IL-4 downregulates gap junction protein connexin 26 to promote HIV-1 infection in macrophages.

ABSTRACT: Macrophages and dendritic cells (DCs) are important targets for HIV-1 replication in vivo. Myeloid cells are collectively more resistant to HIV-1 infection than CD4⁺ T lymphocytes, but interleukin (IL)-4 has been observed to promote macrophage susceptibility to HIV-1 infection. However, the mechanism remains unclear. Herein, we found that IL-4 enhanced HIV-1 infection in myeloid lineage macrophages by downregulating the novel antiviral factor gap junction protein beta 2 (GJB2) located on the cell membrane. In the absence of GJB2, the IL-4-mediated enhancement of HIV-1 replication was largely impaired in primary macrophages. Conversely, IL-6-mediated enhancement of HIV-1 infection was unaffected by GJB2 depletion. GJB2 was constitutively expressed in myeloid cells but not

SUBMITTER: Wang S 

PROVIDER: S-EPMC12607889 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature