2-LTR Circular Viral DNA as a Marker for Human Immunodeficiency Virus Type 1 Infection in Vivo

Non-integrating lentiviral vectors based on the minimal S/MAR sequence retain transgene expression in dividing cells

“…Further sequencing (( Figure S2 and Table S1 in Supporting Information) of the major band in the SNIL group revealed that this band corresponded to the 1-LTR circle (c1-LTR) DNA, which suggested that the SNIL vector was primarily retained as a c1-LTR circular form in the CHO clones. This result is consistent with previous reports showing that c1-LTR is present at a higher concentration than the c2-LTR form in non-integrating lentiviral-transduced cells (Banasik and McCray, 2010;Farnet and Haseltine, 1991;Pauza et al, 1994). LTR circles were also detected in the IL group ( Figure 5C), although they may have been lost during cell division because of the lack of an origin of replication.…”

New insight on the role of extrachromosomal retroviral DNA

“…Amplification of circular E-DNA could easily be substituted for intraactive viral replication. [14][15][16] Several studies of E-DNA have been performed in patients cellular RNA analysis as a measure of viral replication, thus saving time and eliminating reverse transcription of RNA into infected with HIV-1 [17][18][19] or human T cell leukemia virus type I 20,21 as well as in animals infected with simian immunodeficDNA. For these reasons, measurement of the level of circular E-DNA during the course of infection, since it is a marker of ciency virus (SIV), 22 feline leukemia virus 23 , MMLV, 24 equine infectious anemia virus, 25 spleen necrosis virus, 26 avian viral replication, appears to be a simple tool to follow the course of retroviral infections in vivo.…”

“…18,19 Moreover, a decrease in HIV-1 During the past few years, several reports have suggested that circular E-DNA is not simply a dead end product of the unintegrated DNA recovery has been associated with antiretroviral therapy. [30][31][32] It has been suggested that the level of reverse transcription process but rather participates actively in the course of infection.…”

“…41,42 In addition, the short half-life of c1LTR and c2LTR, between 1 and 2 days as mutations introduced into the IN protein simply do not have the same effect on the amount of E-DNA produced. Since has been determined in vivo, 18 does not permit them to be stable templates for viral mRNA transcription. Another reason recovery of RT activity after transient transfection of some INdefective molecular clones of HIV-1 is lower than that of the for the low contribution of E-DNA to the viral RNA pool is likely due to phenomena of promoter interference or wild-type counterpart, 34,36,39,43,44,48 it is likely that these mutants produce a lower amount of E-DNA, thus reducing the occlusion because of close proximity of the two promoters in the case of the c2LTR E-DNA, or the double use of the single amount of E-DNA template for mRNA transcription.…”

“…A lower amount of circular E-DNA is usually viral proteins. Viral proteins translated from mRNAs derived present both in vitro and in vivo at sites of viral replication 18 from E-DNA would be processed by similar pathways as those further ensuring that the major producer of viral mRNA, and transcribed from integrated templates in natural infections and hence protein, is the integrated form of the retrovirus. Howwould thus be in their most native form.…”