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Displaying record number 58286

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HXB2 Location	Pol(101-109) Protease(45-53) DNA(2385..2411)	Pol Epitope Map
Author Location	Protease(45-53)
Epitope	KMIGGIGGF	Epitope Alignment
		Show epitope variants
Epitope Name	KF9
Subtype	B
Species (MHC/HLA)	human(B*15:01)
Immunogen	HIV-1 infection
Country	Germany
Experimental methods	CD8 T-cell Elispot - IFNγ, Chromium-release assay, Other
Keywords	drug resistance

Notes

• To assess associations between CTL driven escape and resistance mutations, KF9 epitopes with protease inhibitor (PI)-initiated mutations were analyzed for recognition by KF9-specific CTL. Some PI mutations like G48V, M46I and I47A in KF9 abrogated CTL recognition, however no evidence was found that the PI mutations are KF9-CTL driven or HLA-B*1501-related. Also, KF9 was not influenced by presence or absence of or the particular therapeutic regimen.
• KF9-epitope mutations were only found in patients who had experienced PI treatments i.e. all potential escape mutations were associated only with usage of drugs. Inexplicably, VL (viral load) was significantly lower in HLA-B*1501+ patients than in -B*1501- patients.

References

Mueller2011 Sandra M. Mueller, Bernd M. Spriewald, Silke Bergmann, Kathrin Eismann, Melanie Leykauf, Klaus Korn, Hauke Walter, Barbara Schmidt, Marie-Luise Arnold, Ellen G. Harrer, Rolf Kaiser, Finja Schweitzer, Patrick Braun, Stefan Reuter, Hans Jaeger, Eva Wolf, Norbert H. Brockmeyer, Klaus Jansen, Claudia Michalik, Thomas Harrer, and German Competence Network for HIV/AIDS. Influence of Major HIV-1 Protease Inhibitor Resistance Mutations on CTL Recognition. J. Acquir. Immune Defic. Syndr., 56(2):109-117, Feb 2011. PubMed ID: 21107269. Show all entries for this paper.

Displaying record number 54658

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HXB2 Location	Pol(101-109) Protease(45-53) DNA(2385..2411)	Pol Epitope Map
Author Location	Protease(45-53 HXB2)
Epitope	KMIGGIGGF	Epitope Alignment
Epitope Name	KF9
Subtype	B
Species (MHC/HLA)	human(B62)
Immunogen	HIV-1 infection
Country	Germany
Experimental methods	CD8 T-cell Elispot - IFNγ
Keywords	escape, mutation acquisition, HLA associated polymorphism, drug resistance

Notes

• To assess HIV-1-specific CTL influence on development and patterns of drug resistance in protease (PR) 94 HLA-typed patients were analyzed. 10 new CTL epitopes were defined statistically and experimentally, and 26 correlations (positive and negative) between HLA class-I alleles and PR mutations - some leading to escape mutations - were detected, demonstrating that CTL epitopes can be predicted based on HLA-amino acid substitution associations.
• Some patient CTL escape mutations were detectable by other CTLs of the same patient. Correlations between resistance mutations, polymorphisms and specific PR inhibitors were not detected.
• HLA-B had the strongest impact on PR sequence change, though HLAs-A and -C also had some impact.
• The authors suggest that CTL escape is active in developing drug-resistance related polymorphisms as well as major and minor mutations in HIV-1 infected persons.
• HIV-1 subtype breakdown in this cohort was follows - 83/94 patients infected with subtype B virus, 3 with subtype C, 4 CRF01_AE, 1 CRF03_AB, 1 CRF15_01B and 2 subtype Ds.
• This newly defined epitope, KMIGGIGGF, KF9, was the optimal HLA-B62 restricted epitope.

References

Mueller2007 Sandra M. Mueller, Birgit Schaetz, Kathrin Eismann, Silke Bergmann, Michael Bauerle, Matthias Schmitt-Haendle, Hauke Walter, Barbara Schmidt, Klaus Korn, Heinrich Sticht, Bernd Spriewald, Ellen G. Harrer, and Thomas Harrer. Dual Selection Pressure by Drugs and HLA Class I-Restricted Immune Responses on Human Immunodeficiency Virus Type 1 Protease. J. Virol., 81(6):2887-2898, Mar 2007. PubMed ID: 17202219. Show all entries for this paper.