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Related Concept Videos

Immunodeficiency Diseases01:25

Immunodeficiency Diseases

Immunodeficiency disorders are conditions in which the immune system's ability to fight infectious disease and cancer is compromised or entirely absent. The immune system comprises a complex network of cells, tissues, and organs that work together to protect the body from potentially harmful invaders. When this system is deficient or not functioning properly, it leaves the body susceptible to infections, diseases, or other complications.
There are three main causes of immunodeficiency disorders...
Sexually Transmitted Infections01:26

Sexually Transmitted Infections

Sexually transmitted infections (STIs) are diseases transmitted primarily through unsafe sexual interactions. Bacteria, viruses, or parasites cause them and can result in severe health complications if untreated.ChlamydiaThe bacterium Chlamydia trachomatis is responsible for the disease Chlamydia, the most common STI in the United States. This peculiar pathogen requires human cells to reproduce, residing intracellularly. The initial infection often goes unnoticed because it typically does not...
Inhibitors of Virion Maturation and Assembly01:19

Inhibitors of Virion Maturation and Assembly

As part of their replication cycle, certain viruses synthesize long precursor proteins called polyproteins within infected host cells. In human immunodeficiency virus (HIV), two major polyproteins are produced: Gag and Gag-Pol. The Gag polyprotein supplies the structural components of the virus, while Gag-Pol includes essential viral enzymes such as reverse transcriptase, integrase, and protease. After synthesis, these polyproteins move to the host cell membrane, where they assemble into an...

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Updated: Jun 27, 2026

Ex Vivo Infection of Human Lymphoid Tissue and Female Genital Mucosa with Human Immunodeficiency Virus 1 and Histoculture
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Ex Vivo Infection of Human Lymphoid Tissue and Female Genital Mucosa with Human Immunodeficiency Virus 1 and Histoculture

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Human immunodeficiency virus per se exerts atherogenic effects.

Ugo Oliviero1, Giovanni Bonadies, Valentina Apuzzi

  • 1Department of Internal Medicine, University Federico II, Naples, Italy.

Atherosclerosis
|December 17, 2008
PubMed
Summary

Human Immunodeficiency Virus (HIV) infection causes early vascular damage, including thickened carotid arteries and impaired blood vessel function, independent of treatment or metabolic issues. This suggests HIV itself contributes to atherosclerosis development.

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Last Updated: Jun 27, 2026

Ex Vivo Infection of Human Lymphoid Tissue and Female Genital Mucosa with Human Immunodeficiency Virus 1 and Histoculture
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Chronic, Acute, and Reactivated HIV Infection in Humanized Immunodeficient Mouse Models
09:54

Chronic, Acute, and Reactivated HIV Infection in Humanized Immunodeficient Mouse Models

Published on: December 3, 2019

Area of Science:

  • Cardiovascular Medicine
  • Infectious Diseases
  • Vascular Biology

Background:

  • Premature atherosclerosis in HIV patients is often linked to highly active antiretroviral therapy (HAART) and metabolic complications.
  • The independent role of Human Immunodeficiency Virus (HIV) infection in promoting atherosclerosis remains unclear.
  • This study investigates whether HIV infection itself contributes to atherogenic effects.

Purpose of the Study:

  • To determine if HIV infection per se induces atherogenic vascular changes.
  • To evaluate the impact of HIV on vascular structure and function in treatment-naïve patients.

Main Methods:

  • Carotid intima-media thickness (IMT) and brachial artery vasodilation (flow-mediated dilation [FMD] and non-dependent vasodilation [NMD]) were measured.
  • 38 treatment-naïve, untreated HIV-infected patients and 41 healthy controls were studied.
  • Controls were matched for metabolic risk factors.

Main Results:

  • HIV patients exhibited significantly higher mean carotid IMT compared to controls (0.85±0.2mm vs. 0.63±0.1mm).
  • Carotid IMT was associated with duration of HIV infection and CD4 T-cell count.
  • Brachial FMD was significantly impaired in HIV patients (8.8±3% vs. 12.2±3% in controls), correlating inversely with HIV viral load (HIV-RNA copies).
  • NMD did not differ significantly between groups.

Conclusions:

  • HIV infection causes early functional and structural vascular alterations, independent of HAART and metabolic factors.
  • Findings support the theory that viral infection contributes to atherosclerosis.
  • Early vascular assessment in HIV-infected patients is recommended.