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  • 1
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    Online Resource
    Multidomain cognitive impairment in non-hospitalized patients with the post-COVID-19 syndrome: results from a prospective monocentric cohort
    Springer Science and Business Media LLC ; 2023
    In:  Journal of Neurology Vol. 270, No. 3 ( 2023-03), p. 1215-1223
    Details
    In: Journal of Neurology, Springer Science and Business Media LLC, Vol. 270, No. 3 ( 2023-03), p. 1215-1223
    Abstract: A fraction of patients with asymptomatic to mild/moderate acute COVID-19 disease report cognitive deficits as part of the post-COVID-19 syndrome. This study aimed to assess the neuropsychological profile of these patients. Methods Assessment at baseline (three months or more following acute COVID-19) of a monocentric prospective cohort of patients with post-COVID-19 syndrome. Multidomain neuropsychological tests were performed, and questionnaires on depression, anxiety, fatigue, sleep, and general health status were administered. Results Of the 58 patients screened, six were excluded due to possible alternative causes of cognitive impairment (major depression, neurodegenerative disease). Of the remaining 52 individuals, only one had a below-threshold screening result on Mini-Mental State Examination, and 13 scored below the cut-off on Montreal Cognitive Assessment. Extended neuropsychological testing revealed a neurocognitive disorder (NCD) in 31 (59.6%) participants with minor NCD in the majority of cases ( n  = 26). In patients with NCD, the cognitive domains learning/memory and executive functions were impaired in 60.7%, complex attention in 51.6%, language in 35.5%, and perceptual-motor function in 29.0%. Cognitive profiles were associated with daytime sleepiness but not with depression, anxiety, sleep quality, total general health status, or fatigue. Conclusion Neurocognitive impairment can be confirmed in around 60% of individuals with self-reported deficits as part of post-COVID-19 syndrome following a mild acute COVID-19 disease course. Notably, screening tests cannot reliably detect this dysfunction. Standard psychiatric assessments showed no association with cognitive profiles. Longitudinal studies are needed to further evaluate the course of neurocognitive deficits and clarify pathophysiology.
    Type of Medium: Online Resource
    ISSN: 0340-5354 , 1432-1459
    URL: Article
    DOI: 10.1007/s00415-022-11444-w
    RVK:
    XA 10000
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 1421299-7
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  • 2
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    Analysis of immune selection as a potential cause for the presence of cleavage site mutation 431V in treatment-naive HIV type-1 isolates
    SAGE Publications ; 2010
    In:  Antiviral Therapy Vol. 15, No. 6 ( 2010-08), p. 907-912
    Details
    In: Antiviral Therapy, SAGE Publications, Vol. 15, No. 6 ( 2010-08), p. 907-912
    Abstract: HIV type-1 (HIV-1) protease (PR) and cleavage site (CS) mutations accumulate in protease-inhibitor-resistant isolates. HIV-1 CS mutation 431V is the most frequent treatment-associated CS mutation; however, little is known about its origin in treatment-naive HIV-1 isolates. Recently, it has been shown that the CS mutation 431V is located within the human leukocyte antigen (HLA)-B*13-restricted cytotoxic T- lymphocyte (CTL) epitope RQANFLGKI (RI9). Therefore, we investigated whether the presence of CS mutation 431V might additionally be related to immune escape. Methods CTL recognition of RI9 and of RI9 variants carrying the 431V or the 436R mutation was analysed by ELISPOT in nine HLA-B*13-positive HIV-1-infected patients. Treatment-naive HIV-1-infected patients with primary drug-resistant HIV-1 isolates ( n=58) or carrying 431V ( n=4) were genotyped for HLA class I alleles. Results ELISPOT analysis showed different patterns of CTL recognition of RI9. CS mutation 431V could abrogate recognition by RI9-specific CTL in a subgroup of patients. Nevertheless, in our study, the occurrence of 431V in treatment-naive HIV-1 without primary drug resistance could not be explained by HLA-B*13-mediated immune selection. In patients with primary drug-resistant HIV-1 isolates, the frequency of HLA-B*13 was not increased and HLA-B*13 did not correlate with CS mutations 436R or 431V. Conclusions HIV-1 CS mutation 431V can abrogate CTL recognition, indicating interactions between development of drug resistance and the CTL response. However, we could not find evidence that the presence of 431V in treatment-naive HIV-1 isolates with and without primary drug resistance is related to immune selection by HLA-B*13 or other HLA class I alleles.
