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Displaying record number 53242

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HXB2 Location	Gag(5-13) p17(5-13) DNA(802..828)	Gag Epitope Map
Author Location	Gag(5-13 SUMA)
Epitope	ASVLSGGEL	Epitope Alignment
Epitope Name	Gag AL9
Subtype	B
Species (MHC/HLA)	human
Immunogen	HIV-1 infection
Patient MHC/HLA	SUMA: A*11:03, A*24:02, B*14:02, B*15:01, C*08:02, C*12:03
Country	United States
Experimental methods	CD8 T-cell Elispot - IFNγ, Chromium-release assay
Keywords	dynamics, acute/early infection, autologous responses, optimal epitope

Notes

• Primary CD8+ T-cell response to Env, Tat and Gag and the extent, kinetics and mechanisms of viral escape were examined in three patients. Rapid escape, within weeks from infection, from HIV specific CTL responses was observed in all three patients, but the kinetics and extent of the escape differed depending on the breadth and co-dominant distribution of CTL-mediated pressure. The two patients that rapidly declined had more focused immunodominant responses, while the single patient that had low viral load and stable CD4 counts for seven years had a broad co-dominant response and less escape.
• The patient SUMA maintained low viral loads and stable CD4 T-cell counts through 7 years of followup. In contrast to more rapid progressors WEAU and BORI, SUMA had a broad response to 24 epitopes, with little immunodominance. Two peptides were somewhat more intensely recognized in acute infection, but this response leveled out early on.
• Only 4 epitopes acquired escape mutations in SUMA over time, and this was 1 of the 20 that remained invariant. A low level response was detected at acute infection that persisted through early infection.
• Dynamics of this response are shown in Fig. S1 of Yang2019 which developed mathematical models with data from Jones2004. Yang2019 concluded that, in general, relative CTL response breadth increased moderately during the first symptomatic month and then remained relatively stable through the first 400 days post-infection. Analysis also suggested slow expansion kinetics for most HIV-specific CTL responses and the presence of intra- and interclonal competition.

References

Jones2004 Nicola A. Jones, Xiping Wei, Darren R. Flower, MaiLee Wong, Franziska Michor, Michael S. Saag, Beatrice H. Hahn, Martin A. Nowak, George M. Shaw, and Persephone Borrow. Determinants of Human Immunodeficiency Virus Type 1 Escape from the Primary CD8+ Cytotoxic T Lymphocyte Response. J. Exp. Med., 200(10):1243-1256, 15 Nov 2004. PubMed ID: 15545352. Show all entries for this paper.

Yang2019 Yiding Yang, and Vitaly V. Ganusov. Defining Kinetic Properties of HIV-Specific CD8(+) T-Cell Responses in Acute Infection. Microorganisms, 7(3):microorganisms7030069 doi, Mar 2019. PubMed ID: 30836625 Show all entries for this paper.

Displaying record number 58188

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HXB2 Location	Gag(5-13) p17(5-13) DNA(802..828)	Gag Epitope Map
Author Location	Gag/Pol(6- CDC-451)
Epitope	ASVLSGGEL	Epitope Alignment
Subtype	B
Species (MHC/HLA)	human
Immunogen	computer prediction
Experimental methods
Keywords	T-cell crossreactivity to human proteins

Notes

• The paper defines potential crossreactivity between HIV-1 and human host proteins. HIV B-clade strain CDC-451 shares 50 7mers and 3 8mers with the human proteome. Of these, 35 are within experimentally-validated epitopes targeted by human immune responses to HIV. The number of common 7mers between the proteomes is 3.7-fold higher than would be expected by chance.
• The 7mers in common with HIV are present in human proteins that, when altered, are associated with AIDS-related symptoms, suggesting that disease symptoms may be caused by autoimmune responses.
• Previously-documented CTL epitope ASVLSGGEL contains 7mer VLSGGEL, which occurs in human gene O75588 : H_YH95C04.1 protein.

References

Lucchese2011 Guglielmo Lucchese, Angela Stufano, Michele Calabro, and Darja Kanduc. Charting the Peptide Crossreactome between HIV-1 and the Human Proteome. Front. Biosci. (Elite Ed.), 3E:1385-1400, 2011. PubMed ID: 21622144. Show all entries for this paper.