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Animal herpes viruses all share some common properties. The structure of herpes viruses consists of a relatively large, double-stranded, linear DNA genome encased within an icosahedral protein cage called the capsid, which is wrapped in a lipid bilayer called the envelope. The envelope is joined to the capsid through a tegument.
Schematic drawing of a Herpesviridae virion. All members of the Herpesviridae share a common structure; a relatively large, monopartite, double-stranded, linear DNA genome encoding 100–200 genes encased within an icosahedral protein cage (with T=16 symmetry) called the capsid, which is itself wrapped in a protein layer called the tegument containing both viral proteins and viral mRNAs and a ...
The lytic phase of infection occurs within mucoepithelial cells while the latent infection of these cells occurs in neurons. These two viruses are the cause of oral and genital herpes. [4] Latency is maintained in a variety of ways, one of which is the latency-associated transcript, or LAT. This long non-coding RNA accumulates in the latent ...
While the infected cell would ordinarily undergo an organized death or be removed by the immune system, the consequences of LAT production interfere with these normal processes. Latency is distinguished from lytic infection; in lytic infection many Herpes virus particles are produced and then burst or lyse the host cell. Lytic infection is ...
During this process HHV-6 utilizes lipid rafts, which are membranous microdomains enriched by cholesterol, sphingolipids, and glycosylphosphatidylinositol-anchored proteins. [25] Early researchers suspected that HHV-6 virions mature in the nucleus; some even incorrectly published this, as they generalized and applied to HHV-6 what was known ...
Herpes simplex, often known simply as herpes, is a viral infection caused by the herpes simplex virus. [5] Herpes infections are categorized by the area of the body that is infected. The two major types of herpes are oral herpes and genital herpes, though other forms also exist. Oral herpes involves the face or mouth.
Entry, or penetration, is the second step in viral replication. This step is characterized by the virus passing through the plasma membrane of the host cell. The most common way a virus gains entry to the host cell is by receptor-mediated endocytosis, which comes at no energy cost to the virus, only the host cell. Receptor-mediated endocytosis ...
In one study, 76% of the 40 examined patients with DRESS exhibited some reactivation of Epstein-Barr virus, HHV-6, or HHV-7. Additionally, HHV-7 is currently suspected as a causative agent of lichen planus. In one dermatologic study, 33 skin biopsies were performed and HHV-7 was found at higher rates in lichen planus lesions.