Nucleotide and amino acid mutations in human immunodeficiency virus corresponding to CD4 + decline

Nucleotide and amino acid mutations in human immunodeficiency virus corresponding to CD4 + decline In a meta-analysis, gene sequences of the HIV-1 V3 and surrounding envelope region from studies examining longitudinally derived blood and plasma human immunodeficiency virus forms were analyzed for changes over disease course. CD4 + counts were used as a marker of disease progression; 58 subjects, followed an average of 56 months, were included. Genetic diversification was found early in disease progression. In mid-progression (CD4 + counts dropping from 488 to 329/mm 3 ) diversification did not increase while loop charge dramatically increased. This is consistent with a charged form that dominates and induces disease progression at this critical time. Although the overall mean increase in loop charge was significant, this increase and the transition to amino acids known to change tropism occurred in only half of the subjects who progressed. Those with rapidly progressing disease (within 2 years post-infection) began with a loop charge similar to the end stage of normal progressors. DNA from blood-cell-derived sequences differed from concurrently obtained plasma counterparts by one nucleotide out of 238, but this difference was not reflected in differences in glycosylation patterns, loop charge, or tropism-conferring amino acids. Plasma-derived forms were poorer predictors of future viral forms than were cell-derived sequences. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Archives of Virology Springer Journals

Nucleotide and amino acid mutations in human immunodeficiency virus corresponding to CD4 + decline

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Publisher
Springer-Verlag
Copyright
Copyright © 2006 by Springer-Verlag
Subject
Biomedicine; Medical Microbiology; Infectious Diseases; Virology
ISSN
0304-8608
eISSN
1432-8798
D.O.I.
10.1007/s00705-005-0693-8
Publisher site
See Article on Publisher Site

Abstract

In a meta-analysis, gene sequences of the HIV-1 V3 and surrounding envelope region from studies examining longitudinally derived blood and plasma human immunodeficiency virus forms were analyzed for changes over disease course. CD4 + counts were used as a marker of disease progression; 58 subjects, followed an average of 56 months, were included. Genetic diversification was found early in disease progression. In mid-progression (CD4 + counts dropping from 488 to 329/mm 3 ) diversification did not increase while loop charge dramatically increased. This is consistent with a charged form that dominates and induces disease progression at this critical time. Although the overall mean increase in loop charge was significant, this increase and the transition to amino acids known to change tropism occurred in only half of the subjects who progressed. Those with rapidly progressing disease (within 2 years post-infection) began with a loop charge similar to the end stage of normal progressors. DNA from blood-cell-derived sequences differed from concurrently obtained plasma counterparts by one nucleotide out of 238, but this difference was not reflected in differences in glycosylation patterns, loop charge, or tropism-conferring amino acids. Plasma-derived forms were poorer predictors of future viral forms than were cell-derived sequences.

Journal

Archives of VirologySpringer Journals

Published: Jun 1, 2006

References

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