title: Complement lysis activity in autologous plasma is associated with lower viral loads during the acute phase of HIV-1 infection.
abstract: BACKGROUND
  To explore the possibility that antibody-mediated complement lysis contributes to viremia control in HIV-1 infection, we measured the activity of patient plasma in mediating complement lysis of autologous primary virus.
  
  
  RESULTS
  Sera from two groups of patients-25 with acute HIV-1 infection and 31 with chronic infection-were used in this study. We developed a novel real-time PCR-based assay strategy that allows reliable and sensitive quantification of virus lysis by complement. Plasma derived at the time of virus isolation induced complement lysis of the autologous virus isolate in the majority of patients. Overall lysis activity against the autologous virus and the heterologous primary virus strain JR-FL was higher at chronic disease stages than during the acute phase. Most strikingly, we found that plasma virus load levels during the acute but not the chronic infection phase correlated inversely with the autologous complement lysis activity. Antibody reactivity to the envelope (Env) proteins gp120 and gp41 were positively correlated with the lysis activity against JR-FL, indicating that anti-Env responses mediated complement lysis. Neutralization and complement lysis activity against autologous viruses were not associated, suggesting that complement lysis is predominantly caused by non-neutralizing antibodies.
  
  
  CONCLUSIONS
  Collectively our data provide evidence that antibody-mediated complement virion lysis develops rapidly and is effective early in the course of infection; thus it should be considered a parameter that, in concert with other immune functions, steers viremia control in vivo.
authors.affiliation: Division of Infectious Diseases, University Hospital Zürich, Zürich, Switzerland.
authors.forename: Michael
authors.initials: M
authors.lastname: Huber
authors.forename: Marek
authors.initials: M
authors.lastname: Fischer
authors.forename: Benjamin
authors.initials: B
authors.lastname: Misselwitz
authors.forename: Amapola
authors.initials: A
authors.lastname: Manrique
authors.forename: Herbert
authors.initials: H
authors.lastname: Kuster
authors.forename: Barbara
authors.initials: B
authors.lastname: Niederöst
authors.forename: Rainer
authors.initials: R
authors.lastname: Weber
authors.forename: Viktor
authors.initials: V
authors.lastname: von Wyl
authors.forename: Huldrych F
authors.initials: HF
authors.lastname: Günthard
authors.forename: Alexandra
authors.initials: A
authors.lastname: Trkola
mesh_terms: D000208:Acute Disease; D000914:Antibodies, Viral / Q000276:immunology*; D000917:Antibody Formation; D002908:Chronic Disease; D003165:Complement System Proteins / Q000276:immunology*; D003430:Cross-Sectional Studies; D015686:Gene Products, env / Q000276:immunology; D015683:Gene Products, gag / Q000276:immunology; D015658:HIV Infections / Q000097:blood / Q000276:immunology* / Q000821:virology*; D015497:HIV-1 / Q000276:immunology* / Q000472:pathogenicity; D006801:Humans; D008137:Longitudinal Studies; D019562:Viral Load; D014766:Viremia / Q000517:prevention & control
chemical_list: D000914:Antibodies, Viral; D015686:Gene Products, env; D015683:Gene Products, gag; D003165:Complement System Proteins