ライフサイエンスコーパス: viral inactivation

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1 dines, resulting in G to A hypermutation and viral inactivation.

2 packaged genome is the dominant mechanism of viral inactivation.

3 es (ROS) did not participate in the detected viral inactivation, a model of virus inactivation based

4 easons for the infectivity of Gammagard, and viral inactivation and removal steps are needed to ensur

5 ods and virus particles was not required for viral inactivation and that reactive oxygen species (ROS

6 -1 KOS was determined by yield reduction and viral inactivation assays.

7 Subsequently, Apo3G triggers viral inactivation by processively deaminating C-->U, wi

8 rt the hypothesis that in vivo intracellular viral inactivation by secretory IgA during transcytosis

9 The antiviral strategy of capsid-targeted viral inactivation (CTVI) was designed to disable newly

10 In one such approach, capsid-targeted viral inactivation (CTVI), nucleases fused to viral coat

11 greater viral reduction which indicate that viral inactivation data in laboratory grade water may no

12 f inactivation kinetic models was fit to the viral inactivation data.

13 ral mutations increased rates of spontaneous viral inactivation (especially D368P) suggests that HIV-

14 Buffer AVL and heat treatments showed total viral inactivation in 100% of samples tested.

15 eat (60 degrees C for 15 min) also showed no viral inactivation in 67% or 100% of samples, respective

16 The antiviral effect of capsid-targeted viral inactivation in our model system, using both proph

17 of blood products, vaccine development, and viral inactivation in vivo.

18 Here, we describe a nonlethal mechanism of viral inactivation in which the lytic granule component,

19 Capsid-targeted viral inactivation is a novel protein-based strategy for

20 s in the environment is highly variable, but viral inactivation is usually complete within months.

21 Intracellular viral inactivation mechanisms such as these could greatl

22 Intracellular viral inactivation mechanisms such as these could greatl

23 itis B and human immunodeficiency virus, and viral inactivation of clotting factor concentrates, were

24 n important cellular context for genetic and viral inactivation of TP53.

25 and factor IX concentrates prepared without viral inactivation procedures showed high frequencies of

26 onal testing for infectious disease markers, viral inactivation processes, and refinement of transfus

27 f aggregation under conditions mimicking the viral inactivation step during monoclonal antibody (mAb)

28 ith blood-borne stages that are resistant to viral-inactivation steps in the manufacturing process, s

29 Viral inactivation was abolished by the addition of a sy

30 ly rapid and kinetically dominant process of viral inactivation, which may partly involve endocytosis

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