CD8+ cells from asymptomatic human immunodeficiency virus-infected individuals suppress superinfection of their peripheral blood mononuclear cells

Barker, Edward; Bossart, Katharine N.; Locher, Christopher P.; Patterson, Bruce K.; Levy, Jay A.

doi:10.1099/0022-1317-77-12-2953

Cited by 35 publications

(21 citation statements)

References 44 publications

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“…The cutoff of 5-fold (0.5 log) was chosen because it is greater than what would be expected from the intrarun variability of viral load assays. Although many approaches and several studies have demonstrated the ability to stimulate viral replication from PBMCs in in vitro cultures (17,18), this is the first report of a rapid, clinical approach to stimulate viral replication in a clinical sample. The percentage of patients with pVL of Ͻ20 cp/ml was expected to be low but not zero based on previous publications quantifying cell-associated unspliced and spliced HIV-1 RNA in patients receiving suppressive antiretroviral therapy (19).…”

Section: Discussionmentioning

confidence: 99%

Identification and Characterization of HIV-1 Latent Viral Reservoirs In Peripheral Blood

Chargin¹,

Yin²,

Song³

et al. 2015

J Clin Microbiol

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Plasma viral load and CD4 counts are effective for clinical monitoring, but they do not give a full representation of HIV-1 quasispecies in cellular reservoirs, the major repository of replication-competent HIV-1 in infected individuals. We sought to develop a diagnostic system that might stimulate the replication-competent HIV-1 reservoirs for enhanced clinical monitoring, including selection of antiretroviral regimens. Whole-blood samples from 45 HIV-infected individuals were collected into 1 ViraStim HIV-1 activation tube and 1 EDTA tube. Samples were tested for viral load and cell type-specific HIV-1 replication. Further, 7 matched activated/nonactivated samples were sequenced using the Trugene HIV-1 genotyping kit. The percentage of patients with replication-competent virus in peripheral blood mononuclear cells (PBMCs) varied, depending on the baseline plasma viral load in the EDTA tubes. Six out of 24 patients with a starting plasma viral load of <20 copies/ml (cp/ml), 6 out of 8 patients with starting viral loads of >20 and <1,000 cp/ml, and 8 out of 13 patients with starting viral loads of >1,000 all showed increases in viral replication of >5-fold. These increases came from cellular reservoirs in blood as determined by simultaneous ultrasensitive subpopulation staining/hybridization in situ (SUSHI). When resistance genotypes in plasma from activation tubes were compared to those from EDTA tubes for 7 patients, all patients showed additional mutations in the activation tube, while 3 patients demonstrated additional genotypic resistance determinants. We show that HIV-1 viral replication can be stimulated directly from infected whole blood. The sequencing results showed that 3 of 7 cases demonstrated additional drug resistance following stimulation.

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Section: Discussionmentioning

confidence: 99%

Identification and Characterization of HIV-1 Latent Viral Reservoirs In Peripheral Blood

Chargin¹,

Yin²,

Song³

et al. 2015

J Clin Microbiol

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“…In addition, controls lacking template were included with each plate. Primers and probe sequences used have been previously described (5,34). ) donor inhibited HIV-1 replication in PHA blasts infected with either the BZ167 isolate (which preferentially uses CXCR4 and CCR3 coreceptors [25]) (Fig.…”

Section: Influenza Virus Stimulation Of Pbmcmentioning

confidence: 99%

Inhibition of Human Immunodeficiency Virus Type 1 Replication prior to Reverse Transcription by Influenza Virus Stimulation

Pinto

Blazevic

Patterson

et al. 2000

J Virol

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It is now recognized that, in addition to drug-mediated therapies against human immunodeficiency virus type 1 (HIV-1), the immune system can exert antiviral effects via CD8 ؉ T-cell-generated anti-HIV factors. This study demonstrates that (i) supernatants from peripheral blood mononuclear cells (PBMC) stimulated with influenza A virus inhibit replication of CCR5-and CXCR4-tropic HIV-1 isolates prior to reverse transcription; (ii) the HIV-suppressive supernatants can be generated by CD4-or CD8-depleted PBMC; (iii) this anti-HIV activity is partially due to alpha interferon (IFN-␣), but not to IFN-␥, IFN-␤, the ␤-chemokines MIP-1␣, MIP-1␤, and RANTES, or interleukin-16; (iv) the anti-HIV activity is generated equally well by PBMC cultured with either infectious or UV-inactivated influenza A virus; and (v) the antiviral activity can be generated by influenza A-stimulated PBMC from HIV-infected individuals. These findings represent a novel mechanism for inhibition of HIV-1 replication that differs from the previously described CD8 anti-HIV factors (MIP-1␣, MIP-1␤, RANTES, and CD8 antiviral factor).

