Initial antibodies binding to HIV-1 gp41 in acutely infected subjects are polyreactive and highly mutated.
dc.contributor.author | Liao, Hua-Xin | |
dc.contributor.author | Chen, Xi | |
dc.contributor.author | Munshaw, Supriya | |
dc.contributor.author | Zhang, Ruijun | |
dc.contributor.author | Marshall, Dawn J | |
dc.contributor.author | Vandergrift, Nathan | |
dc.contributor.author | Whitesides, John F | |
dc.contributor.author | Lu, Xiaozhi | |
dc.contributor.author | Yu, Jae-Sung | |
dc.contributor.author | Hwang, Kwan-Ki | |
dc.contributor.author | Gao, Feng | |
dc.contributor.author | Markowitz, Martin | |
dc.contributor.author | Heath, Sonya L | |
dc.contributor.author | Bar, Katharine J | |
dc.contributor.author | Goepfert, Paul A | |
dc.contributor.author | Montefiori, David C | |
dc.contributor.author | Shaw, George C | |
dc.contributor.author | Alam, S Munir | |
dc.contributor.author | Margolis, David M | |
dc.contributor.author | Denny, Thomas N | |
dc.contributor.author | Boyd, Scott D | |
dc.contributor.author | Marshal, Eleanor | |
dc.contributor.author | Egholm, Michael | |
dc.contributor.author | Simen, Birgitte B | |
dc.contributor.author | Hanczaruk, Bozena | |
dc.contributor.author | Fire, Andrew Z | |
dc.contributor.author | Voss, Gerald | |
dc.contributor.author | Kelsoe, Garnett | |
dc.contributor.author | Tomaras, Georgia D | |
dc.contributor.author | Moody, M Anthony | |
dc.contributor.author | Kepler, Thomas B | |
dc.contributor.author | Haynes, Barton F | |
dc.coverage.spatial | United States | |
dc.date.accessioned | 2017-06-02T12:36:48Z | |
dc.date.available | 2017-06-02T12:36:48Z | |
dc.date.issued | 2011-10-24 | |
dc.description.abstract | The initial antibody response to HIV-1 is targeted to envelope (Env) gp41, and is nonneutralizing and ineffective in controlling viremia. To understand the origins and characteristics of gp41-binding antibodies produced shortly after HIV-1 transmission, we isolated and studied gp41-reactive plasma cells from subjects acutely infected with HIV-1. The frequencies of somatic mutations were relatively high in these gp41-reactive antibodies. Reverted unmutated ancestors of gp41-reactive antibodies derived from subjects acutely infected with HIV-1 frequently did not react with autologous HIV-1 Env; however, these antibodies were polyreactive and frequently bound to host or bacterial antigens. In one large clonal lineage of gp41-reactive antibodies, reactivity to HIV-1 Env was acquired only after somatic mutations. Polyreactive gp41-binding antibodies were also isolated from uninfected individuals. These data suggest that the majority of gp41-binding antibodies produced after acute HIV-1 infection are cross-reactive responses generated by stimulating memory B cells that have previously been activated by non-HIV-1 antigens. | |
dc.identifier | ||
dc.identifier | jem.20110363 | |
dc.identifier.eissn | 1540-9538 | |
dc.identifier.uri | ||
dc.language | eng | |
dc.publisher | Rockefeller University Press | |
dc.relation.ispartof | J Exp Med | |
dc.relation.isversionof | 10.1084/jem.20110363 | |
dc.subject | Adult | |
dc.subject | Cell Lineage | |
dc.subject | Female | |
dc.subject | HIV Antibodies | |
dc.subject | HIV Envelope Protein gp41 | |
dc.subject | HIV-1 | |
dc.subject | Humans | |
dc.subject | Male | |
dc.subject | Mutation | |
dc.subject | Phylogeny | |
dc.subject | Plasma Cells | |
dc.subject | Sequence Analysis, DNA | |
dc.subject | Viral Load | |
dc.subject | Viremia | |
dc.title | Initial antibodies binding to HIV-1 gp41 in acutely infected subjects are polyreactive and highly mutated. | |
dc.type | Journal article | |
duke.contributor.orcid | Gao, Feng|0000-0001-8903-0203 | |
duke.contributor.orcid | Montefiori, David C|0000-0003-0856-6319 | |
duke.contributor.orcid | Alam, S Munir|0000-0003-0941-0703 | |
duke.contributor.orcid | Kelsoe, Garnett|0000-0002-8770-040X | |
duke.contributor.orcid | Tomaras, Georgia D|0000-0001-8076-1931 | |
duke.contributor.orcid | Moody, M Anthony|0000-0002-3890-5855 | |
pubs.author-url | ||
pubs.begin-page | 2237 | |
pubs.end-page | 2249 | |
pubs.issue | 11 | |
pubs.organisational-group | Basic Science Departments | |
pubs.organisational-group | Clinical Science Departments | |
pubs.organisational-group | Duke | |
pubs.organisational-group | Duke Cancer Institute | |
pubs.organisational-group | Duke Human Vaccine Institute | |
pubs.organisational-group | Faculty | |
pubs.organisational-group | Immunology | |
pubs.organisational-group | Institutes and Centers | |
pubs.organisational-group | Medicine | |
pubs.organisational-group | Medicine, Duke Human Vaccine Institute | |
pubs.organisational-group | Medicine, Infectious Diseases | |
pubs.organisational-group | Molecular Genetics and Microbiology | |
pubs.organisational-group | Pathology | |
pubs.organisational-group | Pediatrics | |
pubs.organisational-group | Pediatrics, Infectious Diseases | |
pubs.organisational-group | School of Medicine | |
pubs.organisational-group | Staff | |
pubs.organisational-group | Surgery | |
pubs.organisational-group | Surgery, Surgical Sciences | |
pubs.publication-status | Published | |
pubs.volume | 208 |
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