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Last update 08 May 2025

Simian Acquired Immunodeficiency Syndrome

Last update 08 May 2025

Basic Info

Synonyms

AIDS, Simian, AIDS-サル, AIDS-猿

+ [26]

Introduction

Acquired defect of cellular immunity that occurs naturally in macaques infected with SRV serotypes, experimentally in monkeys inoculated with SRV or MASON-PFIZER MONKEY VIRUS; (MPMV), or in monkeys infected with SIMIAN IMMUNODEFICIENCY VIRUS.

Drugs associated with Simian Acquired Immunodeficiency Syndrome

Azacitidine

Target

DNMT1

Mechanism

DNMT1 inhibitors [+1]

Active Org.

Accord Healthcare SLU [+18]

Originator Org.

Celgene Corp.

Active Indication

Juvenile Myelomonocytic Leukemia [+52]

Inactive Indication

Acute myeloid leukaemia with 11q23 abnormality [+63]

Drug Highest PhaseApproved

First Approval Ctry. / Loc.

United States

First Approval Date19 May 2004

Clinical Trials associated with Simian Acquired Immunodeficiency Syndrome

NCT03643809

/ CompletedNot ApplicableIIT

Epidemiology and Clinico-genetic Correlations of Auto-inflammatory Diseases

Systemic autoinflammatory diseases (SAIDs) are inflammatory conditions caused by a defect of the innate immune system. Most are hereditary, but little is known on recent entities. The investigators aim to (1) establish correlations between the main mutations and symptoms presented by patients (genotype-phenotype correlation), and (2) describe the most recently described clinical, genetic, and demographic characteristics of SAIDs.

Start Date07 Jul 2018

Sponsor / Collaborator

Centre Hospitalier Universitaire de Montpellier

NCT02985190

/ CompletedPhase 2IIT

A Phase II Study of Efficacy and Tolerance of Azacitidine (AZA) In MDS-associated Steroid Dependent/Refractory Systemic Auto-immune and Inflammatory Disorders (SAID)

This study is a phase II of effcicacy and tolerance of azacitidine in patients with myelodysplatic syndrome and steroid dependent or resistent systemic auto-immune and inflammatory disorders

Start Date26 Jan 2017

Sponsor / Collaborator

Groupe Francophone des Myélodysplasies

[+1]

100 Clinical Results associated with Simian Acquired Immunodeficiency Syndrome

100 Translational Medicine associated with Simian Acquired Immunodeficiency Syndrome

0 Patents (Medical) associated with Simian Acquired Immunodeficiency Syndrome

714

Literatures (Medical) associated with Simian Acquired Immunodeficiency Syndrome

01 Jun 2025·Nutrition, Metabolism and Cardiovascular Diseases

Causal effects and mediating pathways of metabolic dysfunction-associated fatty liver disease on novel subtypes of adult-onset diabetes: A two-step Mendelian randomization study

Article

Author: Fan, Yawei ; Luo, Hongping ; Wang, Ting ; Tian, Ye ; Li, Rongrong ; Guan, Yan

