title: HIV-1 dual infection is associated with faster CD4+ T-cell decline in a cohort of men with primary HIV infection.
abstract: BACKGROUND
  In vitro, animal, and mathematical models suggest that human immunodeficiency virus (HIV) co- or superinfection would result in increased fitness of the pathogen and, possibly, increased virulence. However, in patients, the impact of dual HIV type 1 (HIV-1) infection on disease progression is unclear, because parameters relevant for disease progression have not been strictly analyzed. The objective of the present study is to analyze the effect of dual HIV-1 infections on disease progression in a well-defined cohort of men who have sex with men.
  
  
  METHODS
  Between 2000 and 2009, 37 men who had primary infection with HIV-1 subtype B, no indication for immediate need of combination antiretroviral therapy (cART), and sufficient follow-up were characterized with regard to dual infection or single infection and to coreceptor use. Patients were followed to estimate the effect of these parameters on clinical disease progression, as defined by the rate of CD4(+) T-cell decline and the time to initiation of cART.
  
  
  RESULTS
  Four patients presented with HIV-1 coinfection; 6 patients acquired HIV-1 superinfection, on average 8.5 months from their primary infection; and 27 patients remained infected with a single strain. Slopes of longitudinal CD4(+) T-cell counts and time-weighted changes from baseline were significantly steeper for patients with dual infection compared with patients with single infection. Multivariate analysis showed that the most important parameter associated with CD4(+) T-cell decline over time was dual infection (P = .001). Additionally, patients with HIV-1 coinfection had a significantly earlier start of cART (P < .0001).
  
  
  CONCLUSIONS
  Dual HIV-1 infection is the main factor associated with CD4(+) T-cell decline in men who have untreated primary infection with HIV-1 subtype B.
authors.affiliation: Laboratory of Experimental Virology, Academic Medical Center, University of Amsterdam, Netherlands.
authors.forename: Marion
authors.initials: M
authors.lastname: Cornelissen
authors.forename: Alexander O
authors.initials: AO
authors.lastname: Pasternak
authors.forename: Marlous L
authors.initials: ML
authors.lastname: Grijsen
authors.forename: Fokla
authors.initials: F
authors.lastname: Zorgdrager
authors.forename: Margreet
authors.initials: M
authors.lastname: Bakker
authors.forename: Petra
authors.initials: P
authors.lastname: Blom
authors.forename: Jan M
authors.initials: JM
authors.lastname: Prins
authors.forename: Suzanne
authors.initials: S
authors.lastname: Jurriaans
authors.forename: Antoinette C
authors.initials: AC
authors.lastname: van der Kuyl
mesh_terms: D000328:Adult; D018791:CD4 Lymphocyte Count; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D015331:Cohort Studies; D060085:Coinfection / Q000276:immunology* / Q000821:virology*; D018450:Disease Progression; D005838:Genotype; D015658:HIV Infections / Q000276:immunology* / Q000821:virology*; D015497:HIV-1 / Q000145:classification* / Q000235:genetics / Q000302:isolation & purification*; D006801:Humans; D008297:Male; D008969:Molecular Sequence Data; D017422:Sequence Analysis, DNA