%0 Journal Article %A Ikeda, Terumasa %A Molan, Amy M. %A Jarvis, Matthew C. %A Carpenter, Michael A. %A Salamango, Daniel J. %A Brown, William L. %A Harris, Reuben S. %T HIV-1 restriction by endogenous APOBEC3G in the myeloid cell line THP-1 %D 2019 %J Journal of General Virology, %V 100 %N 7 %P 1140-1152 %@ 1465-2099 %R https://doi.org/10.1099/jgv.0.001276 %K HIV-1 restriction %K Vif %K myeloid cell line THP-1 %K APOBEC3G %K G to A hypermutation %I Microbiology Society, %X HIV-1 replication in CD4-positive T lymphocytes requires counteraction of multiple different innate antiviral mechanisms. Macrophage cells are also thought to provide a reservoir for HIV-1 replication but less is known in this cell type about virus restriction and counteraction mechanisms. Many studies have combined to demonstrate roles for APOBEC3D, APOBEC3F, APOBEC3G and APOBEC3H in HIV-1 restriction and mutation in CD4-positive T lymphocytes, whereas the APOBEC enzymes involved in HIV-1 restriction in macrophages have yet to be delineated fully. We show that multiple APOBEC3 genes including APOBEC3G are expressed in myeloid cell lines such as THP-1. Vif-deficient HIV-1 produced from THP-1 is less infectious than Vif-proficient virus, and proviral DNA resulting from such Vif-deficient infections shows strong G to A mutation biases in the dinucleotide motif preferred by APOBEC3G. Moreover, Vif mutant viruses with selective sensitivity to APOBEC3G show Vif null-like infectivity levels and similarly strong APOBEC3G-biased mutation spectra. Importantly, APOBEC3G-null THP-1 cells yield Vif-deficient particles with significantly improved infectivities and proviral DNA with background levels of G to A hypermutation. These studies combine to indicate that APOBEC3G is the main HIV-1 restricting APOBEC3 family member in THP-1 cells. %U https://www.microbiologyresearch.org/content/journal/jgv/10.1099/jgv.0.001276