Journal
JOURNAL OF INFECTIOUS DISEASES
Volume 225, Issue 3, Pages 510-519Publisher
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jiab389
Keywords
newborn; HIV; macrophage; TLR7; TLR8
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Funding
- Laboratory of Dermatology and Immunodeficiencies [LIM56]
- Sao Paulo Research Foundation [2016/16840-6, 2016/01269-1]
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Cord blood macrophages are more susceptible to HIV-1 infection, but treatment with CL097 can enhance their antiviral response and inhibit viral replication. This finding may have potential significance in enhancing neonatal immune response.
Cord blood macrophages are more susceptible to HIV-1 infection. This vulnerability can be reversed under treatment with the type I interferon adjuvant CL097, which triggers inflammatory and antiviral responses in these cells, attenuating viral replication. Vertical transmission is the main mechanism of human immunodeficiency virus type 1 (HIV-1) infection in infants, who may develop high viremia and rapidly progress to AIDS. Innate immunity agonists can control HIV-1 replication in vitro, but the protective effect in the neonatal period remains unknown. Herein, we evaluated the immunomodulatory and antiviral effects of type I interferon (IFN-I) adjuvants on cord blood monocyte-derived macrophages upon HIV-1 infection. Despite the phenotypic and transcriptional similarities between cord blood and adult macrophages, cord blood cells were prone to viral replication when infected with HIV-1. However, treatment with CL097 efficiently promoted the antiviral and inflammatory responses and inhibited HIV-1 replication in cord blood cells in an NF-kappa B and autophagy activation-independent manner. Our data suggest that cord blood macrophages are able to establish antiviral responses induced by IFN-I adjuvants similar to those of their adult counterparts, revealing a potential adjuvant candidate to enhance the neonatal immune response.
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