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Related Concept Videos

Herpes01:28

Herpes

Herpes simplex type 1 (HSV‑1) is a widespread pathogen responsible for orolabial lesions. It is an enveloped, double-stranded DNA (dsDNA) virus belonging to the family Herpesviridae. Once the virus infects a host cell, its double‑stranded DNA genome is delivered into the nucleus, where a coordinated cascade of immediate‑early, early, and late gene expression directs viral DNA replication, structural protein synthesis, and virion assembly. After primary infection of epithelial cells, HSV-1...
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Genital herpes is a sexually transmitted infection primarily caused by herpes simplex virus type 2 (HSV-2), though herpes simplex virus type 1 (HSV-1) is increasingly implicated in genital infections, particularly among younger populations. Transmission occurs mainly through sexual contact, with asymptomatic viral shedding serving as a major route of spread. This characteristic makes HSV-2 difficult to control at a population level, as individuals may unknowingly transmit the virus even in the...
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Cytomegalovirus Disease

Cytomegalovirus (CMV) disease is caused by human cytomegalovirus, a double-stranded DNA virus of the Herpesviridae family. While primary CMV infection is often asymptomatic in immunocompetent individuals, the virus can cause severe disease in neonates and immunocompromised patients. CMV is the most common cause of congenital viral infection in the United States, and a major pathogen in solid organ and hematopoietic stem cell transplant recipients.CMV is transmitted via bodily fluids, sexual...

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Analysis of Simian Immunodeficiency Virus-specific CD8+ T-cells in Rhesus Macaques by Peptide-MHC-I Tetramer Staining
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Human herpesvirus 6A accelerates AIDS progression in macaques.

Paolo Lusso1, Richard W Crowley, Mauro S Malnati

  • 1Unit of Human Virology, San Raffaele Scientific Institute, 20132 Milan, Italy. paolo.lusso@hsr.it

Proceedings of the National Academy of Sciences of the United States of America
|March 16, 2007
PubMed
Summary

Human herpesvirus 6A (HHV-6A) coinfection significantly accelerates simian immunodeficiency virus (SIV) disease progression in macaques. This viral synergy leads to faster CD4(+) and CD8(+) T cell depletion and AIDS development.

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Area of Science:

  • Virology
  • Immunology
  • Primate Models

Background:

  • Human immunodeficiency virus (HIV) causes acquired immunodeficiency syndrome (AIDS), but disease progression varies.
  • Human herpesvirus 6A (HHV-6A), a DNA virus, is suspected to accelerate AIDS progression alongside HIV-1.
  • The role of HHV-6A in vivo as a co-factor in AIDS pathogenesis remains to be fully elucidated.

Purpose of the Study:

  • To investigate the impact of HHV-6A coinfection on the progression of simian immunodeficiency virus (SIV) disease in pig-tailed macaques.
  • To determine if HHV-6A influences the clinical and immunological outcomes of SIV infection in a primate model.

Main Methods:

  • Pig-tailed macaques (Macaca nemestrina) were inoculated with either HHV-6A alone or with both HHV-6A and SIV.
  • Plasma viremia, clinical manifestations, antibody seroconversion, and CD4(+) and CD8(+) T cell counts were monitored.
  • Disease progression and immunological sequelae were compared between singly and dually infected animals.

Main Results:

  • HHV-6A infection in macaques led to rapid viremia, transient symptoms, and seroconversion, confirming susceptibility.
  • SIV-infected macaques showed progressive CD4(+) T cell loss, consistent with AIDS progression.
  • Coinfection with HHV-6A dramatically accelerated AIDS progression, evidenced by early and severe depletion of both CD4(+) and CD8(+) T cells.

Conclusions:

  • HHV-6A coinfection significantly exacerbates SIV-induced immunodeficiency in macaques.
  • These findings provide in vivo evidence that HHV-6A acts as a promoting factor in AIDS progression.
  • HHV-6A may represent a critical co-factor influencing the clinical course of HIV/AIDS in humans.