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Articles by Florencia Pereyra
Total Records ( 2 ) for Florencia Pereyra
  Toshiyuki Miura , Mark A. Brockman , Chanson J. Brumme , Zabrina L. Brumme , Jonathan M. Carlson , Florencia Pereyra , Alicja Trocha , Marylyn M. Addo , Brian L. Block , Alissa C. Rothchild , Brett M. Baker , Theresa Flynn , Arne Schneidewind , Bin Li , Yaoyu E. Wang , David Heckerman , Todd M. Allen and Bruce D. Walker
  Despite reports of viral genetic defects in persons who control human immunodeficiency virus type 1 (HIV-1) in the absence of antiviral therapy, the extent to which such defects contribute to the long-term containment of viremia is not known. Most previous studies examining for such defects have involved small numbers of subjects, primarily focused on subjects expressing HLA-B57, or have examined single viral genes, and they have focused on cellular proviral DNA rather than plasma viral RNA sequences. Here, we attempted viral sequencing from 95 HIV-1 elite controllers (EC) who maintained plasma viral loads of <50 RNA copies/ml in the absence of therapy, the majority of whom did not express HLA-B57. HIV-1 gene fragments were obtained from 94% (89/95) of the EC, and plasma viral sequences were obtained from 78% (61/78), the latter indicating the presence of replicating virus in the majority of EC. Of 63 persons for whom nef was sequenced, only three cases of nef deletions were identified, and gross genetic defects were rarely observed in other HIV-1 coding genes. In a codon-by-codon comparison between EC and persons with progressive infection, correcting for HLA bias and coevolving secondary mutations, a significant difference was observed at only three codons in Gag, all three of which represented the historic population consensus amino acid at the time of infection. These results indicate that the spontaneous control of HIV replication is not attributable to shared viral genetic defects or shared viral polymorphisms.
  Galit Alter , Suzannah Rihn , Hendrik Streeck , Nickolas Teigen , Alicja Piechocka-Trocha , Kristin Moss , Kristen Cohen , Angela Meier , Florencia Pereyra , Bruce Walker and Marcus Altfeld
  Virus-specific CD8+ T cells play a central role in the control< of viral infections, including human immunodeficiency virus< type 1 (HIV-1) infection. However, despite the presence of strong< and broad HIV-specific CD8+ T-cell responses in chronic HIV-1< infection, these cells progressively lose critical effector< functions and fail to clear the infection. Mounting evidence< suggests that the upregulation of several inhibitory regulatory< receptors on the surface of CD8+ T cells during HIV-1 infection< may contribute directly to the impairment of T-cell function.< Here, we investigated the role of killer immunoglobulin receptors< (KIR), which are expressed on NK cells and on CD8+ T cells,< in regulating CD8+ T-cell function in HIV-1 infection. KIR expression< was progressively upregulated on CD8+ T cells during HIV-1 infection< and correlated with the level of viral replication. Expression< of KIR was associated with a profound inhibition of cytokine< secretion, degranulation, proliferation, and activation by CD8+< T cells following stimulation with T-cell receptor (TCR)-dependent< stimuli. In contrast, KIR+ CD8+ T cells responded potently to< TCR-independent stimulation, demonstrating that these cells< are functionally competent. KIR-associated suppression of CD8+< T-cell function was independent of ligand engagement, suggesting< that these regulatory receptors may constitutively repress TCR< activation. This ligand-independent repression of TCR activation< of KIR+ CD8+ T cells may represent a significant barrier to< therapeutic interventions aimed at improving the quality of< the HIV-specific CD8+ T-cell response in infected individuals.
 
 
 
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