About: Mechanisms of HIV non-progression; robust and sustained CD4+ T-cell proliferative responses to p24 antigen correlate with control of viraemia and lack of disease progression after long-term transfusion-acquired HIV-1 infection

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About: Mechanisms of HIV non-progression; robust and sustained CD4+ T-cell proliferative responses to p24 antigen correlate with control of viraemia and lack of disease progression after long-term transfusion-acquired HIV-1 infection Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Mechanisms of HIV non-progression; robust and sustained CD4+ T-cell proliferative responses to p24 antigen correlate with control of viraemia and lack of disease progression after long-term transfusion-acquired HIV-1 infection
Creator	Wang, Bin Dyer, Wayne Geczy, Andrew Sullivan, John Gorry, Paul Learmont, Jennifer Saksena, Nitin Zaunders, John Mcphee, Dale
Source	Medline; PMC
abstract	BACKGROUND: Elite non-progressors (plasma viral load <50 copies/ml while antiretroviral naive) constitute a tiny fraction of HIV-infected individuals. After 12 years follow-up of a cohort of 13 long-term non-progressors (LTNP) identified from 135 individuals with transfusion-acquired HIV infection, 5 remained LTNP after 23 to 26 years infection, but only 3 retained elite LTNP status. We examined the mechanisms that differentiated delayed progressors from LTNP in this cohort. RESULTS: A survival advantage was conferred on 12 of 13 subjects, who had at least one host genetic factor (HLA, chemokine receptor or TLR polymorphisms) or viral attenuating factor (defective nef) associated with slow progression. However, antiviral immune responses differentiated the course of disease into and beyond the second decade of infection. A stable p24-specific proliferative response was associated with control of viraemia and retention of non-progressor status, but this p24 response was absent or declined in viraemic subjects. Strong Gag-dominant cytotoxic T lymphocyte (CTL) responses were identified in most LTNP, or Pol dominant-CTL in those with nef-defective HIV infection. CTL were associated with control of viraemia when combined with p24 proliferative responses. However, CTL did not prevent late disease progression. Individuals with sustained viral suppression had CTL recognising numerous Gag epitopes, while strong but restricted responses to one or two immunodominant epitopes was effective for some time, but failed to contain viraemia over the course of this study. Viral escape mutants at a HLA B27-restricted Gag-p24 epitope were detected in only 1 of 3 individuals, whereas declining or negative p24 proliferative responses occurred in all 3 concurrent with an increase in viraemia. CONCLUSION: Detectable viraemia at study entry was predictive of loss of LTNP status and/or disease progression in 6 of 8, and differentiated slow progressors from elite LTNP who retained potent virological control. Sustained immunological suppression of viraemia was independently associated with preserved p24 proliferative responses, regardless of the strength and breadth of the CTL response. A decline in this protective p24 response preceded or correlated with loss of non-progressor status and/or signs of disease progression.
has issue date	2008-12-11(xsd:dateTime)
bibo:doi	10.1186/1742-4690-5-112
bibo:pmid	19077215
has license	cc-by
sha1sum (hex)	27bafe2069fadba9638ec9eb5ae1afaf3c78cfb8
schema:url	https://doi.org/10.1186/1742-4690-5-112
resource representing a document's title	Mechanisms of HIV non-progression; robust and sustained CD4+ T-cell proliferative responses to p24 antigen correlate with control of viraemia and lack of disease progression after long-term transfusion-acquired HIV-1 infection
has PubMed Central identifier	PMC2633348
has PubMed identifier	19077215
schema:publication	Retrovirology
resource representing a document's body	covid:27bafe2069fadba9638ec9eb5ae1afaf3c78cfb8#body_text
is schema:about of	named entity 'VIRAL LOAD' named entity 'ACQUIRED' named entity 'DIFFERENTIATED' named entity '135' named entity 'BUT' named entity 'COPIES' named entity 'FRACTION OF' named entity 'INFECTION' named entity 'MECHANISMS' named entity 'BACKGROUND' named entity 'T-CELL' named entity 'fraction' named entity 'remained' named entity 'differentiated' named entity 'mechanisms' named entity 'After' named entity 'control' named entity 'viraemia' named entity 'progression' named entity 'p24 antigen' named entity 'HIV' named entity 'HIV-1 INFECTION' named entity 'PROLIFERATIVE' named entity 'TRANSFUSION' named entity 'TINY' named entity 'YEARS' named entity 'HIV INFECTION' named entity 'CD4' named entity 'CONTROL' covid:arg/27bafe2069fadba9638ec9eb5ae1afaf3c78cfb8 named entity 'HIV' named entity 'NON-' named entity 'TRANSFUSION' named entity 'PROGRESSION' named entity 'SUSTAINED' named entity 'ACQUIRED' named entity 'ROBUST' named entity 'DISEASE PROGRESSION' named entity 'FOLLOW-UP' named entity 'STATUS' named entity 'RETAINED' named entity 'INDIVIDUALS' named entity 'COHORT' named entity 'VIRAEMIA' named entity 'RESPONSES' named entity 'MECHANISMS' named entity 'LACK' named entity 'P24 ANTIGEN' named entity 'LONG-TERM' named entity 'IDENTIFIED' named entity 'DELAYED' named entity 'ANTIRETROVIRAL' named entity 'LONG-TERM' named entity 'HIV' named entity 'NON-' named entity 'EXAMINED' named entity 'INFECTED' named entity 'HLA' named entity 'antiviral' named entity 'HIV-1' named entity 'HIV' named entity 'HIV' named entity 'epitope' named entity 'aged population' named entity 'effector' named entity 'infection' named entity 'progressive disease' named entity 'helper T cell' named entity 'primers' named entity 'CD4 T cell' named entity 'Foster City' named entity 'FcγRIIA' named entity 'polymorphisms'

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