T cell-tropic HIV efficiently infects alveolar macrophages through contact with infected CD4+ T cells. Schiff, A E, Linder, A H, Luhembo, S N, Banning, S, Deymier, M J, Diefenbach, T J, Dickey, A K, Tsibris, A M, Balazs, A., Cho, J, Medoff, B, Walzl, G, Wilkinson, R. J, Burgers, W. A, Corleis, B, & Kwon, D. Scientific Reports, 11(1):3890, Nature Publishing Group, feb, 2021.
T cell-tropic HIV efficiently infects alveolar macrophages through contact with infected CD4+ T cells [link]Paper  doi  abstract   bibtex   
Alveolar macrophages (AMs) are critical for defense against airborne pathogens and AM dysfunction is thought to contribute to the increased burden of pulmonary infections observed in individuals living with HIV-1 (HIV). While HIV nucleic acids have been detected in AMs early in infection, circulating HIV during acute and chronic infection is usually CCR5 T cell-tropic (T-tropic) and enters macrophages inefficiently in vitro. The mechanism by which T-tropic viruses infect AMs remains unknown. We collected AMs by bronchoscopy performed in HIV-infected, antiretroviral therapy (ART)-naive and uninfected subjects. We found that viral constructs made with primary HIV envelope sequences isolated from both AMs and plasma were T-tropic and inefficiently infected macrophages. However, these isolates productively infected macrophages when co-cultured with HIV-infected CD4+ T cells. In addition, we provide evidence that T-tropic HIV is transmitted from infected CD4+ T cells to the AM cytosol. We conclude that AM-derived HIV isolates are T-tropic and can enter macrophages through contact with an infected CD4+ T cell, which results in productive infection of AMs. CD4+ T cell-dependent entry of HIV into AMs helps explain the presence of HIV in AMs despite inefficient cell-free infection, and may contribute to AM dysfunction in people living with HIV. Individuals with untreated HIV-1 (HIV) are at increased risk of pulmonary infections with mycobacteria and other bacteria, viruses, and fungi 1-3. The first line of defense against these infections in the lung are alveolar macrophages (AMs), which comprise the vast majority of immune cells in the alveolar space 4,5. AMs from individuals with untreated HIV are dysfunctional, with impaired phagocytic activity 6-8 , proteolytic activity 9 , and bacterial killing 10. The lung is an early site of HIV and simian immunodeficiency virus (SIV) replication in humans, humanized mice and non-human primates (NHPs) 11-15 , and HIV nucleic acids are detectable in AMs in both antiretroviral (ART)-naive and treated individuals 9,16-22. Thus, HIV is found in the lung and in AMs early in the course of HIV-1 infection, but the mechanism of entry of HIV into AMs remains incompletely understood.
@article{Schiff2021,
abstract = {Alveolar macrophages (AMs) are critical for defense against airborne pathogens and AM dysfunction is thought to contribute to the increased burden of pulmonary infections observed in individuals living with HIV-1 (HIV). While HIV nucleic acids have been detected in AMs early in infection, circulating HIV during acute and chronic infection is usually CCR5 T cell-tropic (T-tropic) and enters macrophages inefficiently in vitro. The mechanism by which T-tropic viruses infect AMs remains unknown. We collected AMs by bronchoscopy performed in HIV-infected, antiretroviral therapy (ART)-naive and uninfected subjects. We found that viral constructs made with primary HIV envelope sequences isolated from both AMs and plasma were T-tropic and inefficiently infected macrophages. However, these isolates productively infected macrophages when co-cultured with HIV-infected CD4+ T cells. In addition, we provide evidence that T-tropic HIV is transmitted from infected CD4+ T cells to the AM cytosol. We conclude that AM-derived HIV isolates are T-tropic and can enter macrophages through contact with an infected CD4+ T cell, which results in productive infection of AMs. CD4+ T cell-dependent entry of HIV into AMs helps explain the presence of HIV in AMs despite inefficient cell-free infection, and may contribute to AM dysfunction in people living with HIV. Individuals with untreated HIV-1 (HIV) are at increased risk of pulmonary infections with mycobacteria and other bacteria, viruses, and fungi 1-3. The first line of defense against these infections in the lung are alveolar macrophages (AMs), which comprise the vast majority of immune cells in the alveolar space 4,5. AMs from individuals with untreated HIV are dysfunctional, with impaired phagocytic activity 6-8 , proteolytic activity 9 , and bacterial killing 10. The lung is an early site of HIV and simian immunodeficiency virus (SIV) replication in humans, humanized mice and non-human primates (NHPs) 11-15 , and HIV nucleic acids are detectable in AMs in both antiretroviral (ART)-naive and treated individuals 9,16-22. Thus, HIV is found in the lung and in AMs early in the course of HIV-1 infection, but the mechanism of entry of HIV into AMs remains incompletely understood.},
author = {Schiff, A E and Linder, A H and Luhembo, S N and Banning, S and Deymier, M J and Diefenbach, T J and Dickey, A K and Tsibris, A M and Balazs, AB and Cho, J and Medoff, B and Walzl, G and Wilkinson, Robert J and Burgers, Wendy A and Corleis, B and Kwon, DS},
doi = {10.1038/s41598-021-82066-x},
file = {:C$\backslash$:/Users/01462563/AppData/Local/Mendeley Ltd./Mendeley Desktop/Downloaded/Schiff et al. - 2021 - T cell-tropic HIV efficiently infects alveolar macrophages through contact with infected CD4 T cells.pdf:pdf},
issn = {2045-2322},
journal = {Scientific Reports},
keywords = {Journal Article,OA,fund{\_}ack,original},
mendeley-tags = {OA,fund{\_}ack,original},
month = {feb},
number = {1},
pages = {3890},
pmid = {33594125},
publisher = {Nature Publishing Group},
title = {{T cell-tropic HIV efficiently infects alveolar macrophages through contact with infected CD4+ T cells}},
url = {https://doi.org/10.1038/s41598-021-82066-x},
volume = {11},
year = {2021}
}
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