PMID- 12368301
OWN - NLM
STAT- MEDLINE
DCOM- 20021126
LR  - 20190508
IS  - 0022-538X (Print)
IS  - 1098-5514 (Electronic)
IS  - 0022-538X (Linking)
VI  - 76
IP  - 21
DP  - 2002 Nov
TI  - Equine infectious anemia virus envelope evolution in vivo during persistent 
      infection progressively increases resistance to in vitro serum antibody 
      neutralization as a dominant phenotype.
PG  - 10588-97
AB  - Equine infectious anemia virus (EIAV) infection of horses is characterized by 
      well-defined waves of viremia associated with the sequential evolution of 
      distinct viral populations displaying extensive envelope gp90 variation; however, 
      a correlation of in vivo envelope evolution with in vitro serum neutralization 
      phenotype remains undefined. Therefore, the goal of the present study was to 
      utilize a previously defined panel of natural variant EIAV envelope isolates from 
      sequential febrile episodes to characterize the effects of envelope variation 
      during persistent infection on viral neutralization phenotypes and to define the 
      determinants of EIAV envelope neutralization specificity. To assess the 
      neutralization phenotypes of the sequential EIAV envelope variants, we determined 
      the sensitivity of five variant envelopes to neutralization by a longitudinal 
      panel of immune serum from the source infected pony. The results indicated that 
      the evolution of the EIAV envelope sequences observed during sequential febrile 
      episodes produced an increasingly neutralization-resistant phenotype. To further 
      define the envelope determinants of EIAV neutralization specificity, we examined 
      the neutralization properties of a panel of chimeric envelope constructs derived 
      from reciprocal envelope domain exchanges between selected 
      neutralization-sensitive and neutralization-resistant envelope variants. These 
      results indicated that the EIAV gp90 V3 and V4 domains individually conferred 
      serum neutralization resistance while other envelope segments in addition to V3 
      and V4 were evidently required for conferring total serum neutralization 
      sensitivity. These data clearly demonstrate for the first time the influence of 
      sequential gp90 variation during persistent infection in increasing envelope 
      neutralization resistance, identify the gp90 V3 and V4 domains as the principal 
      determinants of antibody neutralization resistance, and indicate distinct complex 
      cooperative envelope domain interactions in defining sensitivity to serum 
      antibody neutralization.
FAU - Howe, Laryssa
AU  - Howe L
AD  - Department of Infectious Disease and Microbiology, Graduate School of Public 
      Health, University of Pittsburgh, Pittsburgh, Pennsylvania 15261, USA.
FAU - Leroux, Caroline
AU  - Leroux C
FAU - Issel, Charles J
AU  - Issel CJ
FAU - Montelaro, Ronald C
AU  - Montelaro RC
LA  - eng
GR  - R01 AI025850/AI/NIAID NIH HHS/United States
GR  - R01 AI25850/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Virol
JT  - Journal of virology
JID - 0113724
RN  - 0 (Antibodies, Viral)
RN  - 0 (Epitopes, B-Lymphocyte)
RN  - 0 (Glycoproteins)
RN  - 0 (Immunodominant Epitopes)
RN  - 0 (SU protein, equine infectious anemia virus)
RN  - 0 (Viral Envelope Proteins)
SB  - IM
MH  - Amino Acid Sequence
MH  - Animals
MH  - Antibodies, Viral/blood/immunology
MH  - Directed Molecular Evolution
MH  - Disease Progression
MH  - Epitope Mapping
MH  - Epitopes, B-Lymphocyte/genetics/*immunology
MH  - Equine Infectious Anemia/physiopathology/virology
MH  - Glycoproteins/genetics/*immunology
MH  - Horses
MH  - Immunodominant Epitopes/genetics/*immunology
MH  - Infectious Anemia Virus, Equine/genetics/*immunology
MH  - Molecular Sequence Data
MH  - Neutralization Tests
MH  - Phenotype
MH  - Viral Envelope Proteins/genetics/*immunology
PMC - PMC136617
EDAT- 2002/10/09 04:00
MHDA- 2002/11/28 04:00
PMCR- 2002/11/01
CRDT- 2002/10/09 04:00
PHST- 2002/10/09 04:00 [pubmed]
PHST- 2002/11/28 04:00 [medline]
PHST- 2002/10/09 04:00 [entrez]
PHST- 2002/11/01 00:00 [pmc-release]
AID - 0702 [pii]
AID - 10.1128/jvi.76.21.10588-10597.2002 [doi]
PST - ppublish
SO  - J Virol. 2002 Nov;76(21):10588-97. doi: 10.1128/jvi.76.21.10588-10597.2002.