HIV infects cells of the immune system, particularly T CD4 helper cells.
Interaction of viral proteins with the cell, modulate many signaling pathways in the
immune system. This interaction facilitate to the HIV replication, trafficking and
infection. The starting point in signaling pathways is the attachment of HIV envelope
protein gp120 to the CD4 receptor and CCR5 or CXCR4 coreceptor. Such events result
in calcium fluctuation and activation of various Protein Kinase C (PKC) isoforms.
Moreover, it was reported that gp120 mediates chemotaxis and actin cytoskeleton
rearrangement. After the integration of the provirus and gene expression, HIV
regulatory and accessory proteins modulate the enzymatic activity of some of the
protein kinases. Accessory proteins induction of G2 cell cycle arrest is found to reduce
human immune functions through protection against T-cell clonal expansion that would
optimize cellular environment for maximal viral replication. Also induced cell cycle
arrest via a DNA damage-sensitive pathway in HIV infection has been shown. HIV
infects and induces apoptosis of circulating CD4 T and CD34 multi-potent
hematopoietic progenitor cells.
Keywords: ATM, Caspase, CCR5, CXCR4, gp120, Lymphocyte-specific protein
tyrosine kinase, Negative factor, Nuclear factor (NF)-κB, Phospholipase C,
Signaling pathways.