HIV-2: the forgotten AIDS virus

doi:10.1016/j.tim.2008.09.003

Trends in Microbiology

Volume 16, Issue 12, December 2008, Pages 588-595

https://doi.org/10.1016/j.tim.2008.09.003 Get rights and content

HIV type 2 (HIV-2), a closely related retrovirus discovered a few years after HIV type 1, causes AIDS in only a minority of infected individuals. Determining why HIV-2 causes asymptomatic infection in most patients could further our understanding of HIV immunopathogenesis. Studies to date have suggested that both enhanced immune responses and lower viral replication could play a role. We summarize the important findings to date and highlight areas that warrant further exploration.

Section snippets

Studying HIV-2: a natural human model of attenuated HIV infection

Despite 25 years of research an HIV type 1 (HIV-1) vaccine remains elusive. A major obstacle has been lack of knowledge of host immune and viral factors that contribute to protection from infection or disease progression. These elements must be clearly defined for successful HIV vaccine development. Studying simian immunodeficiency virus (SIV) in its natural host, the sooty mangabey, and investigating immune responses in HIV-1 long-term nonprogressors (LTNPs) are the main approaches used to

Origins of HIV-2 and its current distribution

HIV-2 closely resembles SIV_sm from the West African sooty mangabey (Cercocebus torquatus atys), a simian virus that is thought to have entered the human population on at least eight separate occasions, yielding eight distinct HIV-2 groups of which only groups A and B are endemic; with the remainder being single-person infections (reviewed in 2, 3). No significant differences in disease progression, pathogenicity, or transmission have observed between HIV-2 groups A and B, and other HIV-2 groups

Natural history of HIV-2 infection

Although an initial serological survey of asymptomatic Senegalese sex workers [18] raised the possibility that HIV-2 might be a nonpathogenic retrovirus, there were subsequent reports of clinical syndromes in HIV-2 patients indistinguishable from HIV-1 AIDS. Evidence soon emerged that after HIV-2 seroconversion, the AIDS-free survival at 5 years was significantly greater (100% versus 67%) and the CD4⁺ T cell decline was much slower than with HIV-1 (reviewed in Ref. [19]). The clinical features

Is HIV-2 an attenuated virus?

The mild outcome of most HIV-2 infections could be explained by lower viral replication, enhanced host immune control or both. Despite suggestions that HIV-2 might be more attenuated, subsequent studies showed no difference in cytopathicity between HIV-1 and HIV-2 in a lymphoid histoculture model and suggested that co-receptor usage determines the cytopathic effect of both viruses (reviewed in [28]). However, different in vivo viral dynamics are evident in the two infections. VL set points and

Innate immune responses in HIV-2

The TRIM5α pathway emerged in studies of the non-human primates as blocking HIV-1 infection. TRIM5α acts by binding a motif on the viral capsid protein and interfering with later steps in infection by altering the intracellular trafficking of the infecting virion, possibly by activating ubiquitation and degradation. TRIM5α might also limit the accumulation of GAG precursors during retrovirus assembly (reviewed in [38]). Clinical cohort studies have revealed that some TRIM5α variants might

What role does immune activation play in HIV-2 pathogenesis?

The observation that SIV_sm infection of the natural host, the sooty mangabey monkey, leads to high levels of plasma viremia without evidence of immune suppression or disease progression has fuelled speculation that immune activation (which is characteristically low or absent in the SIV-infected sooty mangabey) rather than viral replication, is a fundamental mechanism by which HIV infection leads to disease. What is the relationship between immune activation and disease in HIV-2 infection?

The

HIV-1 and HIV-2 dual infection: lack of protection against HIV-1 from HIV-2 infection

Despite early optimism from Dakar claiming HIV-2 confers a protective effect from HIV-1 coinfection, further West African cohort studies have found no such protection; suggesting HIV-2 might even increase the risk of HIV-1 acquisition (reviewed in [82]). It is not yet clear if this trend is due to biological or behavioral factors and disentangling these issues could prove difficult. Several in vitro studies have also contributed to the debate surrounding HIV-2-mediated protection from HIV-1 (

HIV-2 treatment

Experience with treatment of HIV-2-infected patients with antiretroviral regimens is limited; this is partly due to the geographical restriction of HIV-2 patients to resource-poor settings where ART only recently became available. The potential difficulties in treating HIV-2 infection are summarized in Box 3. It is clear that there is limited information on which to base accurate guidelines for HIV-2 treatment. Given the small size of most HIV-2 cohorts, further advances are unlikely without

