{'fraction_non_alphanumeric': 0.045131485429992894, 'fraction_numerical': 0.026652452025586353, 'mean_word_length': 5.119565217391305, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
HIV-1-Infected Animals Cell Phenotype and Function in Long-Term Chimpanzee NK Cells and Conserved NK Differential NKp 30 Inducibility in

C himpanzees (Pan troglodytes), the closest living relatives of humans (1), are the reservoirs of SIVcpz, the lentivirus most closely related to HIV-1 groups M (pandemic in humans) and N (2). Unlike other primate species, chimpanzees are able to support a persistent infection of specific isolates of HIV-1. Contrary to HIV-1-infected humans, however, they are relatively resistant to the development of AIDS (3). Longitudinal follow-up of chimpanzees experimentally or naturally infected with CCR5-tropic HIV-1 strains or with SIVcpz maintain high plasma virus loads, (4) and normal CD4 T cell levels and have remained asymptomatic (3) with one notable exception (5). They maintain an intact lymphoid microenvironment (6) rich in dendritic cells (DCs) 5 driving effective, low-level, Ag-specific CD4 ϩ and CD8 ϩ T cell responses (7–10) without extensive lymphocyte activation (11–13). Contrary to chimpanzees, only a minority of humans (Ͻ2%) develop an unusually benign clinical course of HIV-1 infection, defined long-term nonprogressive (LTNP) disease (14 –16). LTNP patients respond to long-term HIV infection in a similar way as chimpanzees with respect to the breadth of a HIV-specific CD8 ϩ T cell repertoire and the persistence of virus-specific CD4 ϩ T cell specificity (17–21). These findings are in sharp contrast with the majority of HIV-1-infected humans, where virus replication is only temporarily controlled by a vigorous CD8 ϩ CTL increase during acute infection (22) followed by progressive loss of HIV-1-specific CD4 ϩ cell responses with T cell activation (23–25), impaired CTL function (17, 26 –28), and loss and dysfunction of DC populations (29). Although a variety of both host-and virus-related factors have been described in chimpanzees (2, 4 – 6, 10), none of them alone allows us to fully reconcile the benign course of the infection with a unique correlate that could help explain the breadth and continuous HIV-specific CD8ϩ CTL response. Following encounters with virus-infected or tumor-transformed cells, NK cells provide a first line of defense by Ag-independent recognition of specific triggering ligands that develop through cy-totoxicity and by the release of cytokines and chemokines that, in turn, can activate or recruit multiple cell types (30 –33). Molecules that are predominantly responsible for delivering activating signals leading to peripheral NK cell triggering are the natural cytotoxicity receptors (NCRs) and NKG2D, whereas other surface molecules, including NKp80, NTB-A, 2B4, and the DNAX accessory molecule (DNAM), display a costimulatory effect upon the recognition of their respective ligands on target cells (31, 33, …