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Significantly Lower Plasma Virus Set Point in HIV-2 Infection Than in HIV-1 Infection

Sören Andersson, MD, PhD; Hans Norrgren, MD, PhD; Zacarias da Silva, MD; Antonio Biague, MD; Sana Bamba, MD; Shirley Kwok, PhD; Cindy Christopherson, PhD; Gunnel Biberfeld, MD, PhD; Jan Albert, MD, PhD

Arch Intern Med. 2000;160:3286-3293.

Background  The intriguing differences in the natural course, transmissibility, and epidemiological characteristics of human immunodeficiency virus type 1 (HIV-1) and HIV-2 are still insufficiently explained. Differences in plasma viral load are an obvious possibility, but this has been difficult to investigate because of the lack of tests for HIV-2 RNA.

Objective  To compare plasma HIV RNA load between individuals infected with HIV-1 and HIV-2 in Guinea-Bissau, a West African country with high prevalence and incidence of HIV-1 and HIV-2 infection.

Methods  A total of 102 participants were recruited from ongoing prospective cohort studies. These included 19 HIV-1 and 29 HIV-2 seroincident cases tested at a median of less than 2 years after seroconversion as well as seroprevalent cases with single (9 HIV-1 cases and 31 HIV-2 cases) or dual (n = 14) infections. Plasma HIV RNA levels were determined by a commercial HIV-1 assay and an experimental HIV-2 assay based on the same principles.

Results  The viral set point, ie, the semi-equilibrium reached after seronconversion, was 28-fold lower in recent HIV-2 seroconverters than in recent HIV-1 seroconverters (median, 2500 and 70,000 RNA copies per milliliter, respectively; P<.001). This difference appeared to persist to symptomatic stages of the diseases. Dually infected individuals had lower plasma HIV-1 RNA levels than singly infected individuals.

Conclusions  The differences between HIV-1 and HIV-2 infection are likely to be caused by differences in plasma viral set point and load, but the mechanisms through which HIV-2 infection is contained to a higher degree than HIV-1 remain to be identified.

From the Swedish Institute for Infectious Disease Control and the Microbiology and Tumour Biology Center, Karolinska Institute, Stockholm, Sweden (Drs Andersson, Biberfeld, and Albert); Department of Infectious Diseases, University Hospital, Lund, Sweden (Dr Norrgren); National Public Health Laboratory, Bissau, Guinea-Bissau (Drs da Silva, Biague, and Bamba); and Roche Molecular Systems Inc, Alameda, Calif (Drs Kwok and Christopherson).

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