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Shorter Telomeres in Peripheral Blood Mononuclear Cells from Older Persons with Sarcopenia: Results from an Exploratory Study  [PDF]
Emanuele Marzetti,Maria Lorenzi,Stefano Bonassi,Vanessa Valdiglesias,Francesco Landi,Graziano Onder
Frontiers in Aging Neuroscience , 2014, DOI: 10.3389/fnagi.2014.00233
Abstract: Background: Telomere shortening in peripheral blood mononuclear cells (PBMCs) has been associated with biological age and several chronic degenerative diseases. However, the relationship between telomere length and sarcopenia, a hallmark of the aging process, is unknown. The aim of the present study was therefore to determine whether PBMC telomeres obtained from sarcopenic older persons were shorter relative to non-sarcopenic peers. We further explored if PBMC telomere length was associated with frailty, a major clinical correlate of sarcopenia.
Residual Viremia in Treated HIV+ Individuals  [PDF]
Jessica M. Conway?,Alan S. Perelson
PLOS Computational Biology , 2016, DOI: 10.1371/journal.pcbi.1004677
Abstract: Antiretroviral therapy (ART) effectively controls HIV infection, suppressing HIV viral loads. However, some residual virus remains, below the level of detection, in HIV-infected patients on ART. The source of this viremia is an area of debate: does it derive primarily from activation of infected cells in the latent reservoir, or from ongoing viral replication? Observations seem to be contradictory: there is evidence of short term evolution, implying that there must be ongoing viral replication, and viral strains should thus evolve. However, phylogenetic analyses, and rare emergent drug resistance, suggest no long-term viral evolution, implying that virus derived from activated latent cells must dominate. We use simple deterministic and stochastic models to gain insight into residual viremia dynamics in HIV-infected patients. Our modeling relies on two underlying assumptions for patients on suppressive ART: that latent cell activation drives viral dynamics and that the reproductive ratio of treated infection is less than 1. Nonetheless, the contribution of viral replication to residual viremia in patients on ART may be non-negligible. However, even if the portion of viremia attributable to viral replication is significant, our model predicts (1) that latent reservoir re-seeding remains negligible, and (2) some short-term viral evolution is permitted, but long-term evolution can still be limited: stochastic analysis of our model shows that de novo emergence of drug resistance is rare. Thus, our simple models reconcile the seemingly contradictory observations on residual viremia and, with relatively few parameters, recapitulates HIV viral dynamics observed in patients on suppressive therapy.
Shorter Telomeres May Mark Early Risk of Dementia: Preliminary Analysis of 62 Participants from the Nurses' Health Study  [PDF]
Francine Grodstein, Marieke van Oijen, Michael C. Irizarry, H. Diana Rosas, Bradley T. Hyman, John H. Growdon, Immaculata De Vivo
PLOS ONE , 2008, DOI: 10.1371/journal.pone.0001590
Abstract: Background Dementia takes decades to develop, and effective prevention will likely require early intervention. Thus, it is critical to identify biomarkers of preclinical disease, allowing targeting of high-risk subjects for preventive efforts. Since telomeres shorten with age and oxidative stress, both of which are important contributors to the onset of dementia, telomere length might be a valuable biomarker. Methodology/Principal Findings Among 62 participants of the Nurses' Health Study, we conducted neurologic evaluations, including patient and caregiver interviews, physical exam, neurologic exam, and neuropsychologic testing. We also conducted magnetic resonance imaging (MRI) in a sample of 29 of these women. In these preliminary data, after adjustment for numerous health and lifestyle factors, we found that truncated telomeres in peripheral blood leukocytes segregate with preclinical dementia states, including mild cognitive impairment (MCI); the odds of MCI were 12-fold higher (odds ratio = 12.00, 95% confidence interval 1.24–116.5) for those with shorter telomere length compared to longer telomere length. In addition, decreasing telomere length was strongly related to decreasing hippocampal volume (p = 0.038). Conclusions These preliminary data suggest that telomere length may be a possible early marker of dementia risk, and merits further study in large, prospective investigations.
