ライフサイエンスコーパス: virus-producing cell

1 onic amino acid transporter-1 (mCAT1) in the virus-producing cell.

2 physically tethers virions to the surface of virus-producing cells.

3 ntity of HIV-1 DNA and replication-competent-virus-producing cells.

4 essing of Pr55(gag) was largely inhibited in virus-producing cells.

5 ns, confirming the Gag/TSG101 interaction in virus-producing cells.

6 precursor of the Gag (Pr55(Gag)) of HIV-1 in virus-producing cells.

7 of Vpr also accumulates in the cytoplasm of virus-producing cells.

8 s with rapid turnover of both free virus and virus-producing cells.

9 Vif directly interact with HIV-1 RNA in the virus-producing cells.

10 We show here that HLA class II in the virus-producing cell alters the ratio of three-part to t

11 esses by which Env becomes functional in the virus-producing cell and may assist attempts to interfer

12 It appears that Vif functions in the virus-producing cells and affects viral assembly.

13 l and the relationship between the number of virus-producing cells and plasma virus load has not been

14 infection suggests that the balance between virus-producing cells and the immune response to clear i

15 inhibitory effect of CypA was restricted to virus-producing cells and was TRIM5alpha independent.

16 d with condensed chromatin in the nucleus of virus-producing cells, and cytoplasmic vesicles containi

17 secretion through the exocytic organelles of virus-producing cells, and second after virus binding to

18 cluded from lymphoid B cell follicles, where virus-producing cells are most highly concentrated, sugg

19 eir effects only if target cells, and not if virus-producing cells, are treated with CsA.

20 pecies-specific interactions between Vif and virus-producing cells, as opposed to between Vif and vir

21 hibit the anti-HIV-1 activity of APOBEC3G in virus-producing cells but not in target cells and APE mo

22 gi or UNG2-specific short-interfering RNA in virus-producing cells but not target cells, the virion-a

23 echanisms and induce interferon responses in virus producing cells, but changes in latently infected

24 cent virions, Vif also removes APOBEC3G from virus-producing cells by inducing its ubiquitination and

25 and 15 kDa could be immunoprecipitated from virus-producing cells by the same antibody.

26 iting virion production; delta, loss rate of virus-producing cells; c, clearance rate of free virions

27 We found that antibodies co-expressed in the virus-producing cell can disrupt Env transit to the prop

28 vel of cell-to-cell transmission because the virus-producing cells cannot be easily distinguished fro

29 ermore, we directly demonstrate that >96% of virus producing cells did not express the Ki-67 prolifer

30 idea that Vif functions predominantly in the virus-producing cells during virus assembly.

31 e presence of CypA in the target and not the virus-producing cell enhances HIV-1 infectivity.

32 ctive APO3G mutants transiently expressed in virus-producing cells exhibited significant antiviral ac

33 acrophages were a significant portion of the virus-producing cells found in LNs, intestinal tissues,

34 riction of Env function may serve to protect virus-producing cells from the membrane-disruptive effec

35 Virus producing cells had differentially expressed TSSs

36 Expression of CD4 on the virus-producing cell impairs the release and infectivity

37 their recent infection through contact with virus producing cells in a tissue reservoir.

38 ified macrophages as the principal subset of virus-producing cells in BM over time.

39 The average number of virus-producing cells in peripheral blood is small durin

40 nterleukin 2 (IL-2) or IL-15, could decrease virus-producing cells in the lymphatic tissues.

41 lysis indicated that greater than 95% of the virus-producing cells in these tissues are macrophage an

42 Whether GC TFH are the major HIV-1 virus-producing cells in vivo has not been established.

43 ein are detectable in SIV virions but not in virus-producing cells, indicating that phosphorylation o

44 ed at enhancing immune-mediated clearance of virus-producing cells is of high priority.

45 lthough most HIV originates from short-lived virus-producing cells, it is unlikely that chronic infec

46 t, it was possible to readily isolate stable virus-producing cell lines with titers approaching 10(7)

47 Furthermore, treatment of virus-producing cells or virus particles with raft-disru

48 all groups of rats were injected either with virus-producing cells or with proviral DNA.

49 I molecules and costimulators, EC-stimulated virus-producing cells (p24(high) T cells) do not prolife

50 ree distinct times and locations: (i) in the virus-producing cell prior to viral release, yielding a

51 that expression of either PSGL-1 or CD43 in virus-producing cells reduces the infectivity of progeny

52 Furthermore, overexpression of UBP in virus-producing cells resulted in a significant reductio

53 that expression of A3G, A3F, or murine A3 in virus-producing cells resulted in their virion incorpora

54 nt dispersion of genomes was observed around virus-producing cells, suggesting infection of neighbori

55 the Gag, Pol, and Env proteins of virions or virus-producing cells that correlates with virus infecti

56 e therapy to induce a pseudo-latent state in virus-producing cells, thus transforming HIV-1 into a li

57 , Vif binds to HIV-1 RNA in the cytoplasm of virus-producing cells to form a 40S mRNP complex.

58 Thus, the virus-producing cell type is an important factor in dict

59 aMA) HIV-1 precursor Gag (PrGag) proteins in virus-producing cells using a biotin ligase-tagging appr

60 By electron microscopy on thin sections of virus-producing cells, we observed that some NC mutants

61 The majority of mRNA species present in the virus-producing cells were also detected in Psi- particl

62 Virus-producing cells were subjected to several rounds o

63 uman cells, as well as replication-competent-virus-producing cells, were measured to quantified viral

64 rs decreased HIV-1 Gag protein expression in virus-producing cells, while silencing the m(6)A erasers

65 her studies regarding Vif-RNA interaction in virus-producing cells will be important for studying the

66 Finally, treatment of virus-producing cells with Chk inhibitor protects them f

67 apture NS2-containing protein complexes from virus-producing cells with streptavidin magnetic beads.