HIV-1 infection of mononuclear phagocytic cells: the case for bacterial innate immune deficiency in AIDS

2006 ◽  
Vol 6 (12) ◽  
pp. 794-804 ◽  
Author(s):  
Mahdad Noursadeghi ◽  
David R Katz ◽  
Robert F Miller
Keyword(s):  
Immune Deficiency ◽  
Innate Immune ◽  
Phagocytic Cells ◽  
Hiv 1

scholarly journals Human TRIM5α: Autophagy Connects Cell-Intrinsic HIV-1 Restriction and Innate Immune Sensor Functioning

Viruses ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 320 ◽  
Author(s):  
Alexandra P. M. Cloherty ◽  
Anusca G. Rader ◽  
Brandon Compeer ◽  
Carla M. S. Ribeiro
Keyword(s):  
Therapeutic Potential ◽  
Innate Immune ◽  
Health Concern ◽  
Restriction Factor ◽  
Viral Reservoirs ◽  
Minimal Restriction ◽  
Immunodeficiency Virus ◽  
A Cell ◽  
Species Specific ◽  
Hiv 1

Human immunodeficiency virus-1 (HIV-1) persists as a global health concern, with an incidence rate of approximately 2 million, and estimated global prevalence of over 35 million. Combination antiretroviral treatment is highly effective, but HIV-1 patients that have been treated still suffer from chronic inflammation and residual viral replication. It is therefore paramount to identify therapeutically efficacious strategies to eradicate viral reservoirs and ultimately develop a cure for HIV-1. It has been long accepted that the restriction factor tripartite motif protein 5 isoform alpha (TRIM5α) restricts HIV-1 infection in a species-specific manner, with rhesus macaque TRIM5α strongly restricting HIV-1, and human TRIM5α having a minimal restriction capacity. However, several recent studies underscore human TRIM5α as a cell-dependent HIV-1 restriction factor. Here, we present an overview of the latest research on human TRIM5α and propose a novel conceptualization of TRIM5α as a restriction factor with a varied portfolio of antiviral functions, including mediating HIV-1 degradation through autophagy- and proteasome-mediated mechanisms, and acting as a viral sensor and effector of antiviral signaling. We have also expanded on the protective antiviral roles of autophagy and outline the therapeutic potential of autophagy modulation to intervene in chronic HIV-1 infection.

scholarly journals From Capsids to Complexes: Expanding the Role of TRIM5α in the Restriction of Divergent RNA Viruses and Elements

Viruses ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 446
Author(s):  
Kevin M. Rose ◽  
Stephanie J. Spada ◽  
Rebecca Broeckel ◽  
Kristin L. McNally ◽  
Vanessa M. Hirsch ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Molecular Basis ◽  
Human Population ◽  
Rna Viruses ◽  
Arms Race ◽  
Innate Immune ◽  
Immunodeficiency Virus ◽  
Underlying Mechanisms ◽  
Hiv 1

An evolutionary arms race has been ongoing between retroviruses and their primate hosts for millions of years. Within the last century, a zoonotic transmission introduced the Human Immunodeficiency Virus (HIV-1), a retrovirus, to the human population that has claimed the lives of millions of individuals and is still infecting over a million people every year. To counteract retroviruses such as this, primates including humans have evolved an innate immune sensor for the retroviral capsid lattice known as TRIM5α. Although the molecular basis for its ability to restrict retroviruses is debated, it is currently accepted that TRIM5α forms higher-order assemblies around the incoming retroviral capsid that are not only disruptive for the virus lifecycle, but also trigger the activation of an antiviral state. More recently, it was discovered that TRIM5α restriction is broader than previously thought because it restricts not only the human retroelement LINE-1, but also the tick-borne flaviviruses, an emergent group of RNA viruses that have vastly different strategies for replication compared to retroviruses. This review focuses on the underlying mechanisms of TRIM5α-mediated restriction of retroelements and flaviviruses and how they differ from the more widely known ability of TRIM5α to restrict retroviruses.

scholarly journals The origin of acquired immune deficiency syndrome: Darwinian or Lamarckian?

2001 ◽  
Vol 356 (1410) ◽  
pp. 877-887 ◽  
Author(s):  
Tom Burr ◽  
J. M. Hyman ◽  
Gerald Myers
Keyword(s):  
Immune Deficiency ◽  
Simulated Data ◽  
Immune Deficiency Syndrome ◽  
Acquired Immune Deficiency Syndrome ◽  
Deficiency Syndrome ◽  
Darwinian Evolution ◽  
Immunodeficiency Virus ◽  
Acquired Immune Deficiency ◽  
Hiv 1

The subtypes of human immunodeficiency virus type 1 (HIV–1) group M exhibit a remarkable similarity in their between–subtype distances, which we refer to as high synchrony. The shape of the phylogenetic tree of these subtypes is referred to as a sunburst to distinguish it from a simple star phylogeny. Neither a sunburst pattern nor a comparable degree of symmetry is seen in a natural process such as in feline immunodeficiency virus evolution. We therefore have undertaken forward–process simulation studies employing coalescent theory to investigate whether such highly synchronized subtypes could be readily produced by natural Darwinian evolution. The forward model includes both classical (macro) and molecular (micro) epidemiological components. HIV–1 group M subtype synchrony is quantified using the standard deviation of the between–subtype distances and the average of the within–subtype distances. Highly synchronized subtypes and a sunburst phylogeny are not observed in our simulated data, leading to the conclusion that a quasi–Lamarckian, punctuated event occurred. The natural transfer theory for the origin of human acquired immune deficiency syndrome (AIDS) cannot easily be reconciled with these findings and it is as if a recent non–Darwinian process took place coincident with the rise of AIDS in Africa.