Concluding remarks and future perspectives

HIV-2 infection presents an intriguing puzzle: why does a pathogenic retrovirus fail to cause disease in the majority of infected individuals, yet emulate HIV-1 in the ability to cause AIDS in others? Some key components of the immune armory (such as HIV-specific CD4⁺ T cell responses) are well preserved in HIV-2 infections in contrast to HIV-1 infections. Other factors such as broad NAb responses, which are being fiercely researched for HIV-1 vaccine immunology, are yet to be confirmed in

Acknowledgements

T.I.dS. is supported by a British Infection Society Research Fellowship.

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In-depth analysis of the HIV pandemic at its epicenter in the Congo basin has been hampered by 40 years of political unrest and lack of functional public health infrastructure. In recent surveillance studies (2017-18), we found that the prevalence of HIV in Kinshasa, Democratic Republic of Congo (11%) far exceeded previous estimates.
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The human immunodeficiency virus (HIV) accessory protein Nef plays a major role in establishing and maintaining infection, particularly through immune evasion. Many HIV-2-infected people experience long-term viral control and survival, resembling HIV-1 elite control. HIV-2 Nef has overlapping but also distinct functions from HIV-1 Nef. Here we report the crystal structure of HIV-2 Nef core. The di-leucine sorting motif forms a helix bound to neighboring molecules, and moreover, isothermal titration calorimetry demonstrated that the CD3 endocytosis motif can directly bind to HIV-2 Nef, ensuring AP-2-mediated endocytosis for CD3. The highly conserved C-terminal region forms a α-helix, absent from HIV-1. We further determined the structure of simian immunodeficiency virus (SIV) Nef harboring this region, demonstrating similar C-terminal α-helix, which may contribute to AP-1 binding for MHC-I downregulation. These results provide insights into the distinct pathogenesis of HIV-2 infection.
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HIV type 2 (HIV-2) is considered more benign and has fewer pathogenic consequences than HIV type 1 (HIV-1) for most infected individuals. However, reliable estimates of time to AIDS and mortality among those with HIV-2 infection are absent. We therefore aimed to compare the time to AIDS and mortality, and the CD4 T-cell dynamics between those infected with HIV-1 and HIV-2.
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872 participants tested HIV positive during the 23-year study period: 408 were infected with HIV-1 (183 infected before and 225 infected after enrolment) and 464 were infected with HIV-2 (377 before and 87 after enrolment). The median time from HIV infection to development of AIDS was 6·2 years (95% CI 5·4–7·1) for HIV-1 infection and 14·3 years (10·7–18·0) for HIV-2 infection (p<0·0001). The median survival time after HIV infection was 8·2 years (95% CI 7·5–8·9) for HIV-1 infection and 15·6 years (12·0–19·2) for HIV-2 infection (p<0·0001). Individuals who were infected with HIV-1 or HIV-2 before enrolment showed similar results. Comparison with uninfected individuals indicated limited confounding contribution from natural mortality. Mean CD4 percentages were higher in individuals with HIV-2 than in those with HIV-1 during early infection (28·0% [SE 1·3] vs 22·3% [1·7]; p=0·00094) and declined at a slower rate (0·4% [0·2] vs 0·9% [0·2] per year; p=0·028). HIV-2-infected individuals developed clinical AIDS at higher mean CD4 percentages (18·2%, IQR 7·2–25·4) than HIV-1-infected individuals (8·2%, 3·0–13·8; p<0·0001).
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Swedish International Development Agency, Swedish Research Council, Swedish Society of Medical Research, Medical Faculty at Lund University, and Region Skåne Research and Development.

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Trends in Microbiology

ReviewHIV-2: the forgotten AIDS virus

Section snippets

Studying HIV-2: a natural human model of attenuated HIV infection

Origins of HIV-2 and its current distribution

Natural history of HIV-2 infection

Is HIV-2 an attenuated virus?

Innate immune responses in HIV-2

What role does immune activation play in HIV-2 pathogenesis?

HIV-1 and HIV-2 dual infection: lack of protection against HIV-1 from HIV-2 infection

HIV-2 treatment

Concluding remarks and future perspectives

Acknowledgements

Virology

Lancet

Blood

Virology

Virology

Curr. Biol.

Trends Biochem. Sci.

