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1 viral entry, before the generation of viral reverse transcription products.
2 in the ability of MLV particles to generate reverse transcription products.
3 levels of IAP transcripts, Gag proteins, and reverse transcription products.
4 approximate size expected for a full-length reverse transcription product and with plus-strand stron
6 esult in decreased amounts of early and late reverse transcription products and integrated virus rela
7 at A3G exosomes reduce accumulation of HIV-1 reverse transcription products and steady-state levels o
8 sequencing strategy to characterize nascent reverse transcription products and their precise 3'-term
9 nfection, results in reduced accumulation of reverse transcription products, and is dominant in heter
11 d PBMCs and MDDCs revealed similar levels of reverse transcription products, but increased nuclear im
12 troviruses by preventing the accumulation of reverse transcription products, but the underlying mecha
13 cells revealed that the generation of early reverse transcription products coincides with the timing
14 but not integration, indicating that a viral reverse transcription product comprises the HIV-1 pathog
17 d allows the normal generation of HIV-1 late reverse transcription products, even though HIV-1 infect
19 ucin gene was determined by real-time PCR on reverse transcription products from RNA isolated from hu
20 esistant to other cytosolic sensors of viral reverse transcription products in newly infected cells.
23 ar mass aggregates promote synthesis of long reverse transcription products in vitro by concentrating
25 Quantitative real-time PCR analysis of early reverse transcription products indicated that HIV-1 reve
26 64)K variant was impaired in generating late reverse transcription products, indicating that replicat
27 position, and mediate the integration of the reverse-transcription product into the genome of the hos
28 tion in multiple ways and that inhibition of reverse transcription products is not necessary for TRIM
30 tion, quantitative real-time PCR analysis of reverse transcription products revealed that the mutant
32 unodeficiency virus type 1 (HIV-1), allowing reverse transcription products to accumulate even though
33 HIV replication, including synthesis of late reverse transcription products, two-long terminal repeat
34 antitative methods that monitor formation of reverse transcription products, two-LTR circles and inte
35 photonic microring resonators to detect cDNA reverse transcription products via a subsequent enzymati
37 results indicate that faithful, full-length reverse transcription products were underrepresented in
38 24 production and quantitative PCR for HIV-1 reverse transcription products, whereas treatment of the
39 quantitative real-time PCR analysis of early reverse transcription products, with initiation at the H
40 mRNA synthesis.IMPORTANCE The fates of HIV-1 reverse transcription products within infected cells are
41 acellular viral DNA as well as intracellular reverse transcription products, without affecting HBV RN
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