HSV-1 General overview:
There are Two antigenic types, HSV-1 and HSV-2, that share antigenic cross-reactivity but different Neutralization patterns and are inclined to produce different clinical signs. Man is believed to be the natural host for HSV, but the virus can also be capable Of infecting a variety of animals, such as rodents (good animal models). HSV-2 prevalence is, Generally Speaking, highest at Africa and the Americas, reduced and lowest in Asia. HSV-1 infection is acquired during childhood And adolescence and is markedly more prevalent than HSV-2 infection.
Virions contain one molecule of linear double stranded DNA. Total genome length is 152 kbpt. Genome sequence has terminal repeated sequences; reiterated internally in inverted form; replicated at both ends. Guanine + cytosine ratio 67 %. Each virion contains multiple isomeric forms of genome (i.e. 4 isomeric forms).
How does the infection develop?
Primary infection occurs via a rest from the mucous membranes of the mouth or throat, via the eye or genitals or directly via minor abrasions in the skin. Because of the universal supply of the virus, most individuals are infected with 1-2 decades old; first infection is usually asymptomatic, although there may be minor localized vesicular lesions. Nearby multiplication ensues, followed closely by viremia and systemic disease.
There then follows a life-long latent infection with regular reactivation.During primary disease, the virus enters peripheral sensory nerves and migrates along axons to sensory nerve ganglia in the CNS – allows virus to escape immune reaction! During latent disease of neural cells, viral DNA is maintained as an episome (not incorporated ) with limited expression of particular virus genes necessary for the maintenance of latency – true latency.
The fragile balance of latency may be upset by different disturbances, physical (harm, U.V, hormones, etc) or psychological (stress, emotional upset – perhaps affecting immune system/hormonal equilibrium ).
Use of HSV-1 as gene therapy:
HSV-1 is under active development as a vector for gene therapy. The ability of the LAT promoter to operate throughout latency, which may persist for a lifetime, suggests that this promoter has possible for a lifelong expression of therapeutic genes. Recent success has been reported in clinical trials of engineered HSV-1 against metastatic melanoma tumors.
How could we detect HSV-1 ?
SV-1 qPCR 20x probe combination is a trusted probe for measuring comparative amounts or complete copy amounts of HSV-1 by qualitative PCR. The research contains reverse and forward primers along with some FAM/BHQ-labeled probe specific for glycoprotein D (gD) of HSV-1. This dual-labeled probe is provided with PCR primers in 20x immersion and might be utilized with regular real time PCR reagents. For complete copy quantity calculations, a tube of criteria can also be included containing the target sequence at 1012 copies per watt. These criteria produce linear outcomes at dilutions of 108 to 102 copies per response.
Antigen slides are particularly suited for immunofluorescence but Can also be used in immunohistochemical protocols. Infected cells are mixed with uninfected cells to ensure that every well of the slide has”built in” unwanted controls. Employed with our optimized lineup of pre-mixed secondary antibodies, the antigen shows itself through bright green fluorescence from a dark red background of uninfected cells.Each slide has eight separate wells set in a hydrophobic Teflon mask. Reagents which are incubated on the contaminated cells act as a”bead” on the nicely since the teflon keeps the liquid out. They are supplied in packages of five individually packaged slides and full instructions for use.
Herpes Simplex Type 1 Antigen Slide
Five, eight-well slides with AGMK cells infected with Herpes Simplex type 1 (MacIntyre).