Retroviruses use CD169-mediated trans-infection of permissive lymphocytes to establish infection.

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Bibliographic Details
Title:	Retroviruses use CD169-mediated trans-infection of permissive lymphocytes to establish infection.
Authors:	Sewald, Xaver, Ladinsky, Mark S., Uchil, Pradeep D., Beloor, Jagadish, Ruoxi Pi, Herrmann, Christin, Motamedi, Nasim, Murooka, Thomas T., Brehm, Michael A., Greiner, Dale L., Shultz, Leonard D., Mempel, Thorsten R., Bjorkman, Pamela J., Kumar, Priti, Mothes, Walther
Source:	Science (pre-March 2025). 10/30/2015, Vol. 350 Issue 6260, p563-567. 5p.
Subjects:	Retroviruses, Infection, Mouse leukemia viruses, HIV, Macrophages, Lymphocytes, Virology, B cells, Charts, diagrams, etc.
Abstract:	Dendritic cells can capture and transfer retroviruses in vitro across synaptic cell-cell contacts to uninfected cells, a process called trans-infection. Whether trans-infection contributes to retroviral spread in vivo remains unknown. Here, we visualize how retroviruses disseminate in secondary lymphoid tissues of living mice. We demonstrate that murine leukemia virus (MLV) and human immunodeficiency virus (HIV) are first captured by sinus-lining macrophages. CD169/Siglec-1, an I-type lectin that recognizes gangliosides, captures the virus. MLV-laden macrophages then form long-lived synaptic contacts to trans-infect B-1 cells. Infected B-1 cells subsequently migrate into the lymph node to spread the infection through virological synapses. Robust infection in lymph nodes and spleen requires CD169, suggesting that a combination of fluid-based movement followed by CD169-dependent trans-infection can contribute to viral spread. [ABSTRACT FROM AUTHOR]
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Database:	Psychology and Behavioral Sciences Collection

Description
Abstract:	Dendritic cells can capture and transfer retroviruses in vitro across synaptic cell-cell contacts to uninfected cells, a process called trans-infection. Whether trans-infection contributes to retroviral spread in vivo remains unknown. Here, we visualize how retroviruses disseminate in secondary lymphoid tissues of living mice. We demonstrate that murine leukemia virus (MLV) and human immunodeficiency virus (HIV) are first captured by sinus-lining macrophages. CD169/Siglec-1, an I-type lectin that recognizes gangliosides, captures the virus. MLV-laden macrophages then form long-lived synaptic contacts to trans-infect B-1 cells. Infected B-1 cells subsequently migrate into the lymph node to spread the infection through virological synapses. Robust infection in lymph nodes and spleen requires CD169, suggesting that a combination of fluid-based movement followed by CD169-dependent trans-infection can contribute to viral spread. [ABSTRACT FROM AUTHOR]
ISSN:	00368075
DOI:	10.1126/science.aab2749