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

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Science  30 Oct 2015:
Vol. 350, Issue 6260, pp. 563-567
DOI: 10.1126/science.aab2749

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A close up view of retrovirus spreading

Viral infections typically begin with a small number of viral particles gaining access to the host at a specific tissue site. But how do viruses that cause systemic infections, such as HIV, spread more widely? Sewald et al. visualized how the retroviruses murine leukemia virus (MLV) and HIV spread within lymph nodes in mice (see the Perspective by Hope). Specific macrophages that line the lymph-draining sinuses in lymph nodes first captured the virus using the carbohydrate-binding protein CD169. These macrophages subsequently transferred virus to the B1 subclass of B lymphocytes, which migrated further into the lymph node, disseminating the virus more widely.

Science, this issue p. 563; see also p. 511


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.

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