scholarly journals Lymphocytes are detrimental during the early innate immune response against Listeria monocytogenes

2006 ◽  
Vol 203 (4) ◽  
pp. 933-940 ◽  
Author(s):  
Javier A. Carrero ◽  
Boris Calderon ◽  
Emil R. Unanue
Keyword(s):  
Immune Response ◽  
Listeria Monocytogenes ◽  
Innate Immune Response ◽  
Early Stage ◽  
Bacterial Pathogen ◽  
Interleukin 10 ◽  
Innate Immune ◽  
Type I ◽  
Phagocytic Cells ◽  
Immunodeficient Mice

Mice deficient in lymphocytes are more resistant than normal mice to Listeria monocytogenes infection during the early innate immune response. This paradox remains unresolved: lymphocytes are required for sterilizing immunity, but their presence during the early stage of the infection is not an asset and may even be detrimental. We found that lymphocyte-deficient mice, which showed limited apoptosis in infected organs, were resistant during the first four days of infection but became susceptible when engrafted with lymphocytes. Engraftment with lymphocytes from type I interferon receptor–deficient (IFN-αβR−/−) mice, which had reduced apoptosis, did not confer increased susceptibility to infection, even when the phagocytes were IFN-αβR+/+. The attenuation of innate immunity was due, in part, to the production of the antiinflammatory cytokine interleukin 10 by phagocytic cells after the apoptotic phase of the infection. Thus, immunodeficient mice were more resistant relative to normal mice because the latter went through a stage of lymphocyte apoptosis that was detrimental to the innate immune response. This is an example of a bacterial pathogen creating a cascade of events that leads to a permissive infective niche early during infection.

scholarly journals Whole Exome Sequencing of HIV-1 long-term non-progressors identifies rare variants in genes encoding innate immune sensors and signaling molecules

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Sara Konstantin Nissen ◽  
Mette Christiansen ◽  
Marie Helleberg ◽  
Kathrine Kjær ◽  
Sofie Eg Jørgensen ◽  
...  
Keyword(s):  
Exome Sequencing ◽  
Whole Exome Sequencing ◽  
Rare Variants ◽  
Signaling Molecules ◽  
Innate Immune ◽  
Whole Exome ◽  
Genes Encoding ◽  
Hiv 1

scholarly journals Author response: HIV-1 Vpr antagonizes innate immune activation by targeting karyopherin-mediated NF-κB/IRF3 nuclear transport

2020 ◽  
Author(s):  
Hataf Khan ◽  
Rebecca P Sumner ◽  
Jane Rasaiyaah ◽  
Choon Ping Tan ◽  
Maria Teresa Rodriguez-Plata ◽  
...  
Keyword(s):  
Immune Activation ◽  
Nuclear Transport ◽  
Innate Immune ◽  
Author Response ◽  
Innate Immune Activation ◽  
Hiv 1

scholarly journals Intron-containing RNA from the HIV-1 provirus activates type I interferon and inflammatory cytokines

2017 ◽  
Author(s):  
Sean Matthew McCauley ◽  
Kyusik Kim ◽  
Anetta Nowosielska ◽  
Ann Dauphin ◽  
Leonid Yurkovetskiy ◽  
...  
Keyword(s):  
T Cells ◽  
Antiviral Therapy ◽  
Antiviral Drug ◽  
Cell Types ◽  
Innate Immune ◽  
Type I ◽  
Infected People ◽  
Innate Immune Signaling ◽  
Post Transcriptional Regulation ◽  
Hiv 1

ABSTRACTHIV-1-infected people who take drugs that suppress viremia to undetectable levels are protected from developing AIDS. Nonetheless, these individuals have chronic inflammation associated with heightened risk of cardiovascular pathology. HIV-1 establishes proviruses in long-lived CD4+memory T cells, and perhaps other cell types, that preclude elimination of the virus even after years of continuous antiviral therapy. Though the majority of proviruses that persist during antiviral therapy are defective for production of infectious virions, many are expressed, raising the possibility that the HIV-1provirus or its transcripts contribute to ongoing inflammation. Here we found that the HIV-1 provirus activated innate immune signaling in isolated dendritic cells, macrophages, and CD4+T cells. Immune activation required transcription from the HIV-1 provirus and expression of CRM1-dependent, Rev-dependent, RRE-containing, unspliced HIV-1 RNA. Ifrevwas providedin trans, all HIV-1 coding sequences were dispensable for activation except thosecis-acting sequences required for replication or splicing. These results indicate that the complex, post-transcriptional regulation intrinsic to HIV-1 RNA is detected by the innate immune system as a danger signal, and that drugs which disrupt HIV-1 transcription or HIV-1 RNA metabolism would add qualitative benefit to current antiviral drug regimens.

How HIV-1 lentivirus causes immune deficiency disease

1999 ◽  
Vol 52 (1) ◽  
pp. 59-67 ◽  
Author(s):  
J.A. Habeshaw ◽  
S.E. Wilson ◽  
E.F. Hounsell ◽  
J.S. Oxford
Keyword(s):  
Immune Deficiency ◽  
Deficiency Disease ◽  
Hiv 1
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