Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Inhibitors of Viral Protein Synthesis

Inhibitors of Viral Protein Synthesis

Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...

Inhibitors Of Virion Release

Inhibitors Of Virion Release

Viral replication and dissemination rely on efficient mechanisms for host cell entry, genome replication, assembly, and release. Influenza viruses, such as types A and B, are negative-sense single-stranded RNA viruses with a segmented genome, that depend on two critical surface glycoproteins to carry out these processes: hemagglutinin (HA) and neuraminidase (NA). HA initiates infection by binding to sialic acid residues on the surface of host epithelial cells, facilitating receptor-mediated...

Immune Response Against Viral Pathogens

Immune Response Against Viral Pathogens

The immune system's response to viral infections is a complex and coordinated process involving natural killer (NK) cells, T cell-mediated responses, and antibody-mediated responses.
NK Cells
NK cells are a crucial part of our innate immune system, acting as the first line of defense against viral infections. These cells can recognize and kill infected cells without prior exposure to the virus, effectively slowing down the spread of infection. Additionally, NK cells produce proinflammatory...

Encephalitis ll: Pathophysiology

Encephalitis ll: Pathophysiology

Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Viral load-driven systemic immune exhaustion is an enabler of antibody breadth in HIV infection.

bioRxiv : the preprint server for biology·2026

Same author

Statewide multi-year wastewater sequencing reveals dual origins of HIV-1 signal.

Nature communications·2026

Same author

Evaluating Time-Space Methodologies to Detect Clusters of HIV Transmission: a Comparison of Advanced Methods in Washington State, 2010-2022.

Journal of acquired immune deficiency syndromes (1999)·2026

Same author

Sirtuin2 blockade inhibits replication of human immunodeficiency virus-1 and Mycobacterium tuberculosis in macrophages and humanized mice.

Molecular therapy : the journal of the American Society of Gene Therapy·2026

Same author

Determinants of natural killer cell-mediated antibody dependent cellular cytotoxicity in SARS-CoV-2 antibodies.

PLoS pathogens·2026

Same author

Re-infection with SARS-CoV-2 is associated with increased antibody breadth and potency against diverse sarbecovirus strains.

mBio·2026

Same journal

Identification of a Complex HIV-1 Circulating Recombinant Form (CRF203_cpx) Originating from Three Main Circulating Recombinant Forms in China.

AIDS research and human retroviruses·2026

Same journal

Near Full-Length Genome Characterization of a Novel Second-Generation HIV-1 CRF01_AE/CRF07_BC Recombinant Identified in an MSM Individual in Guizhou, China.

AIDS research and human retroviruses·2026

Same journal

Evolving Indications and Diagnostic Spectrum of Bone Marrow Examination in People with HIV During the Antiretroviral Therapy Era: A 6-Year Retrospective Study.

AIDS research and human retroviruses·2026

Same journal

A Conserved Natural Killer Cell Transcriptional Fingerprint in Rhesus Macaque Models of Acute Viral Infections.

AIDS research and human retroviruses·2026

Same journal

Perceived Ethical Risks of HIV Phylogenetic Research: Insights from Professional Stakeholders in Uganda.

AIDS research and human retroviruses·2026

Same journal

Genomic Characterization of Two Novel Human Immunodeficiency Virus-1 Recombinant Forms (CRF01_AE and B) in Men Who Have Sex with Men in Hebei, China.

AIDS research and human retroviruses·2026

See all related articles

Search research articles

Related Experiment Video

Updated: Jun 24, 2026

Single-cell Quantitation of mRNA and Surface Protein Expression in Simian Immunodeficiency Virus-infected CD4+ T Cells Isolated from Rhesus macaques

Single-cell Quantitation of mRNA and Surface Protein Expression in Simian Immunodeficiency Virus-infected CD4⁺ T Cells Isolated from Rhesus macaques

Published on: September 25, 2018

A decrease in albumin in early SIV infection is related to viral pathogenicity.

Susan M Graham¹, Sarah Holte, Jason T Kimata

¹Department of Medicine, University of Washington, Seattle, Washington 98104, USA. grahamsm@u.washington.edu

AIDS Research and Human Retroviruses

|March 27, 2009

Summary

This summary is machine-generated.

Decreased albumin levels in pig-tailed macaques indicate Simian Immunodeficiency Virus (SIV) infection progression. The extent of albumin decrease correlates with the pathogenicity of the infecting SIV strain.

More Related Videos

An In vitro Co-infection Model to Study Plasmodium falciparum-HIV-1 Interactions in Human Primary Monocyte-derived Immune Cells

An In vitro Co-infection Model to Study Plasmodium falciparum-HIV-1 Interactions in Human Primary Monocyte-derived Immune Cells

Published on: August 15, 2012

Related Experiment Videos

Last Updated: Jun 24, 2026

Single-cell Quantitation of mRNA and Surface Protein Expression in Simian Immunodeficiency Virus-infected CD4+ T Cells Isolated from Rhesus macaques

Single-cell Quantitation of mRNA and Surface Protein Expression in Simian Immunodeficiency Virus-infected CD4⁺ T Cells Isolated from Rhesus macaques

Published on: September 25, 2018

An In vitro Co-infection Model to Study Plasmodium falciparum-HIV-1 Interactions in Human Primary Monocyte-derived Immune Cells

An In vitro Co-infection Model to Study Plasmodium falciparum-HIV-1 Interactions in Human Primary Monocyte-derived Immune Cells

Published on: August 15, 2012

Area of Science:

Veterinary Immunology
Virology
Primate Models

Background:

Circulating albumin decrease predicts disease progression in HIV-infected adults.
Simian Immunodeficiency Virus (SIV) infection in macaques serves as a model for HIV pathogenesis.

Purpose of the Study:

To investigate if albumin levels decrease in pig-tailed macaques during early SIV infection.
To determine if the degree of albumin decrease relates to the pathogenicity of the infecting SIV strain.

Main Methods:

Ten juvenile pig-tailed macaques were inoculated with SIV variants of varying pathogenicity.
Albumin levels were measured in stored serum samples.
Statistical analyses included paired t tests and generalized estimating equations (GEE) modeling.

Main Results:

Albumin levels decreased significantly post-SIV inoculation and during chronic infection.
A significant difference in albumin decrease was observed between infections with early/intermediate versus late SIV variants.
The magnitude of albumin decrease was more pronounced with more pathogenic SIV strains.

Conclusions:

Albumin levels decrease in both early and chronic SIV infection in macaques.
The observed changes in albumin are influenced by the pathogenicity of the infecting SIV strain.
These findings highlight the utility of albumin as a biomarker in SIV pathogenesis studies.