing cells are more

CD57−CD4+ T-cell expression Less frequently seen More CD57− cells are seen

CD4+ T-cell activation level Positive correlation between lipopolysaccharide (LPS) level and proinflammatory cytokines IL-12 and IFN-γ Negative correlation between LPS level and proinflammatory cytokines in HIV-2 individuals with undetectable VL

Susceptibility to the SAMHD1 Myeloid cells are refractory to viral infection Presence of Vpx permits viral infection of myeloid cells through degradation of SAMHD1

Immune activation and T-cell apoptosis Higher immune activation and more apoptosis Less immune activation and less T-cell apoptosis

Nef Does not downmodulate the TCR–CD3 complex Downregulates the TCR–CD3 complex