Prevalence of Kidney Disease in HIV-Infected and Uninfected Rwandan Women  [PDF]
Christina M. Wyatt,Qiuhu Shi,James E. Novak,Donald R. Hoover,Lynda Szczech,Jules Semahore Mugabo,Agnes Binagwaho,Mardge Cohen,Eugene Mutimura,Kathryn Anastos
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0018352
Abstract: In the United States, HIV-related kidney disease disproportionately affects individuals of African descent; however, there are few estimates of kidney disease prevalence in Africa. We evaluated the prevalence of kidney disease among HIV-infected and uninfected Rwandan women.
Association of Low Level Viremia with Inflammation and Mortality in HIV-Infected Adults  [PDF]
Abigail Eastburn, Rebecca Scherzer, Andrew R. Zolopa, Constance Benson, Russell Tracy, Tri Do, Peter Bacchetti, Michael Shlipak, Carl Grunfeld, Phyllis C. Tien
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0026320
Abstract: Background Whether HIV viremia, particularly at low levels is associated with inflammation, increased coagulation, and all-cause mortality is unclear. Methods The associations of HIV RNA level with C-reactive protein (CRP), fibrinogen, interleukin (IL)-6 and mortality were evaluated in 1116 HIV-infected participants from the Study of Fat Redistribution and Metabolic Change in HIV infection. HIV RNA level was categorized as undetectable (i.e., “target not detected”), 1–19, 20–399, 400–9999, and ≥10,000 copies/ml. Covariates included demographics, lifestyle, adipose tissue, and HIV-related factors. Results HIV RNA level had little association with CRP. Categories of HIV RNA below 10,000 copies/ml had similar levels of IL-6 compared with an undetectable HIV RNA level, while HIV RNA ≥10,000 copies/ml was associated with 89% higher IL-6 (p<0.001). This association was attenuated by ~50% after adjustment for CD4+ cell count. Higher HIV RNA was associated with higher fibrinogen. Compared to an undetectable HIV RNA level, fibrinogen was 0.6%, 1.9%, 4.5%, 4.6%, and 9.4% higher across HIV RNA categories, respectively, and statistically significant at the highest level (p = 0.0002 for HIV RNA ≥10,000 copies/ml). Higher HIV RNA was associated with mortality during follow-up in unadjusted analysis, but showed little association after adjustment for CD4+ cell count and inflammation. Conclusion HIV RNA ≥10,000 copies/ml was associated with higher IL-6 and fibrinogen, but lower levels of viremia appeared similar, and there was little association with CRP. The relationship of HIV RNA with IL-6 was strongly affected by CD4 cell depletion. After adjustment for CD4+ cell count and inflammation, viremia did not appear to be substantially associated with mortality risk over 5 years.
Cellular Composition of Cerebrospinal Fluid in HIV-1 Infected and Uninfected Subjects  [PDF]
Emily L. Ho, Rollie Ronquillo, Hermann Altmeppen, Serena S. Spudich, Richard W. Price, Elizabeth Sinclair
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0066188
Abstract: In order to characterize the cellular composition of cerebrospinal fluid (CSF) in a healthy state and in the setting of chronic pleocytosis associated with HIV-1 (HIV) infection, multi-parameter flow cytometry was used to identify and quantitate cellular phenotypes in CSF derived from HIV-uninfected healthy controls and HIV-infected subjects across a spectrum of disease and treatment. CD4+ T cells were the most frequent CSF population and the CD4:CD8 ratio was significantly increased in the CSF compared to blood (p = 0.0232), suggesting preferential trafficking of CD4+ over CD8+ T cells to this compartment. In contrast, in HIV-infection, CD8+ T cells were the major cellular component of the CSF and were markedly increased compared to HIV-uninfected subjects (p<0.001). As with peripheral blood, the CSF CD4:CD8 ratio was reversed in HIV-infected subjects compared to HIV-uninfected subjects. Monocytes, B cells and NK cells were rare in the CSF in both groups, although absolute counts of CSF NK cells and B cells were significantly increased in HIV-infected subjects (p<0.05). Our studies show that T cells are the major cellular component of the CSF in HIV-infected and uninfected subjects. The CSF pleocytosis characteristic of HIV infection involves all lymphocyte subsets we measured, except for CD4+ T cells, but is comprised primarily of CD8+ T cells. The reduced proportion of CD4+ T cells in the CSF may reflect both HIV-related peripheral loss and changes in trafficking patterns in response to HIV infection in the central nervous system.