Virology

Cell

Virology

Genome organization and transactivation of the human immunodeficiency virus type 2

Nature

AIDS as a zoonosis: scientific and public health implications

Science

Identification of a highly divergent HIV type 2 and proposal for a change in HIV type 2 classification

AIDS Res. Hum. Retroviruses

Genetic diversity of human immunodeficiency virus type 2: evidence for distinct sequence subtypes with differences in virus biology

J. Virol.

Tracing the origin and history of the HIV-2 epidemic

Proc. Natl. Acad. Sci. U. S. A.

Genetic characterization of new West African simian immunodeficiency virus SIVsm: geographic clustering of household-derived SIV strains with human immunodeficiency virus type 2 subtypes and genetically diverse viruses from a single feral sooty mangabey troop

J. Virol.

Simian immunodeficiency virus infection in free-ranging sooty mangabeys (Cercocebus atysatys) from the Tai Forest, Cote d’Ivoire: implications for the origin of epidemic human immunodeficiency virus type 2

J. Virol.

Detection and partial characterization of simian immunodeficiency virus SIVsm strains from bush meat samples from rural Sierra Leone

J. Virol.

HIV-2 infection in Bissau, West Africa, 1987-1989: incidence, prevalences, and routes of transmission

J. Acquir. Immune Defic. Syndr.

Age of wife as a major determinant of male-to-female transmission of HIV-2 infection: a community study from rural West Africa

AIDS

Changes in prevalence and incidence of HIV-1, HIV-2 and dual infections in urban areas of Bissau, Guinea-Bissau: is HIV-2 disappearing?

AIDS

Twenty years of prospective molecular epidemiology in Senegal: changes in HIV diversity

AIDS Res. Hum. Retroviruses

Maternal plasma viral RNA levels determine marked differences in mother-to-child transmission rates of HIV-1 and HIV-2 in The Gambia. MRC/Gambia Government/University College London Medical School working group on mother-child transmission of HIV

AIDS

Lower levels of HIV RNA in semen in HIV-2 compared with HIV-1 infection: implications for differences in transmission

AIDS

Parenteral transmission during excision and treatment of tuberculosis and trypanosomiasis may be responsible for the HIV-2 epidemic in Guinea-Bissau

AIDS

Risk factors for HIV-2 seropositivity among older people in Guinea-Bissau. A search for the early history of HIV-2 infection

Scand. J. Infect. Dis.

The natural history of HIV-1 and HIV-2 infections in adults in Africa: a literature review

Bull. World Health Organ.

Kaposi’s sarcoma in the Gambia, West Africa is less frequent in human immunodeficiency virus type 2 than in human immunodeficiency virus type 1 infection despite a high prevalence of human herpesvirus 8

J. Hum. Virol.

Mortality of HIV-1, HIV-2 and HIV-1/HIV-2 dually infected patients in a clinic-based cohort in The Gambia

AIDS

Baseline plasma viral load and CD4 cell percentage predict survival in HIV-1- and HIV-2-infected women in a community-based cohort in The Gambia

J. Acquir. Immune Defic. Syndr.

Plasma RNA viral load predicts the rate of CD4 T cell decline and death in HIV-2-infected patients in West Africa

AIDS

Low peripheral blood viral HIV-2 RNA in individuals with high CD4 percentage differentiates HIV-2 from HIV-1 infection

J. Hum. Virol.

Low level viremia and high CD4% predict normal survival in a cohort of HIV type-2-infected villagers

AIDS Res. Hum. Retroviruses

Equal plasma viral loads predict a similar rate of CD4+ T cell decline in human immunodeficiency virus (HIV) type 1- and HIV-2-infected individuals from Senegal, West Africa

J. Infect. Dis.

Protective immunity against HIV infection: lessons from HIV-2 infection

Future Microbiol.

Plasma viral load in HIV-1 and HIV-2 singly and dually infected individuals in Guinea-Bissau, West Africa: significantly lower plasma virus set point in HIV-2 infection than in HIV-1 infection

Arch. Intern. Med.

Lower human immunodeficiency virus (HIV) type 2 viral load reflects the difference in pathogenicity of HIV-1 and HIV-2

J. Infect. Dis.

Low plasma human immunodeficiency virus type 2 viral load is independent of proviral load: low virus production in vivo

J. Virol.

Plasma viral load, CD4 cell percentage, HLA and survival of HIV-1, HIV-2, and dually infected Gambian patients

Review
HIV-2: the forgotten AIDS virus