PMID- 22555160
OWN - NLM
STAT- MEDLINE
DCOM- 20121212
LR  - 20151119
IS  - 1473-5571 (Electronic)
IS  - 0269-9370 (Linking)
VI  - 26
IP  - 12
DP  - 2012 Jul 31
TI  - HIV-1 envelope diversity 1 year after seroconversion predicts subsequent disease 
      progression.
PG  - 1517-22
LID - 10.1097/QAD.0b013e328354f539 [doi]
AB  - OBJECTIVE: Recent studies have suggested that the dynamics of HIV-1 evolutionary 
      rate reflect the rate of disease progression. We wished to determine whether 
      viral diversity early in infection is predictive of the subsequent disease 
      course. DESIGN: HIV-1 envelope diversity at seroconversion and 1 year thereafter 
      from 89 homosexual participants of the Amsterdam Cohort Studies on HIV infection 
      and AIDS was correlated with clinical endpoints and markers of disease 
      progression. METHODS: Heteroduplex mobility assay (HMA) and sequencing followed 
      by calculation of pairwise genetic distances were applied to determine HIV-1 
      envelope diversity. The HMA pattern (presence or absence of heteroduplexes) and 
      sequence diversity were each tested for correlation with the clinical course of 
      infection. RESULTS: HMA pattern at 1-year postseroconversion was significantly 
      associated with progression to AIDS and AIDS-related death, with presence of 
      heteroduplexes associated with accelerated disease progression. Moreover, not 
      only this dichotomous measure of viral diversity (absence or presence of 
      heteroduplexes), but also genetic diversity itself was associated with disease 
      course. HMA pattern was an independent predictor of accelerated disease 
      progression, also when CCR5 genotype, human leukocyte antigen (HLA)-type, viral 
      load, CD4 T-cell counts, and coreceptor use at viral load set point were included 
      in the analysis. CONCLUSION: Viral diversity early in HIV-1 infection is 
      predictive of the subsequent disease progression. It remains to be established 
      whether viral diversity itself plays a causal role in the increased damage to the 
      immune system or whether it is a reflection of immune pressure or other selective 
      forces.
FAU - Rachinger, Andrea
AU  - Rachinger A
AD  - Department of Experimental Immunology, Sanquin Research, Landsteiner Laboratory, 
      Center for Infection and Immunity Amsterdam (CINIMA), Academic Medical Center of 
      the University of Amsterdam, Amsterdam, The Netherlands.
FAU - Kootstra, Neeltje A
AU  - Kootstra NA
FAU - Gijsbers, Esther F
AU  - Gijsbers EF
FAU - van den Kerkhof, Tom L G M
AU  - van den Kerkhof TL
FAU - Schuitemaker, Hanneke
AU  - Schuitemaker H
FAU - van 't Wout, Angelique B
AU  - van 't Wout AB
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - AIDS
JT  - AIDS (London, England)
JID - 8710219
RN  - 0 (Biomarkers)
RN  - 0 (HLA Antigens)
RN  - 0 (RNA, Viral)
RN  - 0 (Receptors, CCR5)
RN  - 0 (Viral Envelope Proteins)
SB  - IM
MH  - Acquired Immunodeficiency Syndrome/mortality/virology
MH  - Biomarkers/blood
MH  - CD4-Positive T-Lymphocytes
MH  - Disease Progression
MH  - HIV Infections/genetics/*virology
MH  - HIV Seropositivity/genetics/*virology
MH  - HIV-1/genetics/*immunology
MH  - HLA Antigens/immunology
MH  - Heteroduplex Analysis
MH  - Homosexuality, Male
MH  - Humans
MH  - Male
MH  - Prospective Studies
MH  - RNA, Viral/immunology
MH  - Receptors, CCR5/immunology
MH  - Time Factors
MH  - Viral Envelope Proteins/*genetics
MH  - Viral Load
EDAT- 2012/05/05 06:00
MHDA- 2012/12/13 06:00
CRDT- 2012/05/05 06:00
PHST- 2012/05/05 06:00 [entrez]
PHST- 2012/05/05 06:00 [pubmed]
PHST- 2012/12/13 06:00 [medline]
AID - 10.1097/QAD.0b013e328354f539 [doi]
PST - ppublish
SO  - AIDS. 2012 Jul 31;26(12):1517-22. doi: 10.1097/QAD.0b013e328354f539.