Evaluation of GBV-C / HVG viremia in HIV-infected women
Silva, Synara Araújo;Rodrigues, Célia Lima;Campos, Aléia Faustino;Levi, José Eduardo;
Revista do Instituto de Medicina Tropical de S?o Paulo , 2012, DOI: 10.1590/S0036-46652012000100006
Abstract: the present study aimed at standardizing a real-time quantitative polymerase chain reaction assay to evaluate the presence of gbv-c/hgv rna. a "taqman" assay using primers and probe derived from the 5¢ ncr region was developed and validated. two hundred and fifty-three plasma samples from hiv-infected women were tested for gbv-c viremia and antibody against the envelope protein 2. gbv-c rna was detected in 22.5% of the patients whereas the antibody was identified in 25.3% of the cohort. detection of viral rna and of antibodies was mutually exclusive. viral loads showed a mean of 1,777 arbitrary units / ml, being 1.1 and 13,625 arbitrary units / ml respectively the lowest and highest values measured. we conclude that the real-time quantitative polymerase chain reaction method developed is appropriate for the investigation of gbv-c rna since it was shown to be highly specific and sensitive, as well as requiring few steps, preventing contamination and providing additional information as to the relative viremia of carriers, a parameter that must be included in studies evaluating the co-factors influencing the clinical outcome of hiv/aids.
Sleep Disordered Breathing, Fatigue, and Sleepiness in HIV-Infected and -Uninfected Men  [PDF]
Susheel P. Patil, Todd T. Brown, Lisa P. Jacobson, Joseph B. Margolick, Alison Laffan, Lisette Johnson-Hill, Rebecca Godfrey, Jacquett Johnson, Sandra Reynolds, Alan R. Schwartz, Philip L. Smith
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0099258
Abstract: Study Objectives We investigated the association of HIV infection and highly active antiretroviral therapy (HAART) with sleep disordered breathing (SDB), fatigue, and sleepiness. Methods HIV-uninfected men (HIV?; n = 60), HIV-infected men using HAART (HIV+/HAART+; n = 58), and HIV-infected men not using HAART (HIV+/HAART?; n = 41) recruited from two sites of the Multicenter AIDS cohort study (MACS) underwent a nocturnal sleep study, anthropometric assessment, and questionnaires for fatigue and the Epworth Sleepiness Scale. The prevalence of SDB in HIV- men was compared to that in men matched from the Sleep Heart Health Study (SHHS). Results The prevalence of SDB was unexpectedly high in all groups: 86.7% for HIV?, 70.7% for HIV+/HAART+, and 73.2% for HIV+/HAART?, despite lower body-mass indices (BMI) in HIV+ groups. The higher prevalence in the HIV? men was significant in univariate analyses but not after adjustment for BMI and other variables. SDB was significantly more common in HIV? men in this study than those in SHHS, and was common in participants with BMIs <25 kg/m2. HIV+ men reported fatigue more frequently than HIV? men (25.5% vs. 6.7%; p = 0.003), but self-reported sleepiness did not differ among the three groups. Sleepiness, but not fatigue, was significantly associated with SDB. Conclusions SDB was highly prevalent in HIV? and HIV+ men, despite a normal or slightly elevated BMI. The high rate of SDB in men who have sex with men deserves further investigation. Sleepiness, but not fatigue, was related to the presence of SDB. Clinicians caring for HIV-infected patients should distinguish between fatigue and sleepiness when considering those at risk for SDB, especially in non-obese men.
