Person: Robbins, Gregory
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Robbins
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Robbins, Gregory
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Publication Outcomes According to Discharge Location for Persons Who Inject Drugs Receiving Outpatient Parenteral Antimicrobial Therapy(Oxford University Press, 2018) D’Couto, Helen T; Robbins, Gregory; Ard, Kevin; Wakeman, Sarah; Alves, Justin; Nelson, SandraAbstract Background: Opioid use disorder poses a significant public health risk. Persons who inject drugs (PWID) suffer from high mortality and morbidity secondary to serious infectious diseases, often requiring prolonged courses of outpatient parenteral antibiotics. The goal of this study was to determine the outcomes of PWID discharged to home or to a skilled nursing or rehabilitation facility (SNF/rehab) with parenteral antibiotic treatment under an outpatient parenteral antimicrobial therapy (OPAT) program. Methods: This is a retrospective observational study. The study population was identified via hospital and OPAT databases using substance use disorder diagnoses and confirmed through chart review. The study population included hospitalized PWID with injection drug use in the preceding 2 years who were discharged between 2010 and 2015 to complete at least 2 weeks of parenteral antibiotics and monitored by the OPAT program. Retrospective chart review was used to describe patient characteristics and outcomes. Results: Fifty-two patients met inclusion criteria, 21 of whom were discharged to home and 31 were discharged to a SNF/rehab. Of the patients discharged to home, 17 (81%) completed their planned antibiotic courses without complication. Twenty (64%) patients discharged to a SNF/rehab completed the antibiotic courses without complication. Six (11%) patients had line infections, 6 (11%) had injection drug use relapse, and 12 (23%) required readmission. Conclusions: Persons who inject drugs discharged home were not more likely to have complications than those discharged to a SNF/rehab. Home OPAT may be a safe discharge option in carefully selected patients.Publication Phenome-wide Association Study Relating Pretreatment Laboratory Parameters With Human Genetic Variants in AIDS Clinical Trials Group Protocols(Oxford University Press, 2014) Moore, Carrie B.; Verma, Anurag; Pendergrass, Sarah; Verma, Shefali S.; Johnson, Daniel H.; Daar, Eric S.; Gulick, Roy M.; Haubrich, Richard; Robbins, Gregory; Ritchie, Marylyn D.; Haas, David W.Background. Phenome-Wide Association Studies (PheWAS) identify genetic associations across multiple phenotypes. Clinical trials offer opportunities for PheWAS to identify pharmacogenomic associations. We describe the first PheWAS to use genome-wide genotypic data and to utilize human immunodeficiency virus (HIV) clinical trials data. As proof-of-concept, we focused on baseline laboratory phenotypes from antiretroviral therapy-naive individuals. Methods. Data from 4 AIDS Clinical Trials Group (ACTG) studies were split into 2 datasets: Dataset I (1181 individuals from protocol A5202) and Dataset II (1366 from protocols A5095, ACTG 384, and A5142). Final analyses involved 2547 individuals and 5 954 294 imputed polymorphisms. We calculated comprehensive associations between these polymorphisms and 27 baseline laboratory phenotypes. Results. A total of 10 584 (0.17%) polymorphisms had associations with P < .01 in both datasets and with the same direction of association. Twenty polymorphisms replicated associations with identical or related phenotypes reported in the Catalog of Published Genome-Wide Association Studies, including several not previously reported in HIV-positive cohorts. We also identified several possibly novel associations. Conclusions. These analyses define PheWAS properties and principles with baseline laboratory data from HIV clinical trials. This approach may be useful for evaluating on-treatment HIV clinical trials data for associations with various clinical phenotypes.Publication T Cell Activation Markers and African Mitochondrial DNA Haplogroups among Non-Hispanic Black Participants in AIDS Clinical Trials Group Study 384(Public Library of Science, 2012) Hulgan, Todd; Robbins, Gregory; Kalams, Spyros A.; Samuels, David C.; Grady, Benjamin; Shafer, Robert; Murdock, Deborah G.; Selph, Doug; Haas, David W.; Pollard, Richard B.Introduction: Mitochondrial function influences T cell dynamics and is affected by mitochondrial DNA (mtDNA) variation. We previously reported an association between African mtDNA haplogroup L2 and less robust CD4 cell recovery on antiretroviral therapy (ART) in non-Hispanic black ACTG 384 subjects. We explored whether additional T cell parameters in this cohort differed by mtDNA haplogroup. Methods: ACTG 384 randomized ART-naïve subjects to two different nucleoside regimens with efavirenz, nelfinavir, or both. CD4 and CD8 memory and activation markers were available at baseline and week 48 on most subjects. mtDNA sequencing was performed on whole blood DNA, and haplogroups were determined. We studied non-Hispanic black subjects with HIV RNA <400 copies/mL at week 48. Analyses included Wilcoxon ranksum test and linear regression. Results: Data from 104 subjects were included. Major African mtDNA haplogroups included L1 (N = 25), L2 (N = 31), and L3 (N = 32). Baseline age, HIV RNA, and CD4 cells did not differ between L2 and non-L2 haplogroups. Compared to non-L2 haplogroups, L2 subjects had lower baseline activated CD4 cells (median 12% vs. 17%; p = 0.03) and tended toward lower activated CD8 cells (41% vs. 47%; p = 0.06). At 48 weeks of ART, L2 subjects had smaller decreases in activated CD4 cells (−4% vs. −11%; p = 0.01), and smaller CD4 cell increases (+95 vs. +178; p = 0.002). In models adjusting for baseline age, CD4 cells, HIV RNA, and naïve-to-memory CD4 cell ratio, haplogroup L2 was associated with lower baseline (p = 0.04) and 48-week change in (p = 0.01) activated CD4 cells. Conclusions: Among ART-naïve non-Hispanic blacks, mtDNA haplogroup L2 was associated with baseline and 48-week change in T cell activation, and poorer CD4 cell recovery. These data suggest mtDNA variation may influence CD4 T cell dynamics by modulating T cell activation. Further study is needed to replicate these associations and identify mechanisms.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, BruceBackground: 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.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, BruceBackground: 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.