title: 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.
abstract: 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. Arch Intern Med. 2000;160:3286-3293.
authors.affiliation: Swedish Institute for Infectious Disease Control, SE-17182 Solna, Sweden. soren.andersson@orebroll.se
authors.forename: S
authors.initials: S
authors.lastname: Andersson
authors.forename: H
authors.initials: H
authors.lastname: Norrgren
authors.forename: Z
authors.initials: Z
authors.lastname: da Silva
authors.forename: A
authors.initials: A
authors.lastname: Biague
authors.forename: S
authors.initials: S
authors.lastname: Bamba
authors.forename: S
authors.initials: S
authors.lastname: Kwok
authors.forename: C
authors.initials: C
authors.lastname: Christopherson
authors.forename: G
authors.initials: G
authors.lastname: Biberfeld
authors.forename: J
authors.initials: J
authors.lastname: Albert
mesh_terms: D000163:Acquired Immunodeficiency Syndrome / Q000821:virology; D000328:Adult; D000368:Aged; D015153:Blotting, Western; D018791:CD4 Lymphocyte Count; D004492:Edetic Acid; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006169:Guinea-Bissau / Q000453:epidemiology; D015483:HIV Antibodies / Q000097:blood; D015658:HIV Infections / Q000097:blood / Q000453:epidemiology / Q000276:immunology / Q000821:virology*; D006679:HIV Seropositivity / Q000821:virology; D015497:HIV-1 / Q000235:genetics* / Q000276:immunology; D015498:HIV-2 / Q000235:genetics* / Q000276:immunology; D006801:Humans; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D012367:RNA, Viral / Q000097:blood*; D012044:Regression Analysis; D019562:Viral Load
chemical_list: D015483:HIV Antibodies; D012367:RNA, Viral; D004492:Edetic Acid