    Type of Medium: Online Resource
    ISSN: 1359-6535 , 2040-2058
    URL: Article
    DOI: 10.3851/IMP1640
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2010
    detail.hit.zdb_id: 2118396-X
    SSG: 15,3
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  • 3
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    A therapeutic vaccine strategy to prevent Pneumocystis pneumonia in an immunocompromised host in a NHP model HIV and Pneumocystis co-infection
    The American Association of Immunologists ; 2020
    In:  The Journal of Immunology Vol. 204, No. 1_Supplement ( 2020-05-01), p. 82.27-82.27
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 204, No. 1_Supplement ( 2020-05-01), p. 82.27-82.27
    Abstract: Pneumocystis (Pc) is a ubiquitious fungal pathogen that causes pneumonia (PCP) and Pc-related pulmonary sequelae in HIV-infected individuals and other immunocompromised populations. Deficiencies in CD4 T cell populations and immunologic dysfunction can limit humoral immunity and vaccine efficacy in Pc-susceptible populations. The ultimate goal of the field is to develop an effective vaccine that can overcome immune deficits in at risk populations and induce long-lasting protective immunity to Pc. Toward this goals, our laboratory has established a model of PCP co-infection in simian immunodeficiency virus (SIV)-infected non-human primates (NHP). We have previously identified a recombinant protein sub-unit vaccine, KEX1, that induces robust anti-Pc immunity in immune-competent macaques that is durable and prevents Pc pneumonia following simian immunodeficiency virus (SIV)-induced immunosuppression and subsequent Pc challenge (Kling and Norris, 2016). In the present study, we used the SIV model of HIV infection to address whether therapeutic vaccination with KEX1 can be effective following virus-induced immunosuppression. Type I, or invariant natural killer T (iNKT) cells have the potential to provide CD4-independent B cell help. When activated, iNKT cells are capable of rapidly expressing a wide array of cytokines and co-stimulatory molecules that can enhance humoral responses. The central hypothesis of this study is that a therapeutic vaccination strategy can induce invariant natural killer (iNKT) cell-B cell help to boost anti-KEX1 titers and enhance immunity to Pc during virus-induced immunosuppression.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.204.Supp.82.27
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2020
    detail.hit.zdb_id: 1475085-5
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  • 4
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    PML - opportunistische Infektion des Gehirns
    Springer Science and Business Media LLC ; 2023
    In:  InFo Neurologie + Psychiatrie Vol. 25, No. 1 ( 2023-01), p. 24-35
    Details
    In: InFo Neurologie + Psychiatrie, Springer Science and Business Media LLC, Vol. 25, No. 1 ( 2023-01), p. 24-35
    Type of Medium: Online Resource
    ISSN: 1437-062X , 2195-5166
    URL: Article
    DOI: 10.1007/s15005-022-3121-7
    Language: German
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 2529407-6
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  • 5
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    Longitudinal comparison of HIV‐1 plasma viral load and cellular proviral load
    Wiley ; 2014
    In:  Journal of the International AIDS Society Vol. 17, No. 4S3 ( 2014-11)
    Details
    In: Journal of the International AIDS Society, Wiley, Vol. 17, No. 4S3 ( 2014-11)
    Abstract: The goal of antiretroviral treatment (ART) in HIV‐1 infection is the permanent suppression of plasma viral load (pVL) below the currently existing limit of detection of 50 copies/mL (DAIG HIV‐therapy guidelines). Therefore, treatment effectiveness is based on pVL. pVL measurements however do not give any information about the viral reservoir in peripheral blood mononuclear cells (PBMCs). Therefore, the proviral DNA of HIV‐1 could be a useful marker for the investigation of viral reservoirs and monitoring ART in patients showing undetectable pVL. Materials and Methods Seventy‐seven treatment‐experienced HIV‐1 infected patients with pVL 〈 50 copies/mL were randomly selected. pVL and proviral DNA load were measured using the Roche COBAS TaqMan HIV‐1 v2.0 assay. Additionally, CD4+ cell count per mL and the total white blood cell (wbc) count per mL were determined for each patient. Follow‐up data were collected 24 weeks after the time point of the first measurement. Proviral DNA load per mL, CD4+ cell count per mL as well as wbc count per mL were observed over time and differences were estimated using the Mann–Whitney U test. Additionally, correlations between the clinical parameters were analyzed using the two‐sided Pearson correlation analysis. Results Out of the 77 patients, 38 show a significant increase in proviral load per mL over time (p=0,001), whereas 39 patients show a significant decrease (p=0,001). No differences became visible in the CD4+ cell count per mL comparing week 0 and week 24 data. Thirty five patients show a significant increase in wbc count per mL over time (p 〈 0,001), while 42 patients show a significant decrease (p 〈 0,001). A significant correlation of increasing proviral load per mL and wbc count per mL for data of the first (p 〈 0.001) and the second measurement (p 〈 0.001) can be detected, while there are no correlations found between proviral load per mL and CD4+ cell count per mL. Conclusions Our data show that the presence of viral reservoirs in other cell types and not only CD4+ cells is most probable. HIV‐1 proviral DNA seems to be an interesting marker in patients with undetectable pVL and allows the assessment of replication under ART. Nevertheless, further longitudinal studies are needed to assess the usefulness and the clinical significance of this marker.
