ntiviral Response Induced by Toll-Like Receptor (TLR) 7/TLR8 Activation Inhibits Human Immunodeficiency Virus Type 1 Infection in Cord Blood Macrophage

Autor(es)

Pietrobon, Anna J. ^{[1, 2]} ; Yoshikawa, Fabio S. Y. ^{[2, 3]} ; Oliveira, Luana M. ^[2] ; Pereira, Natalli Z. ^[2] ; Matozo, Tais ^[1] ; de Alencar, Bruna C. ^[1] ; Duarte, Alberto J. S. ^[2] ; Sato, Maria N. ^[2]

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Inst Biomed Sci, Dept Immunol, Sao Paulo - Brazil

^[2] Univ Sao Paulo, Med Sch, Trop Med Inst Sao Paulo, LIM 56, Dept Dermatol, Lab Dermatol & Immunodeficiencies, Av Dr Eneas de Carvalho Aguiar 470, 3rd Floor, BR-05403000 Sao Paulo - Brazil

^[3] Chiba Univ, Med Mycol Res Ctr, Div Mol Immunol, Chiba - Japan

• Tipo de documento: Artigo Científico
• Fonte: Journal of Infectious Diseases; v. 225, n. 3, p. 510-519, FEB 1 2022.
• Citações Web of Science: 0

Resumo

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. (AU)

• Processo FAPESP: 16/01269-1 - Imunomodulação de sensores citosólicos de DNA por adjuvantes de interferon tipo I em macrófagos de recém-natos infectados in vitro por HSV-1 e HIV-1
• Beneficiário: Anna Julia Pietrobon
• Modalidade de apoio: Bolsas no Brasil - Mestrado
• Processo FAPESP: 16/16840-6 - Análise de fatores antivirais e exossomas em trofoblastos e monócitos de recém-natos na infecção in vitro por Zika vírus
• Beneficiário: Maria Notomi Sato
• Modalidade de apoio: Auxílio à Pesquisa - Regular