episomal

With adeno-associated viruses and adenoviruses, the genomes remain episomal.

Episomal latency refers to the use of genetic episomes during latency.

AAV-based gene therapy vectors form episomal concatamers in the host cell nucleus.

Both proviral and episomal latency may require maintenance for continued infection and fidelity of viral genes.

Episomal latency is more vulnerable to ribozymes or host foreign gene degradation than provirus latency.

QMCF Technology is an episomal protein expression system that uses genetically modified mammalian cells and specially designed plasmids.

The cccDNA of viruses is also known as episomal DNA or occasionally as a minichromosome.

When the host is stressed, the integrated genome of BSV may be able to recombine out into its episomal form, though the mechanism is not well understood.

In the absence of helper virus or genotoxic factors, AAV DNA can either integrate into the host genome or persist in episomal form.

The Gammaherpesvirinae subfamily is associated with episomal latency established in cells of the immune system, such as B-cells in the case of Epstein-Barr Virus.

Advantages of episomal latency include the fact that the virus may not need to enter the nucleus, and hence may avoid ND10 domains from activating interferon via that pathway.

In mice, the AAV genome has been observed persisting for long periods of time in quiescent tissues, such as skeletal muscles, in episomal form (a circular head-to-tail conformation).

Modification by integrated or episomal DNA has been shown to potentiate longevity in stem cells with such factors as GSK3-β, GATA4, Bcl-2, and HSP-20.

'Diffuse' signals (indicative of episomal HPV), 'diffuse' and 'punctate', or 'punctate' signals alone were demonstrated amongst pre-invasive lesion samples (Figure 2A,2Band 2C).

In dividing cells, AAV DNA is lost through cell division, since the episomal DNA is not replicated along with the host cell DNA.

The development of a yeast-based system that allows stable episomal HPV replication provides a convenient, rapid and inexpensive means to study several aspects of the HPV lifecycle (Angeletti 2002).

EBNA1 is integral in many EBV functions including gene regulation, extrachromosomal replication, and maintenance of the EBV episomal genome through positive and negative regulation of viral promoters.

Herpes virus include Chicken-pox virus and Herpes simplex viruses (HSV-1, HSV-2), all of which establish episomal latency in neurons and leave linear genetic material floating in the cytoplasm.

The demonstration of 1-2 copies of integrated HPV DNA detected as punctate signal begs the question as to why single/low-copy episomal HPV is not also detectable as punctate signal.

An important variant of this cell line is the 293T cell line that contains, in addition, the SV40 Large T-antigen, that allows for episomal replication of transfected plasmids containing the SV40 origin of replication.

These observations are consistent with earlier studies that a punctate signal is representative of integration and a diffuse signal of episomal HPV, and with the theory that integration is an important factor in lesion progression [ 2 12 ] .

When HA-Ppt1p or EGFP-Ppt1p was overexpressed from the GAL1 promoter in a centromeric or episomal plasmid, respectively, indirect immunofluorescence of HA-Ppt1p or direct fluorescence from EGFP-Ppt1p showed that both proteins were also localized throughout the cell.

A possible explanation maybe that that 8 kilo-base single/low-copy episomal HPV sequences may be subject to relatively more degradation and loss from tissues during routine processing than HPV DNA that is physically integrated into the human chromosome ( 50 - 250 mega-base pairs).

If this is the case, then punctate signal detected in carcinomas and high-grade CIN lesions may only represent integration of multiple copies of HPV at sites within the genome, and low-copy episomal (or integrated) DNA may remain sub-threshold on archival FFPE samples.