Table 4.

Cellular and viral factors that influence MTs dynamics during HIV-1 viral egress and maturation.

Cell Factor	Function of the Cellular Factor	Impact on HIV-1 Infection 1
HDAC6	Colocalized with and deacetylates MTs to promote autophagy degradation of Vif and Pr55Gag viral proteins, thus stabilizing the restriction factor A3G, forming an A3G/HDAC6 antiviral complex, an inhibiting HIV-1 viral production and infectiveness.	−
TDP-43	Regulates HDAC6 mRNA and protein levels promoting its antiviral function by tubulin-deacetylation and dependent anti-HIV-1 autophagy. Controls HIV-1 production and the infection capacity of viral particles.	−
SOCS1	Associates with MTs and allows Pr55Gag efficient transport to plasma membrane.	+
IQGAP1	A MTs-associated signaling scaffold protein that impedes viral egress by interacting with HIV-1 Pr55Gag, affecting its distribution and expression at plasma membrane-budding areas.	−
Viral factor	Function of the viral factor	Impact on HIV-1 infection 1, cell-function or viral toxicity 2
Nef	Targets tubulin-deacetylase HDAC6 to stabilize MTs, HIV-1 Pr55Gag and Vif proteins, assuring virus production and the infection capacity of HIV-1.	+
Pr55Gag	HIV-1 Pr55Gag uses MTs-dependent cellular machinery to traffic to the cell-surface in a SOCS1-dependent manner.	+
Tat	Interacts with tubulin leading to the alteration of MTs dynamics and the activation of a mitochondria-dependent apoptotic pathway. Tat uses Bim to facilitate this MTs-associated cell-death signal.	*
Vpr	Modulator of the MTs-dependent endocytic trafficking, negatively affecting phagosome biogenesis and maturation.	*

¹ (+) represents the promotion of HIV-1 replication. (−) represents inhibition of HIV-1 replication. ² (*) represents alteration of cell function or viral toxicity.