Table 1.

Examples of interactions between HIV-1 and host pattern-recognition receptors that are subverted during acute infection

Host pattern-recognition receptor	Expressed by	Cellular location	HIV-1 component(s) recognised	“Intended” outcome(s) of the interaction	Is this subverted by HIV-1?
Langerin	Langerhans cells (LC)	Plasma membrane	Envelope glycoprotein	Virion capture, degradation in Birbeck granules and antigen presentation	Yes if LC are activated: virions are then not degraded, but are transferred to CD4+ T cells.
DC-SIGN	Conventional (c)DCs in tissues	Plasma membrane	Envelope glycoprotein	Virion capture for antigen processing and presentation	Yes. HIV-1 is captured and transferred to CD4+ T cells. Signalling via DC-SIGN also impairs DC functions and (with TLR8 signalling) promotes HIV-1 replication in cDCs.
DCIR	Conventional (c)DCs	Plasma membrane	Envelope glycoprotein	Virion capture for antigen processing and presentation	Yes. HIV-1 is captured and transferred to CD4+ T cells. Signalling via DCIR may also impair DC functions.
TLR7	Plasmacytoid (p)DCs and monocytes	Endocytic vesicles	Viral RNA	Triggering of type 1 IFN and pro-inflammatory cytokine/chemokine production	Yes. HIV-1 is able to repeatedly stimulate pDCs to produce high levels of cytokines/chemokines via this pathway. This promotes HIV-1 replication and spread.
TLR8	Conventional (c)DCs and monocytes	Endocytic vesicles	Viral RNA	Triggering of pro-inflammatory cytokine/chemokine production	Yes. Interaction of HIV-1 with both DC-SIGN and TLR8 promotes virus replication in cDCs.
RIG-I	Most cells	Cytoplasm	Viral RNA	IRF3 activation and triggering of type 1 IFN production	Yes. The HIV-1 protease sequesters RIG-I so that type 1 IFN is not triggered via this pathway.
Unknown DNA sensor	Most cells	Cytoplasm	Viral DNA	IRF3 activation and triggering of type 1 IFN production	Yes. TREX1 digests excess cytoplasmic HIV-1 DNA so that this pathway is not activated. Vpr and Vif also target IRF3 for degradation.
Unknown mechanism dependent on cyclophilin A	Conventional (c)DCs	Cytoplasm	Viral capsid	IRF3 activation and triggering of type 1 IFN production	Not efficiently, perhaps because HIV-1 does not normally replicate efficiently in cDCs. Vpr blocks IRF3 without inducing its degradation.