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Groups of infected mice were sacrificed at day 4 post-infection to determine mouse lung virus loads.
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In addition, a human H5N1 virus isolate with the mutation HA222E was mainly confined to the mouse lung, although virus with the HA222K mutation could be isolated from the mouse brain.
Even in the unprotected mice the lung virus titers were rather low, indicating that some degree of protection was achieved also in these animals (Fig. 2 and Table 2, groups 5 6).
We also report a systematic collection of several corresponding phenotypic variables, including mouse body weights, lung virus titers, viral messenger RNA, and viral genomic RNA for each infected animal.
For virological and pathological examinations, 15 mice per group were intranasally infected with 10 EID50/50 µL of virus, and three mice per group were euthanized at 1, 3, 5, 7 and 9 dpi to examine the growth kinetics of the virus in mouse lung.
Drinking HS decoction also efficiently suppressed replication of the H5N1 virus in mouse lung tissues on days 5 and 7 post infection (log EID50 reduced from 4.42 ± 0.08 to 3.15 ± 0.48 on day 5 and from 5.34 ± 0.32 to 3.75 ± 0.63 on day 7), whereas the inhibitory effect of HS decoction on H5N1 virus replication was completely abolished by depleting MIR2911 with anti-MIR2911 antagomir.
Eigentranscript #2 profile was enriched for transcripts associated with Death Receptor Signaling, Role of Pattern Recognition Receptors in Recognition of Bacteria and Viruses, and Apoptosis Signaling, as well as the Protein Ubiquitination Pathway, which has previously been observed in mouse lung responses following pandemic 1918 influenza virus infection [ 25].
Clinical signs and weight loss after infection correlated well with virus titers in the lungs of infected mice 4 days p.i.No virus was detected in lungs of mice vaccinated with adjuvanted subunit vaccine, while the average lung virus titer of mock-vaccinated mice was 108.1 TCID50/gram lung.
Moreover, our conclusions are based on other factors, which we think are more important, such as survival rate and residual lung virus titer of mice, etc.
Both viruses were able to replicate in mouse lungs; however, the H9N2 virus grew to significant higher titers than the H7N9 virus.
Mouse adapted A/PR/8 virus was propagated in the mouse lung for at least 8 passages.
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