title: Prolonged control of replication-competent dual- tropic human immunodeficiency virus-1 following cessation of highly active antiretroviral therapy.
abstract: BACKGROUND
  While initiation of highly active antiretroviral therapy (HAART) during primary HIV-1 infection occasionally results in transient control of viral replication after treatment interruption, the vast majority of patients eventually experience a rebound in plasma viremia.
  
  
  RESULTS
  Here we report a case of a patient who was started on HAART during symptomatic primary infection and who has subsequently maintained viral loads of < 50 copies/mL for more than nine years after the cessation of treatment. This patient had a high baseline viral load and has maintained a relatively high frequency of latently infected CD4(+) T cells. In addition, he does not have any known protective HLA alleles. Thus it is unlikely that he was destined to become a natural elite controller or suppressor. The mechanism of control of viral replication is unclear; he is infected with a CCR5/CXCR4 dual-tropic virus that is fully replication-competent in vitro. In addition, his spouse, who transmitted the virus to him, developed AIDS. The patient's CD4(+) T cells are fully susceptible to HIV-1 infection, and he has low titers of neutralizing antibodies to heterologous and autologous HIV-1 isolates. Furthermore, his CD8(+) T cells do not have potent HIV suppressive activity.
  
  
  CONCLUSIONS
  This report suggests that some patients may be capable of controlling pathogenic HIV-1 isolates for extended periods of time after the cessation of HAART through a mechanism that is distinct from the potent cytotoxic T lymphocyte (CTL) mediated suppression that has been reported in many elite suppressors.
authors.affiliation: Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA.
authors.forename: Maria
authors.initials: M
authors.lastname: Salgado
authors.forename: S Alireza
authors.initials: SA
authors.lastname: Rabi
authors.forename: Karen A
authors.initials: KA
authors.lastname: O'Connell
authors.forename: Robert W
authors.initials: RW
authors.lastname: Buckheit
authors.forename: Justin R
authors.initials: JR
authors.lastname: Bailey
authors.forename: Amina A
authors.initials: AA
authors.lastname: Chaudhry
authors.forename: Autumn R
authors.initials: AR
authors.lastname: Breaud
authors.forename: Mark A
authors.initials: MA
authors.lastname: Marzinke
authors.forename: William
authors.initials: W
authors.lastname: Clarke
authors.forename: Joseph B
authors.initials: JB
authors.lastname: Margolick
authors.forename: Robert F
authors.initials: RF
authors.lastname: Siliciano
authors.forename: Joel N
authors.initials: JN
authors.lastname: Blankson
mesh_terms: D000595:Amino Acid Sequence; D057134:Antibodies, Neutralizing / Q000276:immunology / Q000378:metabolism; D023241:Antiretroviral Therapy, Highly Active; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000378:metabolism / Q000821:virology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology / Q000378:metabolism / Q000821:virology; D000939:Epitopes / Q000276:immunology / Q000378:metabolism; D015483:HIV Antibodies / Q000276:immunology / Q000378:metabolism; D015658:HIV Infections / Q000188:drug therapy* / Q000635:transmission / Q000821:virology; D015497:HIV-1 / Q000145:classification / Q000276:immunology / Q000472:pathogenicity* / Q000502:physiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D008969:Molecular Sequence Data; D010802:Phylogeny; D019562:Viral Load; D017735:Virus Latency; D014779:Virus Replication
chemical_list: D057134:Antibodies, Neutralizing; D000939:Epitopes; D015483:HIV Antibodies