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SARS-CoV-2 viral persistence in lung alveolar macrophages is controlled by IFN-g and NK cells

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Macaca fascicularis

PROVIDER: GSE243734 | GEO | 2023/09/25

REPOSITORIES: GEO

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SARS-CoV-2 viral persistence in lung alveolar macrophages is controlled by IFN-γ and NK cells.

Project description:Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) RNA generally becomes undetectable in upper airways after a few days or weeks postinfection. Here we used a model of viral infection in macaques to address whether SARS-CoV-2 persists in the body and which mechanisms regulate its persistence. Replication-competent virus was detected in bronchioalveolar lavage (BAL) macrophages beyond 6 months postinfection. Viral propagation in BAL macrophages occurred from cell to cell and was inhibited by interferon-γ (IFN-γ). IFN-γ production was strongest in BAL NKG2r+CD8+ T cells and NKG2Alo natural killer (NK) cells and was further increased in NKG2Alo NK cells after spike protein stimulation. However, IFN-γ production was impaired in NK cells from macaques with persisting virus. Moreover, IFN-γ also enhanced the expression of major histocompatibility complex (MHC)-E on BAL macrophages, possibly inhibiting NK cell-mediated killing. Macaques with less persisting virus mounted adaptive NK cells that escaped the MHC-E-dependent inhibition. Our findings reveal an interplay between NK cells and macrophages that regulated SARS-CoV-2 persistence in macrophages and was mediated by IFN-γ.

| S-EPMC10681903 | biostudies-literature

SARS-CoV-2 viral persistence in lung alveolar macrophages is controlled by IFN-g and NK cells [BALF_Macro_SARS_NHP]

Project description:SARS-CoV-2 RNA generally becomes undetectable in upper airways after a few days or weeks post-infection. It is unclear however if the virus persists in other parts of the body and which mechanism(s) regulate SARS-CoV-2 persistence. We addressed this question in the macaque model. Replication-competent virus was detected in bronchioalveolar lavages (BAL) macrophages beyond 6 months post-infection. SARS-CoV-2 propagated in BAL macrophages from cell-to-cell. IFN-γ inhibited this replication. IFN-γ production within BAL lymphocytes was strongest in NKG2r+CD8+ T and NKG2Alo NK cells and was further increased in NKG2Alo NK cells after Spike protein stimulation. However, IFN-γ production was impaired in NK cells from animals with persisting virus. IFN-γ also enhanced MHC-E expression on BAL macrophages, possibly inhibiting natural killer cell mediated killing. Animals with less persisting virus mounted adaptive NK cells escaping this MHC-E dependent inhibition. Our findings reveal an interplay between NK cells and macrophages mediated by IFN-γ, regulating SARS-CoV-2 persistence in macrophages. Gene expression in bronchoalveolar lavage fluid (BALF) CD64+ Macrophages isolated from 6 healthy donors, 5 randomly chosen wuhan- and 10 omicron infected cynomolgus macaques at least 221 days post-infection, cultured for 8h and profiled with the NanoString nCounter System.

2023-09-25 | GSE243731 | GEO

SARS-CoV-2 viral persistence in lung alveolar macrophages is controlled by IFN-g and NK cells [BALF_BloodNK_SARSWu_NHP]

2023-09-25 | GSE243733 | GEO

SARS-CoV-2 viral persistence in lung alveolar macrophages is controlled by IFN-g and NK cells [BALF_NK_SARSWu_NHP]

2023-09-25 | GSE243732 | GEO

SARS-CoV-2 viral persistence in lung alveolar macrophages is controlled by IFN-g and NK cells

Project description:SARS-CoV-2 viral persistence in lung alveolar macrophages is controlled by IFN-g and NK cells

| PRJNA1019722 | ENA

SARS-CoV-2 viral persistence in lung alveolar macrophages is controlled by IFN-g and NK cells [BALF_NK_SARSWu_NHP]

Project description:SARS-CoV-2 viral persistence in lung alveolar macrophages is controlled by IFN-g and NK cells [BALF_NK_SARSWu_NHP]

| PRJNA1019727 | ENA

SARS-CoV-2 viral persistence in lung alveolar macrophages is controlled by IFN-g and NK cells [BALF_Macro_SARS_NHP]

Project description:SARS-CoV-2 viral persistence in lung alveolar macrophages is controlled by IFN-g and NK cells [BALF_Macro_SARS_NHP]

| PRJNA1019726 | ENA

SARS-CoV-2 viral persistence in lung alveolar macrophages is controlled by IFN-g and NK cells [BALF_BloodNK_SARSWu_NHP]

Project description:SARS-CoV-2 viral persistence in lung alveolar macrophages is controlled by IFN-g and NK cells [BALF_BloodNK_SARSWu_NHP]

| PRJNA1019728 | ENA

SARS-CoV-2 Evades Immune Detection in Alveolar Macrophages

Project description:Respiratory infections, like the current COVID-19 pandemic, target epithelial cells in the respiratory tract. Alveolar macrophages (AMs) are tissue-resident macrophages located within the lung. They play a key role in the early phases of an immune response to respiratory viruses. AMs are likely the first immune cells to encounter SARS-CoV-2 during an infection and their reaction to the virus will have a profound impact on the outcome of the infection. Interferons (IFNs) are antiviral cytokines and among the first cytokines produced upon viral infection. In this study, AMs from non-infectious donors are challenged with SARS-CoV-2. We demonstrate that challenged AMs are incapable of sensing SARS-CoV-2 and of producing an IFN response in contrast to other respiratory viruses, like influenza A virus and Sendai virus, which trigger a robust IFN response. The absence of IFN production in AMs upon challenge with SARS-CoV2 could explain the initial asymptotic phase observed during COVID-19 and argues against AMs being the sources of proinflammatory cytokines later during infection.

| S-SCDT-EMBOR-2020-51252V1 | biostudies-other

SARS-CoV-2 infection in human adult lung alveolar stem cells

Project description: Not available

| EMPIAR-10533 | biostudies-other