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EBV-infected B cells become activated and growth transformed, express a characteristic set of viral latent genes, and acquire the status of proliferating lymphoblastoid cell lines in vitro.
These observations suggest that EBNA1 is a member of a family of viral origin binding proteins that have no apparent orthologue in the human genome, and therefore may represent attractive targets for inhibitors of viral latent replication and persistence.
From the IgM+ and IgM− cell populations cellular DNA and RNA were isolated, cDNAs were prepared and expression of the three viral latent genes EBNA2, LMP1 and LMP2A was analyzed by real-time PCR.
Viral latent gene products rewire B cells to evade the host immune system and propagate the virus [ 15].
One striking feature of EBV-positive BL is the unique pattern of viral latent protein expression, which is restricted to EBNA1.
Studies on HIV-1 latency focused on regulation and reactivation of viral gene expression in the cells in which viral latent infection is already established.
Similar(38)
Cell lines derived from EBV-positive BL tumors, unlike EBV-immortalized B lymphoblastoid cell lines (LCLs), are not dependent on EBV for continued cell growth and proliferation, and maintain a restricted program of viral latent-infection gene expression known as Latency I, in which the only known viral protein expressed is the genome-maintenance protein, EBNA-1.
Little is known about viral, especially latent, infections in anti-TNF-α treatments.
For EBNA 1 expression, both the viral Qp (latent) and Cp/Wp (lytic) promoters were analysed.
There are three types of persistent viral infection: latent, chronic and slow infection [ 2].
The increase in Twist expression is induced by one of the viral oncoprotein, latent membrane protein 1 (LMP1), in the cancer cells.
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