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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...
Multiple Sclerosis l: Introduction01:19

Multiple Sclerosis l: Introduction

Multiple sclerosis is a chronic autoimmune disease of the central nervous system (CNS) that affects the brain, spinal cord, and optic nerves. It is an inflammatory demyelinating disorder and a leading cause of neurological disability in young adults.EpidemiologyMS commonly begins between 20 and 40 years of age and is twice as common in women. Its exact cause remains unclear, but genetic susceptibility contributes, with higher risk in first-degree relatives and identical twins. A greater...
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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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RNA viruses are categorized into positive-strand, negative-strand, or double-stranded groups based on their genomic structure and replication mechanisms. This classification dictates how they exploit host cellular machinery for protein synthesis and replication. Some RNA viruses also utilize reverse transcription as part of their life cycle, further diversifying their replication strategies.Positive-Strand RNA VirusesPositive-strand RNA viruses have genomes that function directly as messenger...
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Cells are sometimes infected by more than one virus at once. When two viruses disassemble to expose their genomes for replication in the same cell, similar regions of their genomes can pair together and exchange sequences in a process called recombination. Alternatively, viruses with segmented genomes can swap segments in a process called reassortment.

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Detection of the Genome and Transcripts of a Persistent DNA Virus in Neuronal Tissues by Fluorescent In situ Hybridization Combined with Immunostaining
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Herpesvirus active replication in multiple sclerosis: a genetic control?

Marta Garcia-Montojo1, Alfonso Martinez, Virginia De Las Heras

  • 1Servicio de Neurología, Hospital Clínico San Carlos, Madrid 28040, Spain.

Journal of the Neurological Sciences
|October 4, 2011
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Genetic factors may influence Human Herpesvirus 6 (HHV-6) replication in multiple sclerosis (MS) patients. MS patients with HHV-6 replication responded less effectively to interferon beta treatment.

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Area of Science:

  • Neuroimmunology
  • Virology
  • Genetics

Background:

  • The etiology of multiple sclerosis (MS) is complex, involving genetic, immunologic, and environmental factors.
  • Human Herpesvirus 6 (HHV-6) is a potential environmental factor implicated in MS pathogenesis.
  • Genetic predisposition may influence susceptibility and disease course in MS.

Purpose of the Study:

  • To investigate if genetic control explains HHV-6 active replication in a subset of MS patients.
  • To determine if MS patients with HHV-6 active replication exhibit distinct clinical characteristics.
  • To explore the relationship between HHV-6 replication, genetic markers, and interferon beta treatment response in MS.

Main Methods:

  • Genotyping of two Single Nucleotide Polymorphisms (SNPs) at the MHC2TA locus and two SNPs at the CD46 locus in 195 MS patients and 195 controls.
  • Polymerase Chain Reaction (PCR) analysis of five serum samples over two years to detect HHV-6 genomes.
  • Comparison of genetic data and HHV-6 detection rates between MS patients and controls, and between treatment responders and non-responders.

Main Results:

  • HHV-6 active replication was detected in 30.2% of MS patients.
  • No significant genetic difference was found between MS patients and controls overall.
  • Significant associations were observed for MHC2TA polymorphisms (rs4774C, rs3087456G) in MS patients with active HHV-6 replication compared to controls.
  • MHC2TA and CD46 showed significant differences when comparing interferon beta responders and non-responders within the MS cohort.
  • MS patients without HHV-6 active replication demonstrated better response to interferon beta treatment.

Conclusions:

  • A potential gene-environment interaction between HHV-6 and MHC2TA/CD46 genes in MS patients is suggested.
  • This interaction warrants further investigation as a possible genetic control mechanism in MS.
  • HHV-6 active replication may be a predictive marker for interferon beta treatment efficacy in MS patients.