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“…The CD8 ϩ antiviral noncytolytic activity has been evidenced with effector cells from HIV-seropositive patients and seems to correlate with the clinical status of infected individuals (4,6,24,40). However, the ability of CD8 ϩ cells from HIV-seronegative donors to inhibit HIV replication has been described but is controversial (26,32,49).…”

mentioning

confidence: 99%

CD8⁺-Cell Antiviral Factor Activity Is Not Restricted to Human Immunodeficiency Virus (HIV)-Specific T Cells and Can Block HIV Replication after Initiation of Reverse Transcription

Borgne

Février

Callebaut

et al. 2000

J Virol

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CD8؉ lymphocytes from human immunodeficiency virus (HIV)-infected patients can suppress in vitro HIV replication in CD4؉ T cells by a noncytolytic mechanism involving secreted CD8 ؉ -cell antiviral factor(s) (CAF). Using an HIV Nef-specific cytotoxic-T-lymphocyte (CTL) line and autologous CD4؉ T cells infected with a nef-deleted HIV-1 virus, we demonstrated that, after a priming antigenic stimulation, this suppression does not require the presence of the specific antigen during the effector phase. Furthermore, using an Epstein-Barr virus (EBV)-specific CTL line from an HIV-seronegative donor, we demonstrated that the ability to inhibit HIV replication in a noncytolytic manner is not restricted to HIV-specific effector cells; indeed, EBV-specific CTL were as efficient as HIV-specific effectors in suppressing R5 or X4 HIV-1 strain replication in vitro. This HIV-suppressive activity mediated by a soluble factor(s) present in the culture supernatant was detectable for up to 14 days following stimulation of EBV-specific CD8؉ cells with the cognate epitope peptide. Following acute infection of CEM cells with an X4 strain of HIV-1, EBV-specific CTL line supernatant containing HIV-suppressive activity did not block virus entry but was shown to interfere with virus replication after the first template switching of reverse transcription. Our results suggest that the noncytolytic control of HIV replication by EBV-specific CD8 ؉ T lymphocytes corresponded to a CAF-like activity and thus demonstrate that CAF production may not be restricted to CTL induced during HIV disease. Moreover, CAF acts after reverse transcription at least for X4 isolate replication inhibition.

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CD8+ cells from asymptomatic human immunodeficiency virus-infected individuals suppress superinfection of their peripheral blood mononuclear cells

Cited by 35 publications

References 44 publications

Identification and Characterization of HIV-1 Latent Viral Reservoirs In Peripheral Blood

Identification and Characterization of HIV-1 Latent Viral Reservoirs In Peripheral Blood

Inhibition of Human Immunodeficiency Virus Type 1 Replication prior to Reverse Transcription by Influenza Virus Stimulation

CD8⁺-Cell Antiviral Factor Activity Is Not Restricted to Human Immunodeficiency Virus (HIV)-Specific T Cells and Can Block HIV Replication after Initiation of Reverse Transcription

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CD8+ cells from asymptomatic human immunodeficiency virus-infected individuals suppress superinfection of their peripheral blood mononuclear cells

Cited by 35 publications

References 44 publications

Identification and Characterization of HIV-1 Latent Viral Reservoirs In Peripheral Blood

Identification and Characterization of HIV-1 Latent Viral Reservoirs In Peripheral Blood

Inhibition of Human Immunodeficiency Virus Type 1 Replication prior to Reverse Transcription by Influenza Virus Stimulation

CD8+-Cell Antiviral Factor Activity Is Not Restricted to Human Immunodeficiency Virus (HIV)-Specific T Cells and Can Block HIV Replication after Initiation of Reverse Transcription

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CD8⁺-Cell Antiviral Factor Activity Is Not Restricted to Human Immunodeficiency Virus (HIV)-Specific T Cells and Can Block HIV Replication after Initiation of Reverse Transcription