Person:
Davis, Benjamin

Profile Picture

Email Address

AA Acceptance Date

Birth Date

Research Projects

Organizational Units

Job Title

Last Name

Davis

First Name

Benjamin

Name

Davis, Benjamin
Author's Publications: search.filters.isAuthorOfPublication.8e2a6076-dcfd-41b4-a570-93fce25d37e8

Search Results

Now showing 1 - 2 of 2
  • Thumbnail Image
    Publication
    Fully Differentiated HIV-1 Specific CD8+ T Effector Cells are More Frequently Detectable in Controlled than in Progressive HIV-1 Infection
    (Public Library of Science, 2007) Draenert, Rika; Rathod, Almas; Verrill, Cori L.; Stone, David R.; Johnston, Mary N.; Flynn, Theresa; Addo, Marylyn Martina; Davis, Benjamin; Gandhi, Rajesh; Robbins, Gregory; Basgov, Nesli; Cohen, Daniel E.; Wurcel, Alysse Gail; Rosenberg, Eric; Altfeld, Marcus; Walker, Bruce
    Background: CD8+ T cells impact control of viral infections by direct elimination of infected cells and secretion of a number of soluble factors. In HIV-1 infection, persistent HIV-1 specific IFN-γ+ CD8+ T cell responses are detected in the setting of disease progression, consistent with functional impairment in vivo. Recent data suggest that impaired maturation, as defined by the lineage markers CD45RA and CCR7, may contribute to a lack of immune control by these responses. Methodology/Principal Findings: We investigated the maturation phenotype of epitope-specific CD8+ T cell responses directed against HIV-1 in 42 chronically infected, untreated individuals, 22 of whom were “Controllers” (median 1140 RNA copies/ml plasma, range less than 50 to 2520), and 20 “progressors” of whom had advanced disease and high viral loads (median 135,500 RNA copies/ml plasma, range 12100 to greater than 750000). Evaluation of a mean of 5 epitopes per person revealed that terminally differentiated CD8+ T cells directed against HIV-1 are more often seen in HIV-1 Controllers (16/22; 73%) compared to HIV-1 progressors (7/20; 35%)(p = 0.015), but the maturation state of epitope-specific responses within a given individual was quite variable. Maturation phenotype was independent of the HLA restriction or the specificity of a given CD8+ T cell response and individual epitopes associated with slow disease progression were not more likely to be terminally differentiated. Conclusions/Significance: These data indicate that although full maturation of epitope-specific CD8+ T cell responses is associated with viral control, the maturation status of HIV-1 specific CD8+ T cell responses within a given individual are quite heterogeneous, suggesting epitope-specific influences on CD8+ T cell function.
  • Thumbnail Image
    Publication
    Impaired hepatitis C virus-specific T cell responses and recurrent hepatitis C virus in HIV coinfection
    (Public Library of Science, 2006) Kim, Arthur; Schulze zur Wiesch, Julian; Kuntzen, Thomas; Timm, Joerg; Kaufmann, Daniel E.; Duncan, Jared E.; Jones, Andrea M.; Wurcel, Alysse G.; Davis, Benjamin; Gandhi, Rajesh; Robbins, Gregory; Allen, Todd; Chung, Raymond; Lauer, Georg; Walker, Bruce
    Background: Hepatitis C virus (HCV)-specific T cell responses are critical for spontaneous resolution of HCV viremia. Here we examined the effect of a lymphotropic virus, HIV-1, on the ability of coinfected patients to maintain spontaneous control of HCV infection. Methods and Findings: We measured T cell responsiveness by lymphoproliferation and interferon-\(\gamma\) ELISPOT in a large cohort of HCV-infected individuals with and without HIV infection. Among 47 HCV/HIV-1-coinfected individuals, spontaneous control of HCV was associated with more frequent HCV-specific lymphoproliferative (LP) responses (35%) compared to coinfected persons who exhibited chronic HCV viremia (7%, p = 0.016), but less frequent compared to HCV controllers who were not HIV infected (86%, p = 0.003). Preservation of HCV-specific LP responses in coinfected individuals was associated with a higher nadir CD4 count (r\(^2\) = 0.45, p < 0.001) and the presence and magnitude of the HCV-specific CD8\(^+\) T cell interferon-\(\gamma\) response (p = 0.0014). During long-term follow-up, recurrence of HCV viremia occurred in six of 25 coinfected individuals with prior control of HCV, but in 0 of 16 HIV-1-negative HCV controllers (p = 0.03, log rank test). In these six individuals with recurrent HCV viremia, the magnitude of HCV viremia following recurrence inversely correlated with the CD4 count at time of breakthrough (r = −0.94, p = 0.017). Conclusions: These results indicate that HIV infection impairs the immune response to HCV—including in persons who have cleared HCV infection—and that HIV-1-infected individuals with spontaneous control of HCV remain at significant risk for a second episode of HCV viremia. These findings highlight the need for repeat viral RNA testing of apparent controllers of HCV infection in the setting of HIV-1 coinfection and provide a possible explanation for the higher rate of HCV persistence observed in this population.