Apoptosis of uninfected cells induced by HIV envelope glycoproteins
Barbara Ahr, Véronique Robert-Hebmann, Christian Devaux, Martine Biard-Piechaczyk
Retrovirology , 2004, DOI: 10.1186/1742-4690-1-12
Abstract: HIV infection usually leads to progressive decline in functionality and number of CD4+ T lymphocytes, resulting in AIDS development [1]. Despite intensive studies, several crucial questions remain to be addressed about the mechanisms through which HIV infection induces T cell death and this subject is one of the most controversial issues in AIDS research.First, T cell loss could be due to direct destruction by the virus. HIV infection results in high T cell activation and turnover, and accelerates both production and destruction of CD4+ T cells [1,2]. Using a mathematical model, Mohri and collaborators have demonstrated that T cell depletion observed in HIV-1 infection was due to an increased turnover of T lymphocytes rather than a decrease in cellular production [3], but the dynamics of T cells in HIV-infected patients remain controversial [4].A strong immune response is a priori beneficial in controlling viral replication. However, independently of viral load, a chronic, heightened activation of the immune system may contribute in a direct manner to progressive CD4+ T cell depletion [4,5]. Two observations corroborate this hypothesis. First, sooty mangabeys, the natural host of simian immunodeficiency virus (SIV), which do not develop AIDS, support high levels of viral replication but fail to exhibit a clear increase in immune activation [6]. In contrast, SIV experimentally transferred to rhesus macaques induces a dramatic increase in immune activation and rapid progression to AIDS and death. In the same way, HIV-1 and HIV-2-infected patients with similar degree of CD4+ T cell depletion show large differences in viral load [7]. CD4+ T cell loss during the chronic phase of HIV/SIV infection is thus more directly related to the overall immune response than the rate of virus replication. Immune activation could drive the progression of HIV disease by destabilizing or progressively changing the homeostatic states of resting T cell populations.Second, T cell apoptosis
ART Suppresses Plasma HIV-1 RNA to a Stable Set Point Predicted by Pretherapy Viremia  [PDF]
Frank Maldarelli ,Sarah Palmer,Martin S King,Ann Wiegand,Michael A Polis,JoAnn Mican,Joseph A Kovacs,Richard T Davey,Diane Rock-Kress,Robin Dewar,Shuying Liu,Julia A Metcalf,Catherine Rehm,Scott C Brun,George J Hanna,Dale J Kempf,John M Coffin,John W Mellors
PLOS Pathogens , 2007, DOI: 10.1371/journal.ppat.0030046
Abstract: Current antiretroviral therapy is effective in suppressing but not eliminating HIV-1 infection. Understanding the source of viral persistence is essential for developing strategies to eradicate HIV-1 infection. We therefore investigated the level of plasma HIV-1 RNA in patients with viremia suppressed to less than 50–75 copies/ml on standard protease inhibitor- or non-nucleoside reverse transcriptase inhibitor-containing antiretroviral therapy using a new, real-time PCR-based assay for HIV-1 RNA with a limit of detection of one copy of HIV-1 RNA. Single copy assay results revealed that >80% of patients on initial antiretroviral therapy for 60 wk had persistent viremia of one copy/ml or more with an overall median of 3.1 copies/ml. The level of viremia correlated with pretherapy plasma HIV-1 RNA but not with the specific treatment regimen. Longitudinal studies revealed no significant decline in the level of viremia between 60 and 110 wk of suppressive antiretroviral therapy. These data suggest that the persistent viremia on current antiretroviral therapy is derived, at least in part, from long-lived cells that are infected prior to initiation of therapy.
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