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Open image in new window Figure 5 Structural mobility of EBOV NP core within virus proliferation.
Therefore, the formation and correct function of RNP is essential for −ssRNA virus proliferation (Sun et al., 2012; Zhou et al., 2013; Ruigrok et al., 2011).
These inhibitors reduced the virus proliferation and this success made the HIV aspartic protease the prime target for AIDS therapies [2].
Although the cell lines for virus proliferation are highly dependent on the type of virus, Vero cell has also been widely used in the detection of chemical's toxicity.
This highly structured element induces valylation of the viral RNA by host cell enzymes and is important for virus proliferation.
As a typical negative-sense single-stranded RNA (−ssRNA) viruses, EBOV possess a nucleocapsid protein (NP) to facilitate genomic RNA encapsidation to form viral ribonucleoprotein complex (RNP) together with genome RNA and polymerase, which plays the most essential role in virus proliferation cycle.
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They are often the result of Epstein-Barr virus (EBV induced proliferation of B-lymphocytes in the setting of immunosuppression.
As Fig. 2A demonstrates, following SubQ virus administration, proliferation of the adoptively transferred OT-1 T cells was restricted primarily to the inguinal lymph nodes draining at the site of SubQ virus administration.
As in figure 4A, once exposed to the SS1 virus, the proliferation rate of cells with elevated Ras/ELK signaling is more prominently reduced as compared with cancer cells with lower Ras/ELK signaling (p<0.05).
In addition, virus driven proliferation of germinal centre (GC) B cells facilitates the amplification of viral episomes and the subsequent generation of a large pool of latent genomes in long lived memory B cells [3].
The first such studies reported that exposure of adult human peripheral blood mononuclear cells (PBMC) to HRSV, IAV, and Sendai virus suppressed proliferation in response to the non-specific mitogen phytohemagglutinin (PHA), an effect that was attributed to the expression of CD54/CD11a/CD18 (ICAM-1/LFA-1) and the interaction between APC and T cells [43], [44].
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