    Type of Medium: Online Resource
    ISSN: 1758-2652 , 1758-2652
    URL: Article
    DOI: 10.7448/IAS.17.4.19669
    Language: English
    Publisher: Wiley
    Publication Date: 2014
    detail.hit.zdb_id: 2467110-1
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  • 6
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    Erratum to: Prevalence and characteristics of hepatitis B and C virus infections in treatment-naïve HIV-infected patients
    Springer Science and Business Media LLC ; 2011
    In:  Medical Microbiology and Immunology Vol. 200, No. 1 ( 2011-2), p. 51-51
    Details
    In: Medical Microbiology and Immunology, Springer Science and Business Media LLC, Vol. 200, No. 1 ( 2011-2), p. 51-51
    Type of Medium: Online Resource
    ISSN: 0300-8584 , 1432-1831
    URL: Article
    DOI: 10.1007/s00430-010-0179-5
    RVK:
    XA 10000
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2011
    detail.hit.zdb_id: 1462140-X
    SSG: 12
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  • 7
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    Antibody response after COVID‐19 vaccination in intravenous immunoglobulin‐treated immune neuropathies
    Wiley ; 2022
    In:  European Journal of Neurology Vol. 29, No. 11 ( 2022-11), p. 3380-3388
    Details
    In: European Journal of Neurology, Wiley, Vol. 29, No. 11 ( 2022-11), p. 3380-3388
    Abstract: This study assessed the prevalence of anti‐SARS‐CoV‐2 antibodies in therapeutic immunoglobulin and their impact on serological response to COVID‐19 mRNA vaccine in patients with intravenous immunoglobulin (IVIg)‐treated chronic immune neuropathies. Methods Forty‐six samples of different brands or lots of IVIg or subcutaneous IgG were analyzed for anti‐SARS‐CoV‐2 IgG using enzyme‐linked immunosorbent assay and chemiluminescent microparticle immunoassay. Blood sera from 16 patients with immune neuropathies were prospectively analyzed for anti‐SARS‐CoV‐2 IgA, IgG, and IgM before and 1 week after IVIg infusion subsequent to consecutive COVID‐19 mRNA vaccine doses and after 12 weeks. These were compared to 42 healthy subjects. Results Twenty‐four (52%) therapeutic immunoglobulin samples contained anti‐SARS‐CoV‐2 IgG. All patients with immune neuropathies (mean age = 65 ± 16 years, 25% female) were positive for anti‐SARS‐CoV‐2 IgG after COVID‐19 vaccination. Anti‐SARS‐CoV‐2 IgA titers significantly decreased 12–14 weeks after vaccination ( p  = 0.02), whereas IgG titers remained stable ( p  = 0.2). IVIg did not significantly reduce intraindividual anti‐SARS‐CoV‐2 IgA/IgG serum titers in immune neuropathies ( p  = 0.69). IVIg‐derived anti‐SARS‐CoV‐2 IgG did not alter serum anti‐SARS‐CoV‐2 IgG decrease after IVIg administration ( p  = 0.67). Conclusions Our study indicates that IVIg does not impair the antibody response to COVID‐19 mRNA vaccine in a short‐term observation, when administered a minimum of 2 weeks after each vaccine dose. The infusion of current IVIg preparations that contain anti‐SARS‐CoV‐2 IgG does not significantly alter serum anti‐SARS‐CoV‐2 IgG titers.
