ライフサイエンスコーパス: simian AIDS

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1 + produces high-level persistent viremia and simian AIDS in both juvenile and newborn rhesus macaques

2 mac239-Nef(+) induced persistent viremia and simian AIDS in rhesus macaques, SIVmac-M4 induced transi

3 tically distinct type D retroviruses such as simian AIDS retrovirus and squirrel monkey retrovirus we

4 een monkeys, one natural host species, avoid simian AIDS by creating a population of T cells that lac

5 Because these animals do not develop simian AIDS despite maintaining high viral loads, there

6 As they do not develop simian AIDS, there is great interest in understanding ho

7 re a natural host of SIV that do not develop simian AIDS.

8 on became persistently viremic and developed simian AIDS.

9 Two animals in the control group developed simian AIDS within 7 to 8 weeks postinfection and were e

10 n retrovirus (SRV) infection can cause fatal simian AIDS in Macaca fascicularis, but many individuals

11 prototypical betaretrovirus responsible for simian AIDS (SAIDS) in rhesus macaques.

12 mphocyte depletion and immune dysfunction in simian AIDS.

13 mangabeys (SM) generally does not result in simian AIDS despite high viral loads and therefore affor

14 f opportunistic infections characteristic of simian AIDS.

15 by 3 logs and accelerated the development of simian AIDS in two of six animals with one developing ea

16 od mononuclear cells, and the development of simian AIDS-defining opportunistic infections.

17 ulated with SIV and monitored until onset of simian AIDS.

18 ks after infection, just before the onset of simian AIDS.

19 In this study, we observed (i) no signs of simian AIDS, (ii) stable SIV loads, (iii) a slow but pro

20 viral replication without clinical signs of simian AIDS.

21 prophylactic immunity sufficient to prevent simian AIDS.

22 SIV(+) monkeys that progress the fastest to simian AIDS.

23 ring chronic asymptomatic infection prior to simian AIDS, SIV-producing cells were more concentrated

24 l swarm and allowed to naturally progress to simian AIDS and potential SIV-associated encephalitis (S

25 s in sooty mangabeys that do not progress to simian AIDS and that maintain stable T-cell numbers desp

26 In 5 macaques that progressed to simian AIDS and death, elevated IL-7 levels were unable

27 developed high virus loads and progressed to simian AIDS.

28 tial for high virus loads and progression to simian AIDS (SAIDS) in SIV-infected adult rhesus macaque

29 ult in immune dysfunction and progression to simian AIDS and that a population of CD3(+)CD4(-)CD8(-)

30 his finding showed that rapid progression to simian AIDS may be accompanied by the selection of CD4-i

31 immune response able to delay progression to simian AIDS.

32 st in the macaque that progressed rapidly to simian AIDS (99 days) and lowest in the macaque that pro

33 o rhesus macaques that progressed rapidly to simian AIDS.

34 SIVmac239-infected macaque that succumbed to simian AIDS at 65 weeks postinfection.

35 thirds of rhesus macaques that succumbed to simian AIDS had myocardial pathology including lymphocyt

36 mentalization was diminished in animals with simian AIDS, which often have low-frequency CTL response

37 accumulation in PC was seen in animals with simian AIDS.

38 n nonhuman primates following challenge with simian AIDS viruses.

39 d in clinical manifestations consistent with simian AIDS.

40 y associated with lymphomas in macaques with simian AIDS.

41 ulation with RhCMV died within 11 weeks with simian AIDS (SAIDS), including activated RhCMV infection

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