Mechanisms of Polymorphonuclear Neutrophil–Mediated Induction of HIV‐1 Replication in Macrophages during Pulmonary Tuberculosis | Zendy

Yoshihiko Hoshino | Zendy; Satomi Hoshino | Zendy; Jeffrey A. Gold | Zendy; Bindu Raju | Zendy; Savita Prabhakar | Zendy; Richard Pine | Zendy; William N. Rom | Zendy; Koh Nakata | Zendy; Michael D. Weiden | Zendy

Open Access

Mechanisms of Polymorphonuclear Neutrophil–Mediated Induction of HIV‐1 Replication in Macrophages during Pulmonary Tuberculosis

Author(s) -

Yoshihiko Hoshino,

Satomi Hoshino,

Jeffrey A. Gold,

Bindu Raju,

Savita Prabhakar,

Richard Pine,

William N. Rom,

Koh Nakata,

Michael D. Weiden

Publication year - 2007

Publication title -

the journal of infectious diseases

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.69

H-Index - 252

eISSN - 1537-6613

pISSN - 0022-1899

DOI - 10.1086/513438

Subject(s) - biology , immunology , virology , microbiology and biotechnology

Pulmonary tuberculosis (TB) can present with polymorphonuclear neutrophil (PMN)-predominant alveolitis. TB accelerates acquired immunodeficiency syndrome by increasing human immunodeficiency virus type 1 (HIV-1) replication and mutation in alveolar macrophages. A 16-kDa CCAAAT/enhancer-binding protein beta (C/EBP beta ) isoform is a strong transcriptional repressor of the HIV long terminal repeat (LTR) in resting alveolar macrophages, leading to latent viral infection; its expression is lost during TB, derepressing the HIV LTR.

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