Mirko Paiardini

ORCID: 0000-0002-7276-3600
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About
Contact & Profiles
Research Areas
  • HIV Research and Treatment
  • Immune Cell Function and Interaction
  • T-cell and B-cell Immunology
  • Cytomegalovirus and herpesvirus research
  • HIV/AIDS Research and Interventions
  • HIV-related health complications and treatments
  • COVID-19 Clinical Research Studies
  • Herpesvirus Infections and Treatments
  • HIV/AIDS drug development and treatment
  • SARS-CoV-2 and COVID-19 Research
  • Immunodeficiency and Autoimmune Disorders
  • Immunotherapy and Immune Responses
  • Virus-based gene therapy research
  • Virology and Viral Diseases
  • Long-Term Effects of COVID-19
  • interferon and immune responses
  • Erythrocyte Function and Pathophysiology
  • Psoriasis: Treatment and Pathogenesis
  • Animal Disease Management and Epidemiology
  • Mosquito-borne diseases and control
  • Blood properties and coagulation
  • CAR-T cell therapy research
  • Viral Infections and Immunology Research
  • Genomics, phytochemicals, and oxidative stress
  • Reproductive System and Pregnancy

Emory University
2016-2025

Emory and Henry College
2003-2025

Emory National Primate Research Center
2012-2024

University of Pennsylvania
2007-2011

Hospital of the University of Pennsylvania
2008

University of Urbino
1995-2006

University of Pittsburgh
2005

The University of Texas Southwestern Medical Center
2003-2005

Harvard University
2003

University of Campania "Luigi Vanvitelli"
2002

The chronic phase of HIV infection is marked by pathological activation the immune system, extent which better predicts disease progression than either plasma viral load or CD4+ T cell count. Recently, translocation microbial products from gastrointestinal tract has been proposed as an underlying cause this activation, based on indirect evidence including detection and specific responses in chronically HIV-infected humans SIV-infected Asian macaques. We analyzed tissues rhesus macaques (RMs)...

10.1371/journal.ppat.1001052 article EN cc-by PLoS Pathogens 2010-08-19

Natural SIV infection of sooty mangabeys (SMs) is nonprogressive despite chronic virus replication. Strikingly, it characterized by low levels immune activation, while pathogenic rhesus macaques (RMs) associated with activation. To elucidate the mechanisms underlying this intriguing phenotype, we used high-density oligonucleotide microarrays to longitudinally assess host gene expression in SIV-infected SMs and RMs. We found that acute was consistently a robust innate response, including...

10.1172/jci40115 article EN Journal of Clinical Investigation 2009-11-23

Abstract HIV-infected humans and SIV-infected rhesus macaques experience a rapid dramatic loss of mucosal CD4+ T cells that is considered to be key determinant AIDS pathogenesis. In this study, we show nonpathogenic SIV infection sooty mangabeys (SMs), natural host species for SIV, also associated with an early, severe, persistent depletion memory from the intestinal respiratory mucosa. Importantly, kinetics in SMs similar SIVmac239-infected macaques. Although induces same pattern target...

10.4049/jimmunol.179.5.3026 article EN The Journal of Immunology 2007-09-01

Abstract The immunodeficiency that follows HIV infection is related to the virus-mediated killing of infected CD4+ T cells, chronic activation immune system, and impairment cell production. In this study we show in HIV-infected individuals loss IL-7R (CD127) expression defines expansion a subset CD8+ specific for as well other Ags, phenotypic (i.e., CCR7 CD62 ligand with enrichment activated and/or proliferating cells) functional production IFN-γ, but not IL-2, decreased ex vivo...

10.4049/jimmunol.174.5.2900 article EN The Journal of Immunology 2005-03-01

ABSTRACT The mechanisms underlying the AIDS resistance of natural hosts for simian immunodeficiency virus (SIV) remain unknown. Recently, it was proposed that SIV avoid disease because their plasmacytoid dendritic cells (pDCs) are intrinsically unable to produce alpha interferon (IFN-α) in response RNA stimulation. However, here we show (i) acute infections associated with a rapid and robust type I IFN vivo , (ii) pDCs principal producers IFN-α/β at peak infection lymphatic tissues, (iii)...

10.1128/jvi.02612-09 article EN Journal of Virology 2010-05-20

While CD8+ T cells are clearly important in controlling virus replication during HIV and SIV infections, the mechanisms underlying this antiviral effect remain poorly understood. In study, we assessed vivo of lymphocyte depletion on lifespan productively infected chronic SIVmac239 infection rhesus macaques. We treated two groups animals that were either lymphocyte-depleted or controls with antiretroviral therapy, used mathematical modeling to assess presence absence lymphocytes. found that,...

10.1371/journal.ppat.1000747 article EN cc-by PLoS Pathogens 2010-01-28

Antiretroviral therapy (ART) suppresses viral replication in HIV-infected individuals but does not eliminate the reservoir of latently infected cells. Recent work identified PD-1+ follicular helper T (Tfh) cells as an important cellular compartment for persistence. Here, using ART-treated, SIV-infected rhesus macaques, we show that CTLA-4+PD-1− memory CD4+ cells, which share phenotypic markers with regulatory were enriched SIV DNA blood, lymph nodes (LN), spleen, and gut, contained...

10.1016/j.immuni.2017.09.018 article EN publisher-specific-oa Immunity 2017-10-01

In rhesus macaques (RMs), experimental depletion of CD4+ T-cells prior to SIV infection results in higher viremia and emergence CD4-independent SIV-envelopes. this study we used the recombinant anti-CD4 antibody CD4R1 deplete RM SIVmac251 investigate sources increased viral burden lifespan productively infected cells. CD4-depleted animals showed (i) set-point load two-logs than controls; (ii) macrophages constituting 80% all vRNA+ cells lymph node mucosal tissues; (iii) substantial expansion...

10.1371/journal.ppat.1004467 article EN cc-by PLoS Pathogens 2014-10-30

Despite successful control of viremia, many HIV-infected individuals given antiretroviral therapy (ART) exhibit residual inflammation, which is associated with non-AIDS-related morbidity and mortality may contribute to virus persistence during ART. Here, we investigated the effects IL-21 administration on both inflammation in ART-treated, SIV-infected rhesus macaques (RMs). Compared animals only ART, RMs ART showed improved restoration intestinal Th17 Th22 cells a more effective reduction...

10.1172/jci81400 article EN Journal of Clinical Investigation 2015-11-08

The persistence of HIV reservoirs, including latently infected, resting CD4+ T cells, is the major obstacle to cure infection. CD32a expression was recently reported mark cells harboring a replication-competent reservoir during antiretroviral therapy (ART) suppression. We aimed determine whether CD32 marks or transcriptionally active infected cells. Using peripheral blood and lymphoid tissue ART-treated HIV+ SIV+ subjects, we found that most circulating memory CD32+ expressed markers...

10.1126/scitranslmed.aar6759 article EN Science Translational Medicine 2018-04-18

Whole-genome sequencing and comparative genomic analysis of immune-related genes Cercocebus atys Macaca mulatta identify candidate genes, such as ICAM2 TLR4, that may explain the AIDS resistance C. atys. Sooty mangabeys are a primate model for non-pathogenic simian immunodeficiency virus (SIV) infection. Guido Silvestri colleagues sequenced genome captive sooty mangabey from Yerkes National Primate Research Center in Atlanta, Georgia. They compared this with sequences other primates suggest...

10.1038/nature25140 article EN cc-by Nature 2018-01-01
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