    Type of Medium: Online Resource
    ISSN: 1351-5101 , 1468-1331
    URL: Issue
    URL: Article
    DOI: 10.1111/ene.v29.11
    DOI: 10.1111/ene.15508
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 2020241-6
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  • 8
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    Progressive Multifocal Leukoencephalopathy: Pathogenesis, Diagnostic Tools, and Potential Biomarkers of Response to Therapy
    Ovid Technologies (Wolters Kluwer Health) ; 2023
    In:  Neurology
    Details
    In: Neurology, Ovid Technologies (Wolters Kluwer Health)
    Abstract: JC polyomavirus (JCV) establishes an asymptomatic latent and/or persistent infection in most of the adult population. However, in immunocompromised individuals, JCV can cause a symptomatic infection of the brain, foremost progressive multifocal leukoencephalopathy (PML). In the last two decades, there has been increasing concern among patients and the medical community as PML was observed as an adverse event in individuals treated with modern (selective) immune suppressive treatments for various immune-mediated diseases, especially multiple sclerosis (MS). It became evident that this devastating complication also needs to be considered beyond the patient populations historically at risk, including those with hematological malignancies or HIV-infected individuals. We review the clinical presentation of PML, its variants, pathogenesis, and current diagnostic approaches. We further discuss the need to validate JCV-directed interventions and highlight current management strategies based on early diagnosis and restoring JCV-specific cellular immunity, which is crucial for viral clearance and survival. Lastly, we discuss the importance of biomarkers for diagnosis and response to therapy, instrumental in defining sensitive study endpoints for successful clinical trials of curative or preventive therapeutics. Advances in understanding PML pathophysiology, host and viral genetics, and diagnostics, in conjunction with novel immunotherapeutic approaches indicate that the time is right to design and carry out definitive trials to develop preventive options and curative therapy for JCV-associated diseases.
    Type of Medium: Online Resource
    ISSN: 0028-3878 , 1526-632X
    URL: Article
    DOI: 10.1212/WNL.0000000000207622
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2023
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  • 9
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    Table_2.xlsx
    Frontiers Media SA ; 2022
    In:  Frontiers in Immunology Vol. 13 ( 2022-12-6)
    Details
    In: Frontiers in Immunology, Frontiers Media SA, Vol. 13 ( 2022-12-6)
    Abstract: Pneumocystis is a ubiquitous fungal pathogen that causes pneumonia (PCP) and pulmonary sequelae in HIV-infected individuals and other immunocompromised populations. With the success of anti-retroviral therapy for HIV-infected individuals the frequency of PCP in that population has decreased, however, PCP remains a significant cause of morbidity and mortality in individuals with hematologic and solid malignancies, and in individuals treated with immunosuppressive therapies for autoimmune diseases, and following bone marrow and solid organ transplantation. Despite the clinical need, there is no approved vaccine to prevent PCP in vulnerable populations. The ultimate goal of the field is to develop an effective vaccine that can overcome immune deficits in at risk populations and induce long-lasting protective immunity to Pneumocystis . Toward this goal, our laboratory has established a model of PCP co-infection in simian immunodeficiency virus (SIV)-infected non-human primates (NHP) and identified a recombinant protein sub-unit vaccine, KEX1, that induces robust anti- Pneumocystis immunity in immune-competent macaques that is durable and prevents PCP following simian immunodeficiency virus (SIV)-induced immunosuppression. Type I, or invariant natural killer T (iNKT) cells have the potential to provide B cell help under conditions of reduced CD4+ T cell help. Methods In the present study, we used the SIV model of HIV infection to address whether therapeutic vaccination with the iNKT cell-activating adjuvant α-galactosylceramide (α-GC) and KEX1 (α-GC+KEX1) can effectively boost anti- Pneumocystis humoral immunity following virus-induced immunosuppression. Results Immunization of antigen-experienced NHPs with α-GC+KEX1 during the early chronic phase of SIV-infection significantly boosted anti- Pneumocystis humoral immunity by increasing memory B cells and antibody titers, and enhanced titer durability during SIV-induced immunosuppression. This therapeutic vaccination strategy boosted anti- Pneumocystis immune responses during SIV-infection and contributed to protection against Pneumocystis co-infection in KEX1-vaccinated macaques. Conclusion These studies present a novel strategy for stimulating durable anti- Pneumocystis humoral immunity in the context of complex, chronic SIV-induced immunosuppression and may be further applied to immunization of other immunosuppressed populations, and toward other common recall antigens.
    Type of Medium: Online Resource
    ISSN: 1664-3224
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.3389/fimmu.2022.1036658
    DOI: 10.3389/fimmu.2022.1036658.s001
    DOI: 10.3389/fimmu.2022.1036658.s002
    DOI: 10.3389/fimmu.2022.1036658.s003
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2606827-8
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  • 10
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    Association of cerebrospinal fluid brain-binding autoantibodies with cognitive impairment in post-COVID-19 syndrome
    Elsevier BV ; 2023
    In:  Brain, Behavior, and Immunity Vol. 109 ( 2023-03), p. 139-143
    Details
    In: Brain, Behavior, and Immunity, Elsevier BV, Vol. 109 ( 2023-03), p. 139-143
    Type of Medium: Online Resource
    ISSN: 0889-1591
    URL: Article
    DOI: 10.1016/j.bbi.2023.01.006
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2023
    detail.hit.zdb_id: 1462491-6
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