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Displaying record number 61607

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HXB2 Location	Pol(90-98) Protease(34-42) DNA(2352..2378)	Pol Epitope Map
Author Location	Pol
Epitope	`EEINLPGRW`	Epitope Alignment
		Show epitope variants
Epitope Name	B44-EW9 Pol
Species (MHC/HLA)	human(B*44)
Immunogen	HIV-1 infection
Experimental methods	Other
Keywords	escape

Notes

Proof of principle is given to show that HIV-1 genome sequence from short reads can be used to reconstruct actual whole genome haplotypes including immune escape mutations. 30 whole genome haplotypes from subject 9213 were reconstructed longitudinally and published. Mutations are found to change depending on linkage and resulting clonal interference shows that selection coefficients to study HIV evolution must be estimated for complete haplotypes and not individual escapes.
Subdominant Pol epitope, EW9, EEINLPGRW was present as WT in haplotypes studied, at days 0-476, but had begun escape by day 476 for Patient 9213. Mutations seen were EEIkLPGRW (N4K) and anchor residue change, EdINLPGRW (E2D).

References

Pandit2014 Aridaman Pandit and Rob J. de Boer. Reliable Reconstruction of HIV-1 Whole Genome Haplotypes Reveals Clonal Interference and Genetic Hitchhiking among Immune Escape Variants. Retrovirology, 11:56, 4 Jul 2014. PubMed ID: 24996694. Show all entries for this paper.

Displaying record number 61612

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HXB2 Location	Pol(90-98) Protease(34-42) DNA(2352..2378)	Pol Epitope Map
Author Location	Pol
Epitope	`EEINLPGRW`	Epitope Alignment
		Show epitope variants
Epitope Name	Pol B44-EW9
Subtype	B
Species (MHC/HLA)	human(B*44)
Immunogen	HIV-1 infection
Patient MHC/HLA	9213: A01, A24, B38, B44, C*04
Country	Germany, Switzerland, United States
Experimental methods	CD8 T-cell Elispot - IFNγ, Other
Keywords	escape, acute/early infection, assay or method development

Notes

A high throughput whole HIV-1 genome deep sequencing platform combining 454 pyrosequencing with novel assembly and detection of low-frequency variants was used to quantify early stage, poorly represented variants. Application of this method to longitudinal samples from subject 9213 suggests that during acute infection early, low-frequency mutations result from viral adaptation to strong host cellular immune responses during the early decline of peak viral load (VL). Rapid viral escapes from the most dominant immune responses, however, correlate with the loss of this initial viral control.
Non-dominant WT Pol epitope EEINLPGRW was targeted during acute infection in patient 9213 and is present at days 0 (100%), 3 (100%), 59 (100%), 165 (80.1%), 476 (39.4%) being lost by the subsequent time point, d1543 (frequency of haplotype in parentheses). Mutations arise from d165 onwards.
Epitope EW9, EEiNLPGRW, is different from the consensus B, EEMNLPGRW.

References

Henn2012 Matthew R. Henn, Christian L. Boutwell, Patrick Charlebois, Niall J. Lennon, Karen A. Power, Alexander R. Macalalad, Aaron M. Berlin, Christine M. Malboeuf, Elizabeth M. Ryan, Sante Gnerre, Michael C. Zody, Rachel L. Erlich, Lisa M. Green, Andrew Berical, Yaoyu Wang, Monica Casali, Hendrik Streeck, Allyson K. Bloom, Tim Dudek, Damien Tully, Ruchi Newman, Karen L. Axten, Adrianne D. Gladden, Laura Battis, Michael Kemper, Qiandong Zeng, Terrance P. Shea, Sharvari Gujja, Carmen Zedlack, Olivier Gasser, Christian Brander, Christoph Hess, Huldrych F. Günthard, Zabrina L. Brumme, Chanson J. Brumme, Suzane Bazner, Jenna Rychert, Jake P. Tinsley, Ken H. Mayer, Eric Rosenberg, Florencia Pereyra, Joshua Z. Levin, Sarah K. Young, Heiko Jessen, Marcus Altfeld, Bruce W. Birren, Bruce D. Walker, and Todd M. Allen. Whole Genome Deep Sequencing of HIV-1 Reveals the Impact of Early Minor Variants Upon Immune Recognition During Acute Infection. PLoS Pathog., 8(3):e1002529, 2012. PubMed ID: 22412369. Show all entries for this paper.