BACKGROUND AND AIMBased on an in-depth understanding of diabetes heterogeneity, five novel subtypes of adult-onset diabetes have been identified. This study investigates the differential impact of metabolic dysfunction-associated fatty liver disease (MAFLD) on these subtypes using a Mendelian randomization (MR) approach, while also exploring modifiable mediating factors.METHODS AND RESULTSGenetic variants associated with MAFLD were selected at the genome-wide significance threshold (P < 5 × 10^-8), with 16 variants used to assess causal associations with the risk of severe autoimmune diabetes (SAID), mild obesity-related diabetes (MOD), severe insulin-resistant diabetes (SIRD), severe insulin-deficient diabetes (SIDD), and mild age-related diabetes (MARD). Two-step MR was used to estimate total, direct, and mediated effects, analyzing 55 potential mediators across five domains. The primary method used was inverse variance weighting (IVW) along with a series of sensitivity analyses to ensure robustness of the results. Genetically predicted MAFLD was significantly associated with increased risk of MARD (OR = 1.171, 95 % CI 1.091-1.256), SIDD (OR = 1.158, 95 % CI 1.056-1.270), and SIRD (OR = 1.267, 95 % CI 1.119-1.434), with suggestive evidence for SAID (OR = 1.161, 95 % CI 1.016-1.327), but no association with MOD. Among all subtypes, waist-to-hip ratio adjusted for BMI (WHRadjBMI) was a common mediator, with liver fat, alanine aminotransferase (ALT), gamma-glutamyl transferase, fasting insulin (FI), and BMI mediating at least three subtypes. Liver fat accounted for the largest proportion of mediation (43.63 %-73.09 %), followed by ALT (8.99 %-17.93 %) and FI (6.81 %-13.04 %).CONCLUSIONThis study underscores the causal relationship between MAFLD and specific diabetes subtypes, highlighting the importance of integrated management of liver lipid metabolism, abdominal obesity, and blood glucose regulation. These findings support personalized intervention strategies.

01 Apr 2025·The American Journal of Emergency Medicine

Case report: Hyponatremia due to syndrome of inappropriate antidiuresis associated with normal pressure hydrocephalus

Article

Author: Martin, Julia ; McCoin, Nicole ; Marcum, Samuel

Hyponatremia is common in hospitalized patients. Syndrome of inappropriate antidiuresis (SIAD) is a known cause of hyponatremia, with many different causes. Normal pressure hydrocephalus-related SIAD with resultant hyponatremia is a less known association. This case report is of a 77-year-old male with known normal pressure hydrocephalus (NPH) presenting with acute mental status changes and severe hyponatremia and found to have SIAD due to his NPH. A lumbar puncture quickly improved both his confusion and hyponatremia. The association between SAID and NPH is important as the management may require a lumbar puncture to improve symptoms. Emergency physicians must know this association to help make correct diagnoses and guide treatment.

01 Apr 2025·Brain Research Bulletin

Differential tissue and cellular distribution of chemokine C-C motif ligand 2 in grey/white matters of healthy and simian immunodeficiency virus infected monkey

Article

Author: Xiong, Huangui ; Zhu, Junyi ; Shi, Xue ; Li, Hongjun ; Zhao, Huangying ; Zhang, Jingdong

Previous studies have shown that CCL2 concentration is higher in cerebrospinal fluid than in plasma of health and human immunodeficiency virus (HIV) infected individuals, suggesting an extra source of CCL2 in brain. Brain cellular CCL2 has been broadly studied in cultured cells and its in-vivo cellular distribution has been investigated in rodent experimental autoimmune encephalomyelitis model. However, its cellular distribution in grey and white matter (GM, WM) remains elusive. We explored this issue using healthy and simian immunodeficiency virus (SIV) infected monkeys and found: 1) Neurons were a major source of CCL2-like immunoreactivity (CCL2-ir) in normal GM, and corpus callosum (CC) ependyma showed high density of CCL2-ir. 2) Upon SIV infection, CCL2-ir was strikingly raised in GM neurons, and in CC ependyma. 3) Brain vascular-perivascular cells were a large source of CCL2-ir in normal GM and WM, which was relatively larger in CC WM than in GM. 4) Vascular-perivascular CCL2-ir proportional areas were significantly enhanced by SIV infection in both GM and CC WM. 5) Microglia seemed not to express CCL2 in healthy brain. Microglia-marker and CCL2-ir co-labeled cells were significantly increased by SIV infection. 6) A vast of macrophage-like cells were situated along infected CC ependyma, suggesting a large number of monocytes be crossing ependyma, which may be related to establishment of viral reservoir. In conclusion, our study provides valuable insights into the cellular sources and alterations of CCL2 in the monkey brain under normal and SIV-infected conditions, which may promote better understanding of CCL2 in related neurological processes.

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Simian Acquired Immunodeficiency Syndrome

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