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Figure 1.

Viral patterns that activate the immune system.

A virion can be envisioned as a concentration of different patterns recognized by the immune system: virtually all of its components can be used to start a response before the T cell compartment is active.

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Figure 2.

Some effects of viral interaction with DCs.

Certain viruses, like RSV, infect DCs, replicate in them, and cause them to mature, while others, like several herpesviruses, dengue virus, and influenza virus, replicate and hinder maturation. Viruses like HPV do not replicate in DCs and are only presented as antigens, while others, like HIV, are concentrated and delivered to their target organs by DCs, which thereby increase the chances of virions to infect cells.

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Figure 3.

The infectious synapse model.

At the site of mucosal entry, DCs concentrate HIV-1 via DC-SIGN. Virions are stored either in “virosomes”, where their infectivity is even preserved, or (and?) on the DC surface and, once in the lymph node, DCs deliver them actively to target CD4+ T cells. Several molecules are involved in this event that closely resembles the transmission of acetylcholine along the nerve (synapse), in that virions are actively transported in vesicles along actin fibers and released outside the cells where they immediately find their receptors, which have been concentrated on the T cell side. This mechanism may be active also for other viruses, like HCV and SARS coronavirus.

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